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The Sun Research Project

May 5th 2015

Brian Rose

The sun is the most vital component of our solar system, but many people know very
little about it and the full effects of its rays. It warms our planet every day, provides the
light by which we see and allows for life on earth, but from a dermatological standpoint
also has a wide array of undesirable side effects. This research paper will examine how
ultraviolet rays affect us, how sunscreen works, and how it is measured.
How do UVA and UVB affect us?
The sun emits a spectrum of radiation that spans from infrared to ultraviolet. Light
within the visible portion of this spectrum has wavelengths ranging from 380 to 780
nanometers (nm). The ultraviolet band of the spectrum spans 100 to 380 nm, this short
wavelength, high-energy radiation is able to interact with human cells, initiating and
accelerating reactions and biochemical processes in the human body, some of them
beneficial, others detrimental. (Dash, 2009)
Ultraviolet or UV radiation is part of the electromagnetic spectrum that reaches the
earth from the sun. These rays come from variety of sources including the sun, tanning
beds, and fluorescent lights. (Xu, 2001) UVA wavelengths are outside of the visible
spectrum, making it invisible to the naked eye. These rays play an important role in
conditions such as photoaging, cellular DNA damage, genetic mutations such as cancer,
and the synthesis of melanin. UV wavelengths are classified as UVA, UVB, or UVC each
with different defining characteristics and wavelengths.
UVA rays have the longest wavelength at 320380 nanometers. (Xu, 2001) This
radiation is responsible for dermatoheliosis or photoaging (UVA=aging) and the
tanning effect produced when the body produces melanin to absorb the suns rays. UVA
rays account for up to 95% of the UV radiation reaching the Earths surface. These rays
have the ability to pass through the ozone layer, reaching the earth, and even deep sea
layers of the ocean. They are present with relatively equal intensity during all daylight
hours throughout the year. (Dash, 2009)UVA rays can penetrate through clothing,
clouds and glass. UVA rays contribute to skin aging and wrinkling because they are able
to penetrate into the dermis, whereas UVB rays can only reach the epidermis.
UVB rays have a wavelength of 290 nm - 320 nanometers and are the primary cause of
skin reddening and sunburn (UVB=burning). These rays tend to damage the skin's
superficial epidermal layers. This radiation plays a key role in the development of skin
cancer but can also contribute to tanning and photoaging. These rays are somewhat
filtered by the ozone layer but the majority penetrates through. UVB rays do not
significantly penetrate glass, clothing or other materials. This wavelengths intensity

varies by season, location, and time of day. The most significant amount of UVB hits
Canada between 10 AM and 4 PM from April to October. (Fourtanier, 2008) However,
UVB rays can burn and damage your skin year-round, especially at high altitudes and on
reflective surfaces such as snow or ice, which reflect approximately 80 percent of the
rays.
UVC rays have the shortest wavelength, 100-290 nanometers and are the most
dangerous and damaging of all UV rays. These rays have the shortest wavelength and
the most energy of all UV rays; thankfully these rays do not reach the earths surface
because they are completely absorbed by the ozone layer. However astronauts are at risk
of this type of radiation, through a process called electroplating the astronauts visor is
covered in a thin layer of gold to protect from solar radiation. (Xu, 2005)

Photo
courtesy
of
skincance
r.org/prev
ention

Skin color in humans is primarily due to


the production of melanin, polymers of
oxidized tyrosine that form dark-colored
granules in the skin. (Dash, 2009)This
pigment is dark brown colored, giving it
the ability to absorb UV light and protect
the skin beneath it from DNA damage.
Because of this protective ability,
melanin is known as a photoprotectant, a
substance that can protect an organism
from damage caused by the absorption of
photons from a radiating source,
particularly the sun. (Dash, 2009)

