Potential health risks of sunscreen

It has been suggested that this article be merged into Sunscreen. (Discuss) Proposed since April 2008.

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Sunscreen protects against two common forms of skin cancer, squamous cell carcinoma (SCC) and basal cell carcinoma (BCC), and several sunscreen ingredients protect against tumor development in photocarcinogenicity tests in mice. However, there is some evidence, largely arising from correlational studies and in vitro experiments, that particular sunscreen ingredients (such as oxybenzone, benzophenone, octocrylene, or octylmethoxycinnamate) may be linked to increased risks of malignant melanoma, a rarer but more deadly form of skin cancer. It has also been linked to Vitamin D deficiency.[1] The broad areas of concern are:

• potentially carcinogenic properties of some sunscreen ingredients
• Vitamin D deficiency caused by reduced exposure to ultraviolet light
• incomplete protection against the full ultraviolet spectrum combined with increased time spent in the sun

This leads to a sunscreen controversy within the academic community. It is known that some sunscreens only protect against UVB radiation, and not against the more dangerous UVA spectrum. A number of class-action lawsuits allege that sunscreen manufacturers misled consumers into believing that these products provided full sun protection. The vitamin D hypothesis is not as widely accepted but continues to generate scholarly debate. Most health authorities and medical associations have concluded that on the whole, sunscreen use is beneficial, but there is not yet a thorough consensus.

Malignant melanoma has been found more frequently in sunscreen users compared to non-users in some studies.^[1] Other studies found fair skinnned people used more suncreen and had more skin cancer, but did not address cause and effect.^{[2][3][4][5][6][7]} A meta-analysis of 9067 patients from 11 case–control studies found no association between sunscreen use and development of malignant melanoma. It was suggested that sunscreens block the natural warnings and adaptations mediated by UVB, but allow damage from UVA to go unchecked^[8].

However, these claims could not be supported in three meta-analyses.^[9][10] (Huncharek and Kupelnick, 2000, Annals Epidemiol. vol. 10, p. 467.)

The only evidence suggesting a relationship between sunscreen and melanoma is correlational, and thus cannot be used to establish a causal relationship.

Even though it is rare, malignant melanoma is responsible for 75 % of all skin cancer-related death cases, making it the most lethal form of skin cancer.^[11][12] Many scientists argue that the sun-avoiding health message does increase some forms of skin cancer.^[13]

There is a correlation between high UV exposure, especially during childhood, and the risk to develop melanoma,^[14][15][16] resulting in a WHO recommendation for persons under 18 to avoid sunbeds.^[17]

Authors who claim that sunscreen use causes melanoma have speculated that this occurs by one of the following mechanisms:

• the absence of UVA filters combined with a longer exposure time of the sunscreen user^{[2][18][19][20]}
• less vitamin D generation in sunscreen users.
• By reducing the exposure of the skin to UVB radiation, sunscreen suppresses the skin's production of the natural photoprotectant, melanin,^[21] and the lack of melanin leads to an increased risk of melanoma.^[2]
• free radical generation by sunscreen chemicals that have penetrated into the skin.^{[22][23][24][25][26]}
• pathogenic cytotoxicity and carcinogenicity of micronized titanium or zinc oxide nanoparticles.^[27]

Some sunscreen ingredients may damage cells when illuminated. ^{[28][29][30][31]} PABA causes DNA damage in human cells.^[32] PABA was banned as a sunscreen ingredient several years after these findings were published. Phenylbenzimidazole (PBI) causes DNA photodamage when illuminated while in contact with bacteria or human keratinocytes.^[26][33][34]

Some sunscreen ingredients generate Reactive oxygen species when exposed to UV-A,^[35] which can increase carbonyl formation in albumin^[36] and damage DNA. It is also well-known that DNA alterations are necessary for cancer to occur.

Many sunscreen ingredients generate singlet oxygen under illumination.^[37] Several popular UV-filters have been demonstrated to generate free radicals.^[36]

Kerry Hanson et al. have shown for the three sunscreen ingredients octocrylene, octylmethoxycinnamate, and benzophenone-3 that after the sunscreen chemicals had time to absorb into the skin the number of ROS and free radicals is higher for the sunscreen user than for the non-user.^[25] Such an increase in ROS might increase the chance of melanoma, but this hypothesis has not been tested.

