Can Using a Sunscreen Be Worse than Using a Tanning Bed? The Health Implications of a UVB Biased Sunscreen.

The New Study that Shows How a UVB Sunscreen Can Be Worse than a Tanning Bed

The Role of Long Wave UVA in Skin Cancer

There is an unrelenting rise in skin cancer rates in North America with an annual increase around 2-3 % over the past 3 decades. In the UK there was an alarming increase of 40% in the past 4 years. Empirical analysis of global skin cancer rates suggest that rates are levelling off or decreasing in countries with higher UVA-Protection Factor (UVA-PF) levels in sunscreens (2015 Sunscreen Symposium, Florida, September 2015). The compelling evidence for the primary role of UVA - particularly the UVA1 or longwave UVA -  in the genesis of skin cancer – comes from a number of scientific studies over the past 15 years (Halliday 2002, Agar 2004, Noonan 2012, Rünger 2012). This is logical and intuitive as UVA is more abundant than UVB and penetrates deeper into the skin.

The primary objectives of photoprotection  must be to prevent rising rates for skin cancer, reduce health care expenditures for a disease with potentially preventable aspects, and to reduce other effects of UV radiation, like photoaging and immune suppression. The continual 2-3% annual rise in skin cancer rates for North America shows that the current approach has failed. Critical analysis argues that ineffective UVB biased sunscreens are an important contributory factor. Cancer prevention and immune protection  from sunscreens in humans is dependent on protection from UVA and cannot be predicted from the SPF (sun protection factor), more a measure of UVB attenuation.

There is  a logical and evidence-based argument that the exclusive use of balanced sunscreens, which provide spectral homeostasis or uniform protection at every wavelength can reduce cancer rates and photoaging. The current  science confirms that UVB causes direct DNA damage, whereas UVA results in direct DNA damage and indirect effects from ROS (reactive oxygen species), photoimmunosuppression, and disruption of repair mechanisms.  UVB initiates and modulates the damage cycle but UV (particularly UVA1) completes the process. Photoprotection with traditional UVB biased sunscreens with little or no UVA protection must now be abandoned and a new clinical strategy adopted by doctors and as a public health policy.

How Can A UVB Biased Sunscreen Do More Harm than Good?

There is another powerful bit of evidence that implicates the widespread use of UVB-biased sunscreens, with little or no UVA1 protection, in rising skin cancer rates and visible photoaging at younger ages. Daily use of UVB biased sunscreens that dominate the market, exposes the patient to asymmetric UVA1 radiation, similar to a tanning bed. More people develop skin cancer because of tanning than develop lung cancer because of smoking. One indoor UV tanning session increases users’ risk of developing squamous cell carcinoma by 67 percent and basal cell carcinoma by 29 percent. People who first use a tanning bed before age 35 increase their risk for melanoma by 75 percent.  

There is an important  parallel between the asymmetric UVA1 from tanning bed exposure and using a UVB-biased sunscreen, either on vacation or every day. This crucial fact escapes our regulators, most physicians including dermatologists, and the cosmetic industry. 

Vacation exposure over 2 weeks with typical sunscreens for protection could be double the radiation received from 10  eight minute tanning bed exposures. In extreme cases of recreational sun exposure where sunscreens providing suboptimal broad-spectrum protection are used, the UV insult to the skin is likely to result in higher cumulative exposures than commonly employed sunbed practices (Diffey et al).

This occurred to me several years ago but the science and physics was beyond my capability. I kept asking Uli Osterwalder- one of the authors in the study and a friend- about this obvious concern, until they finally did the calculations. It is a computer derived analysis that suggests the wrong sunscreen - UVB-biased - may be more dangerous than tanning bed exposure. Both provide asymmetric UVA radiation to your skin. There is another cautionary aspect to this. The vacation model is more acute and intense but what about everyday exposure if using a UVB-biased sunscreen? Many outdoor occupations reach or exceed the vacation exposure.