Melanin provides an important function in human biology but also plays a role in many
other organisms of the animal kingdom. In the same way that melanin provides skin and
hair colour, it also provides the colour of birds plumage, amphibians and reptiles
skin/scales, and other animals fur. Pigmentation in animals provides bright colours that
attract mates in the animal kingdom and is used for camouflage. Squids also release an
ink composed mostly of melanin to distract and confuse its predators.
In humans; skin, hair and eyes contain all contain melanin. This pigment is produced by
melanocytes, special skin cells located in the basal layer of the epidermis. The process of
melanin production in the skin is called melanogenesis, and is initiated after cellular
damage following exposure to UV radiation.
Melanogenesis is the production of melanin by specialized cells called melanocytes.
(Knowland, 1993) About 5-10% of the cells in the epidermis layer of the skin are

melanocytes. Upon exposure to UV radiation, DNA within the cells nucleus becomes
damaged; this triggers cytokines, molecules that communicate with other cells, to
stimulate melanin production. Melanin synthesis begins in the liver where
phenylalanine is converted to tyrosine. (Xu, 2001) The oxidation of L-Tyrosine to LDOPA is then catalysed resulting in L-DOPA oxidizing to DOPAquinone. (Dash,
2009)This product then produces either eumelanin or pheomelanin in granules
dispersed throughout the body. Eumelanin is found in the hair, skin and irises/pupils
and is very dark brown in color. Pheomelanin is also found in the hair and skin. This
type of melanin is pink or red in color and is less effective against UV radiation. These
pigments form a protective covering in the inner layers of the epidermis, absorbing UV
rays and inhibiting cellular DNA damage.
Light-skinned people have a low basal level of melanogenesis taking place. They are
prone to skin damage from the sun because of their lack of melanin. (Xu, 2001) People
with darker colored skin produce much higher levels of the pigment and have a much
greater degree of natural protection from the sun. (Xu, 2001) These differences in skin
color originated from the evolution of ancestors in areas with differing amounts of
sunlight and UV radiation.
If melanin ever fails to completely absorb ultraviolet radiation and DNA is damaged, a
second chemical process is activated. Apoptosis or programmed cell death occurs every
day in the human body when cells are defective or unhealthy. (Hughes, 2013)When UV
radiation penetrates into cells it damages cellular membranes which could cause
irregular cell division and mutations potentially leading to skin cancer and other
diseases harmful to the bodys health. (Hughes, 2013) This damage is recognized by the
body which sends signals to kick-start apoptosis.
When apoptosis takes place proteins called caspases break down the cellular
components needed for survival (nucleus, mitochondria), and produce enzymes known
as DNases, which destroy the DNA in the nucleus of the cell. (Haywood, 2003)
Macrophages then clean away any debris leaving no trace of the original cell. This
process prevents future complications by preemptively removing any threats.
Ultraviolet DNA damage can be usually counteracted with DNA repair, melanogenesis,
apoptosis and sometimes free radical neutralization; however if all of these response
mechanisms fail then skin cancer can occur. (Haywood, 2003) The process in which
skin cancer develops by way of ultraviolet radiation is called photocarcinogenesis.
(Reisz, 2004) Malignant skin tumors are the most common tumors in humans and their
incidence is steadily increasing in our country and worldwide in the last decades.
Although a lot of factors may contribute to the development of skin tumors such as
ionizing radiations, viruses, arsenic, tar derivatives, genetic factors, immunologic status
and others, the most important environmental factor is the ultraviolet radiation from

the sunlight or from artificial sources.(Reisz, 2004) In recent years several studies have
been performed to investigate the role of UVR in tumorogenesis which demonstrated
they can cause irreversible changes in cell genetic material, initiation, promotion and
progression of tumors. So, exposure to UVR induces photocarcinogenesis which plays a
key role in the development of the three most common types of skin cancer: basal cell
carcinomas, squamous cell carcinomas, [collectively named non-melanoma skin cancer
(NMSC)], and melanomas that derive from melanocytes. (Cho, 2007) All of these skin
cancers are usually formed with increased exposure to sunlight, increase with age and
susceptibility related to skin pigmentation.
Photocarcinogenesis is a complex multistage process involving mutation of DNA genes
and the transformed cells escape from immunosurveillance and undergo clonal
expansion. (Dash, 2009) UVB photons are directly absorbed by nuclear DNA of
keratinocytes with transfer energy, causing its damage. If mutagenic photoproducts are
not repaired before DNA replication they will lead to mutation in cancer relevant genes,
almost always producing thymine dimers; before mutating into lesions which eventually
manifest as one of the three main types of skin cancer.
The type of skin cancer is determined by where the tumor lies in the skin. Squamous cell
carcinoma occurs on the surface layer of skin, or in the squamous cells. (Dalerba, 2007)
Basal cell carcinoma occurs slightly deeper, in the basal cells. Both of these cancers
occur within the epidermis and are both classified as nonmelanomatous skin cancers,
which are less severe than melanoma. (Dalerba, 2007)Melanoma occurs within the
melanocytes which are responsible for melanin synthesis.
What products are available for sun protection around the world?
The effects of UV radiation cause a multitude of problems including burns,
dermatoheliosis, and skin cancer. Fortunately companies have developed cosmetics to
combat these effects before they happen. Sunscreen is defined as a topical product
containing UV filters that absorb or reflect ultraviolet radiation preventing future
damage. (Uyama, 2005)
The active ingredients in sunscreen are known as UV filters. There are two main
subgroups of these filters, physical and chemical. Both achieve the same results;
protecting the skin from UV rays, but by different methods.
Physical filters work by sitting on top of skin and either reflecting or scattering UV rays.
Zinc oxide and titanium dioxide are common examples of this type of filter. Zinc oxide
can block against both UVA and UVB rays, covering the whole spectrum, while titanium
dioxide only delivers protection from UVB rays. Both ingredients work well, but have a
tendency to leave a white cast on skin.

