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Do sunscreens really protect us?
Do sunscreens really protect us?
As a nation our sun exposure habits have become dysfunctional. We live and
work increasingly indoors. We are only in direct sunlight for minutes a day,
shuttling between home, office and supermarket shielded by the windows of
cars, buses or trains. This low-level of UV exposure contrasts with the holiday
habits of most of the British population. The overseas holiday is so widely
accepted as an annual ritual that holidays within the UK now have a novelty to
them: where for Blair it was the Tuscany villas, now it is the Camerons’
Cornish “staycation” [1]. With the overseas holiday comes the expectation of
a tan.
In younger age groups, especially for women, there is a societal
pressure to be tanned. The cult of celebrity equates a tan with attractiveness,
desirability and health. With the indestructible feeling of youth and a belief in
modern and future medicine, the young are often cavalier when it comes to
protecting themselves from the sun, especially when the immediate payout
(for most) of a tan is socially rewarded. This phenomenon has made some
interesting news stories in recent years, including a travel firm running a
competition for photos of the worst sunburns [2], and the mother who allowed
her 5 month old son to develop sunburn necessitating hospital admission [3].
In Wales, with its notably tanned celebrities (Gavin Henson, Charlotte Church
et al.), there has been a recent push to ban coin-operated non-attended
tanning booths [4]. These booths allowed under-16s to re-use them
immediately and repeatedly, exposing themselves to levels of UV certain to
cause harm [4].
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Do sunscreens really protect us?
Why does it matter how much sun exposure we have (or don’t have)? Whilst
the public conscious is dimly aware that the sun is dangerous, the public’s
understanding of the risks is poor – perhaps why so many choose the short
term benefit of a tan, given an ill-informed weighing of the risks and benefits of
UV exposure. Over- or under-exposure to sunlight can damage our health in
a number of different ways.
Sunlight is a large sample of the electromagnetic spectrum and at the Earth’s
surface can be considered as 4 wavelength regions: ultraviolet B (UVB, 280315 nm), ultraviolet A (UVA, 315-400 nm), visible light (400-760 nm) and
infrared (760-106 nm) [5]. Infrared waves are the ‘warmth’ of sunlight and are
widely regarded as safe – infrared light bulbs are used as food warmers in
restaurants. Excluding the effects of visible light on the retina, UVA and UVB
are the biologically active components of sunlight [5]. UVB rays are of higher
energy than UVA [6]. Only a small proportion of UVB reaches the dermis and
causes injury by direct DNA damage, whereas UVA penetrates the dermis
and causes damage through the generation of reactive oxygen species [6].
The skin pathologies caused by the UV component of sunlight can be divided
into chronic and acute.
Chronic changes include photo-ageing, actinic
keratoses, keratoacanthomata and malignancies associated with UV
exposure: basal cell carcinoma, squamous cell carcinoma and malignant
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Do sunscreens really protect us?
melanoma [7].
UVA and UVB have differing roles in mediating these
changes, probably because of their different penetrations and mechanisms of
molecular injury. Sunburn is caused by UVB, but there is increasing evidence
that the other pathologies, including photo-ageing are caused by both UVA
and UVB, perhaps in synergy [8].
Sunlight can exacerbate pre-existing diseases and is often helpful in making
the diagnosis. The photosensitive rash of systemic lupus erythematosus is
the best example. Rosacea, psoriasis, Darier’s disease and herpes simplex
infections can all be worsened by sunlight exposure [9].
Acute pathologies caused by sunlight include sunburn (solar erythema) and
photosensitivity reactions which can be caused by UV or visible light. Patients
who have taken a photosensitising drug or had contact with photosensitising
plants are at particular risk.
Photosensitivity is the only dermatological
pathology that visible light is known to cause. There are a number of very
rare acute reactions to light, including polymorphic light eruption, solar
urticaria, actinic prurigo, juvenile spring eruption, hydroa vacciniforme,
photosensitive eczema, porphyrias, pellagra and xeroderma pigmentosum [9].
Proving the efficacy by comparing sunscreens (with a strong theoretical
argument for benefit and small risks [discussed later]) to placebo (no benefits,
no risks) is ethically questionable, especially for exquisitely UV-sensitive
conditions such as xeroderma pigmentosum. Achieving statistical proof is
further complicated by the low incidence of these conditions.
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Do sunscreens really protect us?
Sunscreen was developed in the 1930s answering a demand for protection
from sunburn due to the fashion for tanning in light skinned populations [10].
Early sunscreens attempted to block UVB preventing sunburn and providing
some protection from chronic UV responses. Compounds used in sunscreens
can be divided into two classes: physical or chemical blockers.