If tanning beds cause higher risks for skin cancer, then providing a patient with a UVB biased sunscreen that gives a similar UV radiation profile, relative to the right conditions of exposure and time, should also be considered as an undesirable measure. For doctors involved with rejuvenation, prescribing a balanced sunscreen that gives adequate UVA1 protection is a responsible practice standard. This is an integral part of post treatment care after rejuvenation procedures. Without balanced protection, the patient resumes accelerated photoaging from UVA1 exposure and the  treatment benefit is quickly lost. Repeat treatments will then be required more quickly. 

What Is A Better Alternative?

Adequate but safe UVA1 protection is only attainable with filters like zinc oxide (>20%), zinc oxide (>15%) plus 7.5% titanium dioxide or encapsulated octinoxate, bemotrizinol, and bisoctrizole – insoluble particle type filters with no entry into our bodies. Regrettably,  the last two safe and highly effective insoluble particle filters, have yet to be approved by Health Canada and the FDA, despite their global use in every other country over the past 15 years.

Most UVB-biased sunscreens use the soluble filters that penetrate skin into blood and even tissues like receptors in the brain. The group includes oxybenzone (benzophenone), homosalate, octisalate, octocrylene, non-encapsulated or regular octinoxate, and 4-methyl benzilidene camphor. They are more active in UVB and shortwave UVA (UVA2). Some UVA1 activity comes from avobenzone, another soluble filter that obtains tissue levels. It enters the body and is unstable in sunlight. Most parents and pregnant women are unaware that these filters (used in over 80% of our sunscreens) gain entry to our bodies, reason enough to avoid them.

There is a principle in endocrinology – isoform function – whereby chemicals with the same structure likely bind to the same hormone receptor and generally have the same effects. Hence avobenzone and octisalate very likely exert the same toxic effects as oxybenzone and homosalate, known to be hormone disruptors. Oxybenzone and its structural cousin avobenzone are now the leading causes of photocontact allergy (Warshaw 2012). A 2015 report (Downs et al) confirms other studies over the past decade that oxybenzone washing of sea-bathers is genotoxic, kills larvae of reproducing coral, and converts the planula from a motile to a sessile state by ossification. Oxybenzone found in 65% of our poses a hazard to coral reef conservation and threatens the resiliency of coral reefs to climate change.

Recommendations for Practitioners and Consumers:

You are faced with a simple choice in selecting a safe and effective sunscreen:

·       UVB- biased products with tiny soluble organic filters that give incomplete protection (inadequate UVA1 protection) and are implicated with adverse effects on our health and the environment. They are likely a root cause of rising cancer rates and early photoaging.

·       A balanced or truly broad spectrum sunscreen using insoluble filters, large particles that remain on the skin, have no known adverse effects on human health or the environment, and give you better protection, where the right combination can approach that of textiles and staying out of the sun.

·      Balanced sunscreens using insoluble particle type UV filters with no entry into blood of mother or fetus are safe to use in pregnancy. More egregious to me, is the fact that nearly all physicians fail to advise pregnant women and parents about percutaneous absorption of soluble filters and their possible hormone disrupting and carcinogenic effects. As a former obstetrician, I appreciate the persuasive simplicity that anything safe to use in pregnancy is safe to use for everyone.

The Latest Science in Sunscreens and Protection: What You Need To Know

For this third post, I thought I would pass on interesting and relevant scientific news from recent meetings I attended with my wife, Dr. Sharyn Laughlin. The Annual Meeting of the Photomedicine Society and the Annual Meeting of The American Academy of Dermatology were held in March 2014.

More evidence was presented by Dr. Thomas Ruenger for the role of UVA in inducing enzymes that promote the breakdown of collagen and elastin as an important mechanism for photoaging. The findings presented also show that the effect of longwave UVA is the most pronounced and much greater than the effect of UVB. Over the past decade, there has been a volume of evidence from scientific studies that confirm the important effect that UVA has on photoaging and the induction of cellular damage, leading to all forms of skin cancer. This should come as no surprise to anyone – including those who still do not acknowledge the inherent dangers of UVB-biased sunscreens that give unbalanced protection, and allow the effects of UVA to be mostly unabated and cumulative.