Chemical filters work by converting UV radiation into harmless energy. As their


chemical bonds absorb UV radiation, components of the sunscreen slowly break down
and release heat. (Hughes, 2013) Common ingredients of this type of filter are
avobenzone, oxybenzone, Tinosorb M, Tinosorb S, Mexoryl SX and Mexoryl XL.
Chemical sunscreens tend to use a combination of ingredients to protect against the full
spectrum of UV rays. Most chemical filters offer both UVA and UVB blocking
capabilities and photostability; however Avobenzone tends to degrade upon exposure to
light. Many sunscreens will often use a combination of both physical and chemical UV
blockers to achieve optimal results.
COMMON UV FILTERS
PHYSICAL
FILTERS
(Inorganic
Sunscreen
Filters)

Active Ingredient
Zinc Oxide (ZnO)

Range
UVB,
UVA1,
UVA2

Max %
25%

Function
Absorbs and
blocks UVA and
UVB rays and
therefore is
considered
broadspectrum

Notes
Photostable; Less likely
to cause irritation;
Responsible for a
sunscreens white
cast; FDA approved.

Titanium Dioxide
(TiO2)

UVB,
UVA2

25%

Other Names:
- CI Pigment white 6
- Titanium peroxide
- CI 77891
- Pigment white 6
Avobenzone

Reflects and
blocks UVA and
UVB rays,
however, it
doesnt protect
against the
whole range of
UVA rays.

Photostable; Less likely


to cause irritation but
may cause breakouts for
some people;
Responsible for a
sunscreens white
cast; FDA approved.

UVA1

3%

Absorbs full
spectrum UVA
rays

Very photounstable;
Degrades in light; Oilsoluble; Tends to be
unstable when there is
octinoxate; Can be
stabilized by Tinosorb,
Meroxyl SX, and other
UV filters or photostabilizers; Not
irritating to skin; FDA
approved

UVA1,
UVA2

3%

Absorbs UV
rays, then
releases the UV
rays as thermal
energy; No skin
penetration

Photostable; Watersoluble; Doesnt protect


against the entire UV
spectrum; FDAapproved Patent held by
L'Oral

UVA2

3%

Absorbs UV
rays, then

Photostable; Oilsoluble; Used

Other Names:
- CI 77947
- Nogenol
- Pigment white 4
- Zinc gelatin

CHEMICAL
FILTERS
(Organic
Sunscreen
Filters)

Graph courtesy of
skinacea.com/UVfilter

Other Names:
- Butyl methoxy-dibenzoylmethane
- Parsol 1789
- Eusolex 9020
- Escalol 517
- BMBM
- BMDBM
Mexoryl SX

Other Names:
- Terephthalylidene
dicamphor sulfonic acid
- TDSA
Mexoryl XL

Other Names:
- Drometrizole trisiloxane
- Ecamsule
Helioplex

UVB,
UVA1

6%

releases the UV
rays as thermal
energy; No skin
penetration
Absorbs UV
rays

synergistically with
Meroxyl SX; Not yet
approved by the FDA.
Helioplex is a mix of
avobenzone +
oxybenzone, a
combination that offers
broad spectrum
protection and stability;
Not water proof; Patent
held by Neutrogena;
FDA approved