Physical
blockers (zinc oxide, titanium dioxide) reflect UV light preventing it from
reaching the epidermis [6]. Chemical blockers absorb the UV and release it at
a different, non-toxic wavelength [6]. The efficacy of sunscreen has been
measured using the sun protection factor (SPF). This measures the ratio
between the time needed to develop sunburn with and without the sunscreen.
As an example, a person using SPF15 who normally burns in 10 minutes, can
expect to burn after 150 minutes of exposure. Doubling an SPF does not half
the UV dose at the epidermis: SPF15 blocks 94% of UVB and SPF30 blocks
97% [6]. The FDA are phasing out the complicated SPF to replace it with
simpler categories of protection: low (SPF2-15), medium (15-30), high (30-50)
and highest (50+) [11]. An SPF makes no statement about the protection
conferred against UVA. There are differences in the UVA protection between
different physical blockers – with titanium dioxide inferior to zinc oxide [12] –
and a number of chemical blockers offer little or no UVA protection [13]. In
Europe, UVA protection is currently scored with a star rating, frequently
printed on the reverse of the bottle.
Epidemiological studies of skin cancer have established a strong link between
skin cancer and sunburn history [14]. Animal models of skin cancers show
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Do sunscreens really protect us?
the protective effect of sunscreen [15-17]. There is however no model for
melanoma [14].
More recently, UVA has been implicated in skin cancer
pathogenesis [18].
A similar evidence base exists for the link between
smoking and lung cancer and a number of other diseases, including coronary
heart disease [19]. In the UK, a smoking ban in 2007 resulted in a 2.4%
reduction in emergency admissions for myocardial infarction, equating to 1200
fewer admissions a year [19].
A similar result might be expected with
widespread usage of sunscreen, with the UV protection afforded by
sunscreen reducing cancer rates.
Large case-control studies report the
opposite effect, where sunscreen use is associated with an increased risk of
melanoma [14].
Population studies also show an increased rate of skin
cancer despite wider availability of sunscreen [20]. Sunscreen use by schoolaged children is associated with an increased risk of basal cell carcinoma and
more acquired melanocytic naevi – predictors of future malignant melanoma
[21-23].
One explanation for this discrepancy is that sunscreen provides
effective protection from sunburn, but not from UV-induced DNA damage [14].
Users of sunscreen spend longer in the sun, as they are protected from
sunburn and therefore feel protected from carcinogenic damage [24]. Most
sunscreens offer low protection against UVA and modest to good protection
against UVB [11]. ‘Un-blocked’ UVA might contribute to the increased cancer
rates in sunscreen users, as the delay in sunburn development (due to UVB)
allows for a larger UVA exposure.
Exposure to UV radiation does not affect only the skin.
associated
pathologies
of
the
eye,
Page 5 of 14
including
There are UV-
photokeratitis
and
Do sunscreens really protect us?
photoconjunctivitis in the short term and cataracts, pterygium and squamous
cell carcinoma of the cornea or conjunctiva with chronic exposure [25]. The
World Health Organisation estimates that of the 18 million people in the world
rendered blind by cataracts, 5% (0.9 million) are attributable to UV exposure
[25].
As mentioned earlier, herpes simplex infection of mucosal epithelium
can be exacerbated by UV light. These ‘non-skin’ UV-associated pathologies
will not be influenced by the use or otherwise of sunscreen.
Wearing
sunglasses in sunlight is an important step in protecting eyes from UV
damage and a hat will provide ophthalmological and dermatological protection
for the face and neck.
Despite the numerous pathological associations, UV exposure does have
benefits to health [25]. Vitamin D can be synthesised in the skin by the action
of UVB light on dehydrocholesterol and is a fat-soluble vitamin. There is
evidence that sunscreens can prevent vitamin D production in skin [26].
Vitamin D has two recognised biological roles. The first role is in calcium
metabolism and appropriate bone mineralisation depends on vitamin D.
Vitamin D deficiency causes rickets in children and osteoporosis and
osteomalacia in adults. These diseases carry a significant impact on quality
of life. A model of the effects of UV exposure predicted that in the year 2000
between 1.3 and 1.7 million disability-adjusted life years (DALYs) were lost to
the UV-related pathologies already discussed [7]. Modelling a UV exposure
of 0 generated the prediction of 3,304 million DALYs lost to rickets,
osteomalacia and osteoporosis [7]. From these data, UV exposure can be
considered a positive factor in global health.
Page 6 of 14
The balance for Western
Do sunscreens really protect us?
populations is probably more equivocal, as high-fat Western diets will deliver
a larger component of the vitamin D requirement.
Vitamin D’s second role is immunomodulation. The early mice studies linking
UV exposure with carcinogenesis demonstrated a UV-mediated suppression
of anti-tumour responses [27]. Transplant of the UV-induced tumours into
immunocompetent hosts resulted in tumour rejection [28].
recipients did not reject the tumours [28].