Our Skin: A Work of Art Worth Saving

Not everything in science needs a study. Many definitive studies cannot be done in humans for ethical and practical reasons. Sometimes critical thinking, cognitive analysis, deductive reasoning – fancy terms for common sense – is all that is required. UVA penetrates to the deeper dermis where the important elements regulating genetics, immunity, and cell function reside, while UVB barely penetrates through the epidermis. UVA is ubiquitous, essentially the same at any latitude and time of day, and is 15-16 times more potent than the dose of UVB that only accounts for 5% of the UV band. It should be logical that the adverse effects of UV radiation may have more to do with UVA than UVB. Erythema or redness of the skin, the first sign of sunburn, and the eventual sunburn, is commonly believed by many people (even some physicians), to be UVB (290-320 nm) mediated skin damage, with a minor contribution from UVA-2 (320-340 nm). It is the basis of the sun protection factor (SPF) that is a label standard that indicates the degree to which a sunscreen reduces the sunburn reaction. The new labelling rules to be adopted in N. America changes the meaning of SPF to denote sunburn protection factor, a more accurate definition. It should convey to the consumer that SPF is a measure of the sunscreen’s ability to reduce or protect from sunburn but is not an adequate measure of protection to other adverse effects of the sun. The erythema-sunburn reaction and its genesis is actually more complex and is also related to UVA-1 effects.

Anyone who has had a sunburn by not applying a sunscreen on a very cloudy day has experienced a UVA sunburn. It is a deeper burn and much more painful that the usual sunburn that starts with UVB initiation. A sunscreen that completely blocks only UVB will not always prevent sunburn and over time a gradual or delayed sunburn develops to the UVA part of the sun. UVB is more efficient in causing sunburn and produces the immediate redness. UVA accounts for 95% of UV exposure and this higher absolute amount contributes to erythema. The early or mainly UVB initiated sunburn reaction, is a protective response telling you to get out the sun when the damage is early and more superficial. Continued sun exposure, even with a sunscreen of high SPF, but minimal UVA-1 protection, eventually leads to a more severe sunburn and the deeper damage that causes irreversible consequences- photoaging and the DNA changes that may lead to cancer many years down the road. SPF values > 15 can only be attained if the UV filters used are reducing transmission of UVA-2 and UVA-1, but is primarily a measure of UVB attenuation.

Industry consultants continue to push the trend arguing for high SPF sunscreens with values > 50 even approaching 100. There is a minor photometric basis for using a higher SPF. Looking at the transmission, rather than what is blocked does show that SPF 30 gives twice the protection than SPF 15, a SPF 60 twice that of SPF 30 and four times SPF 15. An SPF 15 blocks 93.3% of incident UV compared to 96.6% with SPF 30, a difference of 3.3% for doubling the concentration of filters. However, considering what gets through by counting photons of light shows that only half the amount gets through with the higher SPF. The higher SPF also compensates for the lower application amounts used by consumers in practice than the amount applied for laboratory SPF testing. There is some truth in a consumer thinking that a higher SPF allows you better protection and a SPF 30 allows you to stay out twice as long as a SPF 15. The danger is that the higher SPF will have some UVA protection but not nearly enough, if it does not contain one of the limited number of filters that give adequate UVA-1 protection. I am cynical enough to think that industry pushes high SPF sunscreens knowing that the public assumes they are better in every respect. Given a choice between a SPF 30 and a SPF 50, always select the more balanced sunscreen with better UVA-1 protection. This is easy to do in the UK or Europe. Look for Boots 4 or 5 stars in the UK or a UVA-PF to SPF ratio of > 1/3 in Europe. The more this ratio approaches 1, the better the sunscreen is for affording you balanced and proper protection. North American consumers have no such ability  to use the label metrics for selection. The new rule of using a Critical Wavelength (CW) of 370 nm or greater as proof of truly broad spectrum activity, particularly the most important UVA-1 extinction, will not necessarily be valid.

