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Skin Cancer Induced by Pollution-Mediated ROS

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Handbook of Oxidative Stress in Cancer: Mechanistic Aspects

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Abstract

The incidence of skin cancer is indeed alarming. More people are diagnosed with skin cancer each year than all other cancers combined. In the USA, one in five will develop skin cancer by the age of 70; each year, more than 24,000 Americans die of skin cancers – the most lethal of which are increased by environmental pollution. Physicians have realized for decades that UVB initiates skin cancer, but only recently have medical researchers learned that UVA interacts with airborne pollutants synergistically to initiate and promote skin cancer. Also, ubiquitous environmental pollutants – including ozone, polycyclic aromatic hydrocarbons (PAHs), nitrogen oxides, volatile organic compounds (VOCs) – generate reactive oxygen species (ROS) which oxidize epidermal lipids, inducing a cascade of cellular stress reactions that can initiate skin cancer. Furthermore, environmental toxins are carried on the surface and within the core of particulate matter (PM). This PM can be absorbed cutaneously to deep epidermal layers and can enter the dermis through hair follicles as well as via blood flow after respiratory pulmonary absorption. The xenobiotic pollutants act by binding to the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor found in all types of skin cells – keratinocytes, melanocytes, fibroblasts, and dermal dendritic cells. For full protection from the environmental damage (extrinsic aging and skin cancer), certainly sunscreens that filter UVA as well as UVB are necessary, but sunscreens are not enough! To combat the dangerous oxidative damage induced by airborne pollutants, correctly formulated topical antioxidants can effectively protect.

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Abbreviations

4-ABP:

4-aminobiphenyl

ARNT:

AHR nuclear translocator

AHR:

aryl hydrocarbon receptor

AHRR:

AHR repressor

BaP:

benzo[a]pyrene

BCC:

basal cell carcinoma

bFGF:

basic fibroblast growth factor

BPDE:

BaP diol epoxide

CAP:

concentrated ambient particles

CO:

carbon monoxide

COX-1, −2:

cyclooxygenase-1, −2

CPD:

cyclobutane pyrimidine dimer

cSRC:

“cellular sarcoma,” photo oncogene tyrosine-protein kinase

CYP:

cytochrome P450

EGFR:

epidermal growth factor receptor

ERK-1,-2:

extracellular signal-regulated kinase-1,-2

FICZ:

6-formylindolo[3,2b]carbazole

GPx:

glutathione peroxidase

HNE:

4-hydroxy-2-nonenal (protein adduct)

H2O2:

hydrogen peroxide

HSP-27,-32,-70,-90:

heat shock proteins-27,-32,-70,-90

ICAM:

intercellular adhesion molecule

IcdP:

indole [1,2,3-cd]pyrene

Iℓ-1α,-1b,-8:

interleukin-1α,-1b,-8

LDH:

lactate dehydrogenase

MAPK:

mitogen-activated protein kinases

MCP-1:

monocyte chemoattractant protein-1

MED:

minimal erythema dose

MMP:

matrix metalloproteinases

NF-κB:

nuclear factor of kappa-light-chain polypeptide gene enhancer in B-cells

NNN:

N-nitrosonornicotine

NOx:

nitrous oxide

NO2:

nitrogen dioxide

NRF2:

nuclear transcription factor (erythroid-derived 2)-like2

8-OHdG:

8-hydroxy deoxyguanosine

O3:

ozone

PAH:

polycyclic aromatic hydrocarbons

PM:

particulate matter

PM10, PM2.5:

PM with diameter ≤10 μm, ≤2.5 μm

ppm:

parts per million

PR:

progesterone receptor

PRE:

progesterone response element

PRP:

progesterone receptor + progesterone complex

PUVA:

psoralen plus UVA

RHE:

reconstructed human epidermis

ROS:

reactive oxygen species

SCC:

squamous cell carcinoma

SOD-1:

superoxide dismutase-1

TCDD:

tetrachlorodibenzo-p-dioxin

TGF-β:

transforming growth factor β

TIMP:

tissue inhibitors of metalloproteinases

TNF-α,-β:

tumor necrosis factor-α,-β

Trp:

tryptophan

UFP:

ultrafine particles (<100 nm)

UV:

ultraviolet

VCAM:

vascular cell adhesion molecule

VOC:

volatile organic compounds

WHO:

World Health Organization

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Acknowledgments

The author thanks Xueyan Zhou, MD, MS, for research assistance and Heather Nolan, MA, for excellent artistic rendition of the figures, research assistance, editing, and typing.

Conflicts of Interest

The author declares no conflict of interest with any aspect of the publication.

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Authors and Affiliations

  1. Department of Dermatology, The Mount Sinai Icahn School of Medicine, New York, NY, USA

    Karen E. Burke

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  1. Karen E. Burke
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Editors and Affiliations

  1. Department of Biochemistry and Biophysics, University of Kalyani, Kalyani, West Bengal, India

    Sajal Chakraborti

  2. Department of Veterinary Pathobiology, University of Missouri, Columbia, MO, USA

    Bimal K. Ray

  3. CSIR-Indian Institute of Chemical Biology, Kolkata, India

    Susanta Roychoudhury

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Burke, K.E. (2022). Skin Cancer Induced by Pollution-Mediated ROS. In: Chakraborti, S., Ray, B.K., Roychoudhury, S. (eds) Handbook of Oxidative Stress in Cancer: Mechanistic Aspects. Springer, Singapore. https://doi.org/10.1007/978-981-15-9411-3_2

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