DNA, in particular, is susceptible to damage caused by photo-excited compounds.^[33]

Between 1% and 10% of some sunscreen ingredients are absorbed into the body through the skin.^{[22][38][39][40][41][42][22][24][43]} See^[44] , ^[45]

The absorption of the sunscreen ingredients into the skin does not occur instantaneously, but the sunscreen concentration in the deeper levels of the skin increases over time.^[25] For this reason the amount of time between the topical application of sunscreen and the end of the illumination period is an important parameter in experimental studies. Illumination of those sunscreen chromophores which have penetrated the stratum corneum amplifies the generation of ROS.^[25]

All studies except for one ^[46] have found that sunscreens protect mice against melanoma. ^[47][48][49]

In 2008, a clinical study showed that the application of sunscreen prevents SCC, BCC and actinic keratosis. The study included 60 transplant patients who received immunosuppression, a group of persons with a particularly high risk to develop skin cancer. The patients were very compliant, using sunscreen 5.6 days per week on average. The control group was recruited retrospectively and consisted of 60 transplant patients equally matched for age, skin type and kind of transplant organ. The control group had been instructed to use sunscreen as well, but were not provided with cost-free sunscreen and showed very poor compliance.

After 24 months, the sunscreen group showed a 53% reduction of actinic keratosis, while the control group showed an increase of 38%. The difference in the development of SCC and BCC were also highly significant. Non-significant results included a slight decrease of herpes and warts and a slight increase in acne in the sunscreen group.^[50][51]

Lawsuits have been filed against sunscreen manufacturers.^[52]

These lawsuits limit themselves to the absence of UV-A filters.

In August 2007, the United States Food and Drug Administration tentatively concluded that "the available evidence fails to show that sunscreen use alone prevents skin cancer[...]"^[53]

Sunscreen ingredients are not tested in Europe, Japan or Australia for photocarcinogenic effects before being introduced to the market. Even in the US, most sunscreens sold in 2008 have not passed regulatory testing either, due to a grandfather clause. Three new sunscreen active ingredients introduced in the US since 1978 have fulfilled new testing requirements.^[54]

The use of sunscreen with a sun protection factor (SPF) of 8 inhibits more than 95% of vitamin D production in the skin.^[55][56] Recent studies showed that, following the successful "Slip-Slop-Slap" health campaign encouraging Australians to cover up when exposed to sunlight to prevent skin cancer, an increased number of Australians and New Zealanders became vitamin D deficient.^[57] Ironically, there are indications that vitamin D deficiency may lead to skin cancer.^[58] To avoid vitamin D deficiency, vitamin supplements can be taken. Also, according to the Wikipedia article on vitamin D, ". . . adequate amounts of vitamin D3 can be made in the skin after only ten to fifteen minutes of sun exposure at least two times per week to the face, arms, hands, or back without sunscreen." This applies "in sunlight when the UV index is greater than 3. . . . which occurs daily within the tropics [and] during the spring and summer seasons in temperate regions". With sunscreen, the required exposure would be longer: if 95% of vitamin D production is inhibited, then it proceeds at only 5%, or 1/20^th, the normal rate, and it would take 20 times as long—200 to 300 minutes (3-1/3 to 5 hours), twice a week—of sun exposure to the face, arms, hands, or back for adequate Vitamin D to be made in the skin. Obviously, the required time would decrease with increased body exposure area, as when wearing a swimsuit on a beach, a very common setting where sunscreen is used. By this math, it is apparent that vacationers who spend hours on the beach each day with sunscreen on may make more vitamin D in a week of vacation than they do during a typical week in their lives with no sunscreen, if they spend most of their non-vacationing time inside houses, offices, and other buildings where they get almost no sun exposure. Also, it is worth noting that, as the Vitamin D article states, "with longer exposure to UVB rays, an equilibrium is achieved in the skin, and the vitamin simply degrades as fast as it is generated". The above article makes clear that vitamin D overdose is nearly impossible from natural sources, including food sources.

• Melanoma
• tanning activator
• sun protective clothing
• Vitamin D