The CW is a measure of the wavelength at which 90% of the area under the absorption or extinction curve occurs. This relates to broad spectrum activity as to achieve this CW of 370 nm, usually requires a significant UVA absorbance. However, the threshold of 370 nm can be attained by some sunscreens with little overall UVA-PF, particularly in the more problematic UVA-I spectrum approaching 400 nm. Sunscreens with low UVA-PF  and those with moderate UVA-PF can both have the same CW of 370 nm. The shape of the extinction curve is a factor and a UVB biased sunscreen SPF 30, with inadequate or a low UVA-PF  < 10 can attain the same CW of 370 nm as a sunscreen with UVA-PF of ≥ 10. One would fail the EU criteria but both would pass in the USA and Canada, under new regulations being enforced this year. My preference for adequate UVA protection is that SPF 30 values should have a UVA-PF exceeding 20 with the ratio approaching 1. More about these considerations in a later post.

The other important topics discussed at these meetings included the use of anti-inflammatory(AI) agents

Can a diet rich in anti-oxidants protect you from the sun?

or antioxidants (AO) in sunscreens, and the role for oral photoprotection as a component of a sun protection strategy. The use of AI ingredients will be discussed in detail in a future post. Dr. Salvador Gonzales  reviewed the present status of oral nutrients that afford some measure of UV protection, and its use in oral photoprotection is increasing in Europe at an annual rate of about 5%. He also reminded us that a lifetime UV radiation exposure is attained 1/3 through vacation, compared to 2/3 from every day or non-vacational time. This supports our view that a balanced sunscreen is for daily use all year round. In addition 70-80% of sunburns occur can occur in your backyard. Dr. Mary Matsui presented evidence that certain nutrient and botanical ingredients applied on the skin are a source of non-sunscreen photoprotection. The list of useful agents for oral or topical photoprotection is extensive. Some of these and other agents also may reduce skin damage from visible light (400-770 nm) and near infrared (IRA at 770 -1400 nm), now shown to be relevant in addition to UV in the genesis of adverse effects from sunlight. This an area I am presently researching at CyberDERM. While developing a balanced sunscreen that mimics the UV protection afforded by black clothing or shade, we are identifying the single best antioxidant to add to the formula. Some of the effects of UV and IRA on inducing immune suppression may also be reduced by oral therapy. Longer wavelengths UVA-1 near 400 nm and visible through IRA at 400- 1400 nm, tend to produce deeper damage to the dermis. Oral antioxidants may be more rational and efficient than topical application. The concept of skin therapy from within via the dermal blood vessels is not new. I recall an ad-campaign from many years ago- “have you taken your skin care today”? For therapy to cell damage in the dermis, ingestion and delivery by the dermal blood supply seems more logical than topical administration, which requires absorption through the epidermis, and the agent is not always sure to reach the deep dermis. We are also working on an antioxidant mix for oral supplementation that best achieves all the objectives. For now it appears that taking 2 Gms. of Vitamin C and 1200 IU of Vitamin C increases the minimal erythema dose –  the visible sign of sun damage – by 20% after 1 week and 40% at 3 months (Gonzales et al). Flavonoids and the subgroups- anthocyandins, catechins, flavonols, and isoflavones – all play important roles in modulating and inhibiting the various adverse effects. A diet rich in blue and red berries, red or purple grapes, 1-2 glasses of red wine/day, dark chocolate, green and white teas, apples, broccoli, onions and scallions, kale, soybeans, hot peppers, apricots and celery, provides Flavonoids. This diet with Vitamin C and E as described above may be a useful adjunctive measure to using a balanced sunscreen and sun avoidance  for those at greater risk of cancer and photodamage. These nutrients, along with ingesting curcumin, resveratrol, and pomegranate, are already recommended for a myriad of health benefits. Skin cancer is considered an occupational disease in some provinces of Germany, and in Canada we need a National Occupational Strategy for those involved in outdoor work. For these workers and anyone at higher risk for skin cancer, a dietary approach as outlined is a complementary and responsible self- help initiative.