UV-exposed
Together these experiments
implicate UV-generated vitamin D as an important immunomodulator. The
immune effects of vitamin D are still not fully understood. Locally produced
vitamin D activates the innate immune system by, for example, increasing
production of antimicrobial peptides (e.g. cathelicidin) by monocytes and
macrophages [27]. Vitamin D has the opposite effect on the adaptive system,
with an inhibitory effect on T cell differentiation and plasma cell development
[27]. There are associations between a gene (CYP27B1) involved in vitamin
D metabolism and human autoimmune diseases, including type 1 diabetes
[29], linking disturbances of vitamin D metabolism with immune pathology. It
has been shown that responses to particular tumour vaccination strategies
can be enhanced with pre-vaccine UV exposure [27].
As vitamin D has
activatory and inhibitory effects on components of the immune system, it is
the balance of these effects is critical in determining the overall outcome of
vitamin D signalling. This balance is likely to be disturbed by a number of
other immunological signals, not least the presence of microbial products.
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Do sunscreens really protect us?
Immunomodulation with UV light therapy can be used in the treatment of
dermatological diseases, most notably psoriasis. Light therapy is given as a
narrower spectrum (311-313nm) of UVB than found in sunlight [27]. UVB
radiation disturbs cytokine signalling in psoriatic skin, suppressing IL-23 and
IL-17, integral parts of the Th17 differentiation pathway [27]. Narrow band
UVB probably causes little or no vitamin D production [27], and so presumably
acts independently of vitamin D. Supplementing UVB therapy with topical
vitamin D has a synergistic effect and is commonplace in the treatment of
psoriasis. UVA can also be used in light therapy, often in conjunction with
psoralen, a photosensitiser.
Can the next generation of sunscreens keep the benefits of UV exposure
whilst still mitigating its deleterious effects? There are a number of promising
lines of research. The first is examining UV protection afforded by microbial
products. Microbes have been exposed to UV light for a substantial portion of
their evolution – since the composition of the atmosphere stabilised. There
are a number of microbially produced sunscreens, including mycosporins and
bacterial melanins, which are now reaching the market for human sunscreens
[5].
Nanoparticles of zinc oxide and titanium dioxide have re-popularised
these physical barriers, as new formulations are less conspicuous [30]. Some
of these nanoparticles can be found systemically, raising the possibility of
trans-dermal drug delivery by nanoparticle carriage [30]. Perhaps the most
intriguing research is based on coral’s photo-protection mechanism.
A
mycosporin-like amino acid (MAA) sunscreen is synthesised by algae living
within the coral structure [31].
This MAA is passed to the coral host via
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Do sunscreens really protect us?
exocytosis from the algae [31], where it is presumed to prevent photobleaching.
The same MAA molecule has been identified in tropical fish,
suggesting that the MAA can travel up the food chain [32]. This is the first
description of the enteric delivery of a sunscreen. If this MAA can be massproduced, and it proves safe in mammals, this might provide a novel
approach offering better UV protection and, by being tablet-based, improved
concordance, sparing the user regular re-application after swimming,
toweling, sweating or prolonged exposure. A pragmatic alternative is to use
UV-meters to formally quantify exposure, allowing individuals to tailor their
activities for adequate vitamin D synthesis without excessive UV dosing [14].
In summary, there is no straightforward answer to the question ‘do
sunscreens really protect us?’. In principle, sunscreens provide protection
from UVB-mediated pathologies, including sunburn and - at least in vitro and
in animal models - from dermatological malignancy. They also provide some
protection for UVA-mediated pathology. The data concerning sunscreen use
by humans is more conflicting.
Perhaps sunscreen provides a false
protection, preventing sunburn and therefore allowing an increased exposure
to carcinogenic levels of UV. Responsible use of sunscreen probably does
prevent skin cancer, so the best advice to give to a single patient remains to
use sunscreen (high SPF, with UVA protection), alongside emphasizing the
importance of judicious use, hats, sunglasses and seeking shade in the early
afternoon (12-3pm). Sunscreens are not harmless, they do have the potential
to cause disease, through vitamin D deficiency.
The systemic effects of
vitamin D deficiency (rickets, osteoporosis and osteomalacia) are significant
Page 9 of 14
Do sunscreens really protect us?
sources of morbidity worldwide and their link with little or no UV exposure well
described. The World Health Organisation has predicted a larger DALY loss
with no UV exposure than with no improvements in sun protection.
Immunomodulation via local effects of vitamin D is less well understood and
could include immunosuppression or autoimmune disease predisposition.
Light therapy suggests the existence of other immunomodulatory pathways
independent of vitamin D. Whilst appropriate use of sunscreen does protect
us from dermatological malignancy, whether they provide a definite overall
health improvement is unclear. This assessment hinges on the possibility of a
undefined immunomodulatory pathway independent of vitamin D, alongside
our growing understanding of vitamin D and its immunological function.
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