Higher-energy UVB rays are the primary cause of sunburn and bind directly to DNA, causing pre-cancerous mutations. However, the sun’s more numerous lower-energy UVA rays penetrate deeper into skin tissue and are most responsible for generating free radicals that may damage DNA and skin cells (Marrot 2005), promote skin aging (Wlasckek 2001), and cause skin cancer (Wittgen 2007).
Sunscreens can help reduce UV-related free radical damage by diverting the radiation from the skin, but the ingredients themselves can break down and release their own free radicals in the process. When the sunscreen molecules absorb UV energy, keeping it from the skin, the molecules dispel the excess energy by releasing free radicals. In a delicate balancing act, an effective sunscreen prevents more free radical damage (from UV radiation) than it creates through its own generation of free radicals. In other words, it reduces UV exposure without itself damaging skin. Sunscreen makers commonly add antioxidants to their products to soak up free radicals from either UV radiation or sunscreen itself.
Most of the US-approved UV filters release free radicals – octylmethoxycinnamate, oxybenzone, avobenzone, octocrylene, titanium dioxide, zinc oxide, Padimate O, PABA, menthyl anthranilate, and Mexoryl SX (Allen 1996, Beeby 2000, Cantrell 1999, Damiani 2007 & 2010, Dondi 2006, Hidaka 2006, Knowland 1993, Sayre 2005, Serpone 2002). Some benzophenones, octisalate and Mexoryl appear to produce no free radicals (Allen 1996, Fourtanier 2008).
Sunscreens typically do more good than harm in this regard, but they could be better. (Popov 2009, Serpone 2006, Haywood 2003). Tests show that sunscreens generally reduce formation of free radicals – one study found a 45 percent reduction at typical amounts and a 55 percent reduction at the recommended use amount of 2 mg/cm2. This would be equivalent to a “free radical protection factor” of 2, not the 15 to 50 SPF common for sunburn protection (Haywood 2003).
The balance may shift if people apply too little sunscreen or reapply infrequently. For example, a study found that for three common sunscreens, the amount of free radicals caused by sunscreens exceeded the amount on untreated skin after one hour (Hanson 2006).
Recent studies measured free radical protection factors of around 2 to 4 for chemical and titanium dioxide-based sunscreens (Haywood 2012). Unsurprisingly European sunscreens were better, averaging a protection factor of 13 in 12 European products (Wang 2011). In a European study, the UVA protection factor and free radical skin protection factors were highly correlated, and the three sunscreens with inadequate UVA protection had the worst free radical protection (Wang 2012).
FDA’s recent standard for UVA protection is far less stringent and leaves US manufacturers with only three ingredients to combat free radical damage. This situation will not improve until FDA sets tighter restrictions for UVA protection, approves new sunscreen chemicals or develops a standard requirement for reducing free radical damage.
Some sunscreen ingredients or formulations may be more damaging to skin than others. Both nano-size zinc oxide and titanium dioxide from sunscreens react strongly with UV light (Dunford 1997) and may damage skin cells (Sharma 2009). Manufacturers typically use coatings that reduce activity (Popov 2009, Serpone 2006). Furthermore, the crystal structure of titanium dioxide (anatase vs. rutile) also appears to affect its potency in generating free radicals (Lu 2008).
The UV filter Padimate O causes skin damage through an entirely different mechanism. It fell out of favor when evidence emerged that it reacts with other compounds to form a mutagenic contaminant (Loeppky 1991) and causes a dramatic increase in DNA strand breaks compared to untreated skin (Gulson 1999).
It is difficult to gauge the effectiveness of a particular sunscreen formulation at combating free radicals. Zastrow (2004) has proposed an Integrated Sun Protection index that would quantify the degree of free radical formation under UV light.