Currently the best way to protect your skin is with a broad spectrum sunscreen; however
other topical products can lessen the effects of UV radiation and neutralize free radicals.
Antioxidants such as Vitamin C, Vitamin E, and Carotenoids, such as beta-carotene have
photoprotective abilities when administered topically and orally. (Hughes, 2013)
Ultraviolet radiation absorption is responsible for the production of free radicals in
damaged cells. When weak bonds split, a molecule with an odd, unpaired electron is
formed; this is called a free radical. (Fourtanier, 2008) The problem with free radicals is
that they are generally very unstable and react quickly with other compounds, trying to
capture the needed electron to gain stability. A free radical will attack the nearest stable
molecule, taking its electron and stabilizing. However, now that the other molecule has
lost electron it becomes a radical itself, beginning a chain reaction. When this process
cascades it can cause disruption within a cell. (Wardman, 2003)
Some free radicals arise normally during metabolism and they are sometimes
purposefully created to neutralize viruses and bacteria within the body. However,
environmental factors such as pollution, radiation, cigarette smoke and herbicides can
also spawn free radicals. (Wardman, 2003) Normally, the body can handle free radicals
by using antioxidants like ascorbic acid or tocopherol to neutralize them, but if
antioxidants are unavailable, or if free-radical production becomes excessive, damage
can occur; especially in later life when cell processes begin to fail. (Wardman, 2003)
The vitamins C and E are known to protect the body against the destructive effects of
free radicals. Antioxidants neutralize free radicals by donating one of their own
electrons, ending the electron donation reaction. The antioxidants dont become free
radicals after donating an electron because they are stable even after losing an electron.
These antioxidants act as scavengers, helping to prevent cell and tissue damage that
could lead to cellular damage and disease.
Vitamin E or tocopherol is the most efficient chain-breaking antioxidant available and
the primary defender against oxidation. It is used to neutralize lipophilic free radicals.

(Hughes, 2013) Vitamin C or ascorbic acid is the most abundant water-soluble


antioxidant in the body. It acts primarily in cellular fluid combating hydrophilic freeradical formations caused by pollution and cigarette smoke.
Apart from their ability to neutralize free radicals in the body, these antioxidants have
also been shown to attenuate the formation of sunburn cells, thymine dimers and other
UV-induced morphologic skin changes when applied topically and exposed to UV
radiation. (Burnett, 2011)
How is sunscreen measured, and common myths?
In regards to sunscreen, terminology is important to understand what goes on the skin,
how it functions, and why. SPF is the most common rating system of sunscreen in North
America. SPF stands for Sun Protection Factor and is a measure of a sunscreen's ability
to prevent UVB rays from damaging the skin. The number following SPF is the fraction
of sunburn-producing UVB rays that reach the skin. For example, "SPF 15" means that
1/15th of the burning radiation will reach the skin. This number is also an
approximation of how long a person can be in the sun without burning. By multiplying
the SPF factor by the length of time it takes for him or her to suffer a burn without
sunscreen you can find the amount of time before burning occurs. A person with an
average Caucasian skin tone, Fitzpatrick Scale III, takes on average 10 minutes to
develop a burn. (Burnett, 2011)If this person applies an SPF 15 sunscreen it will take
approximately 150 minutes before they burn. An alternate way to think about it is in the
percentage of UV rays each SPF blocks. SPF 15 blocks 93% of UVB rays, SPF 30 blocks
97% of UVB rays, and SPF 50 blocks 98% of UVB rays. (Burnett, 2011)
Photo
courtesy
of
photoder
matology
.com

As stated before, the SPF scale is only a measurement of UVB radiation. In North
America the label broad spectrum is used to denote that sunscreens protect from both
UVA and UVB rays. According to the Food and Drug Administration sunscreens may be
labeled broad spectrum if they provide protection against both UVA and UVB radiation
according to FDA-sanctioned test methods. Currently no scale of efficiency regarding
UVA rays is used in North America; however many other countries make use of UVA

