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.