measurement factors on their products. In Europe, Asia, and Australia different systems
are used. PPD or Persistent Pigment Darkening is a reaction used throughout Europe to
measure UVA level sunscreen efficiency. PPD readings are taken at 2-4 hours of sun
exposure. (Dalerba, 2007) The PPD method uses UVA radiation to cause a persistent
darkening or tanning of the skin instead of measuring erythema or reddening of the
skin. (Kanavy, 2007) UVA rays can penetrate further than UVB rays, reaching the
melanocytes in the basal layer of the epidermis kickstarting melanogenesis and resulting
in immediate skin darkening unlike UVB radiation. (Dalerba, 2007) The PPD method
functions similarly to SPF in that theyre both in vitro tests and represent the fraction of
UV radiation reaching the skin. Sunscreen with a PPD rating of 10 should theoretically
allow a person 10 times as much UVA exposure than usual. (Kanavy, 2007)
The American Academy of Dermatology recommends everyone uses a sunscreen every
day that is broad-spectrum, SPF 30 or greater and water resistant. Sunscreen should be
worm everyday even when it is cloudy, many people believe that clouds block and filter
out UV radiation but thats a misconception. The broken cloud effect has been
observed regularly in the last century. In this process UV rays bounce off the sides of
dense clouds and refract and scatter millions of times through the water particles
resulting in stronger UV radiation than a clear sky at ground level. (Kanavy, 2011)
A common myth often used to rationalize not wearing sunscreen revolves around
Vitamin D synthesis. Our bodies can produce some vitamin D following exposure to the
Suns UVB radiation. However, after a limited amount of sun exposure (approximately
five minutes), vitamin D production ends because the max amount has been reached.
Any further UV exposure will break down vitamin D into inactive compounds.
Furthermore, sun exposure increases your risk of skin cancer and accelerated skin
aging. The only non-damaging way to obtain vitamin D is through diet, such as leafy
greens, and supplements.
In conclusion the sun is an important part of life for humans and other organisms. Its a
critical part of the solar system but concerning dermatology it almost only has harmful
applications. Ultraviolet radiation can cause free radical damage, photoaging and skin
cancer in the human body. Therefore, everyone should wear sunscreen daily to protect
from this type of damage and lower the rising worldwide incident rates of skin cancer.

APA References
1. Dash, Madhab Chandra; Dash, Satya Prakash (2009). Fundamentals Of
Dermatology 3E. Tata McGraw-Hill Education. p. 213. ISBN 978-1-259-08109-5.
Retrieved 18 October 2013.

2. Xu, C.; Green, Adele; Parisi, Alfio; Parsons, Peter G (2001). "Photosensitization of
the Sunscreen Octyl p-Dimethylaminobenzoate b UVA in Human Melanocytes
but not in Keratinocytes.". Photochemistry and Photobiology 73 (6): 600604.
3. Knowland, John; McKenzie, Edward A.; McHugh, Peter J.; Cridland, Nigel A.
(1993). "Sunlight-induced mutagenicity of a common sunscreen ingredient."
4. M.C.B. Hughes; G.M. Williams; P. Baker; A.C. Green (June 4, 2013). "Sunscreen
and Prevention of Skin Aging" 158 (11). Annals of Internal Medicine. pp. 781
790.
5. Burnett M.E., Wang S.Q. (April 2011). "Current sunscreen controversies: a critical
review". Photodermatology, Photoimmunology & Photomedicine 27
6. "Sunscreen FAQs". American Academy of Dermatology. Retrieved July 22, 2014.
7. Haywood, R.; Wardman, P.; Sanders, R.; Linge, C. (2003). "Sunscreens
inadequately protect against ultraviolet-A-induced free radicals in skin:
implications for skin aging and melanoma?". The Journal of investigative
dermatology
8. Moyal, D.; Fourtanier, A. (2008). "Broad-spectrum sunscreens provide better
protection from solar ultraviolet-simulated radiation and natural sunlightinduced immunosuppression in human beings". Journal of the American
Academy of Dermatology
9. Fourtanier A (October 1996). "Mexoryl SX protects against solar-simulated UVRinduced photocarcinogenesis in mice". Photochem Photobiol 64 (4): 68893.
10. Meredith P, Riesz J (February 2004). "Radiative relaxation quantum yields for
synthetic eumelanin". Photochemistry and Photobiology
11. Kim, Y.-J.; Uyama, H. (15 May 2005). "Tyrosinase inhibitors from natural and
synthetic sources: structure, inhibition mechanism and perspective for the
future". Cellular and Molecular Life Sciences
12. Kanavy, Holly E.; Gerstenblith, Meg R. (2011). "Ultraviolet Radiation and
Melanoma". Seminars in Cutaneous Medicine and Surgery
13. Dalerba, P.; Cho, R. W.; Clarke, M. F. (2007). "Cancer stem cells: models and
concepts". Annu. Rev. Med. 58: 267284.
doi:10.1146/annurev.med.58.062105.204854

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