Melanoma is one of the deadliest forms of skin cancer, originating in melanocytes—the cells responsible for producing melanin, the pigment that gives skin its color. It’s a cancer largely caused by UV damage from the sun, making it especially common in individuals with red hair, freckles, or pale skin. Most melanomas can be traced back to severe sunburns—the kind that make your skin peel. These burns inflict DNA damage, setting off a cascade that, over time, allows mutated cells to grow, forming moles. Some of these moles may eventually transform into melanomas—aggressive, metastatic cancers that can spread rapidly and become life-threatening.
This brings us to a troubling paradox. For decades, public health campaigns have emphasized the importance of protecting our skin from UV radiation. Sunscreen use has skyrocketed. People now wear hats, seek shade, and don long clothing to avoid sunburn. With all this effort, you’d expect melanoma rates to drop. But instead, the opposite has happened: melanoma incidence continues to rise substantially (Figure 1). Why?
The answer might lie not in the absence of sun protection but in what we’re using for protection.
How Cancer Develops: Initiation and Promotion
To understand the potential risks posed by these sunscreen ingredients, it’s essential to explore the process of cancer formation. Skin cancer (and basically all cancers) arises in three stages: initiation, promotion and progression. In the initiation stage, cells sustain DNA damage, and for skin cancer, often from UV radiation or a chemical insult. For these damaged cells to progress into cancer, there must be a promotion stage involving chronic inflammation or other stimuli that drive their proliferation.
Laboratory studies with mice highlight this process. Applying a DNA-damaging chemical to their skin alone rarely leads to cancer. However, when followed by a promoting agent that causes inflammation, cancer formation becomes much more likely. This dual requirement—initiation followed by promotion—illustrates how chronic exposure to harmful agents can push damaged cells toward malignancy.
Now consider sunscreen: some products may not only initiate DNA damage but also promote chronic inflammation or cell turnover, creating conditions that favor cancer development.
A Closer Look at Common Sunscreens
Popular sunscreen brands contain endocrine disrupting chemicals and/or carcinogens- chemicals that directly cause DNA damage and can initiate and/or promote cancer. Let’s break down what these chemicals are and how they can cause cancer.
Many sunscreens contain chemicals that directly cause DNA damage. Sunscreens were found to be contaminated with benzene- a known carcinogen. Easily absorbed by the skin, benzene can generate reactive metabolites like benzene oxide and benzoquinone, which can directly bind to DNA in melanocytes, causing mutations. DNA damage in melanocytes can initiate changes that promote uncontrolled growth. Benzene metabolism also produces reactive oxygen species (ROS), which also damages DNA.
Even if not contaminated with a carcinogen, many sunscreens contain chemicals listed as “UV Filters” that break down and can directly cause DNA damage. Octocrylene, octylmethoxycinnamate, benzophenone-3, and avobenzone generate ROS when exposed to sunlight and therefore will cause oxidative stress and damage DNA. Melanocytes, which already experience oxidative stress due to melanin synthesis, are particularly vulnerable to this additional insult.
These DNA damage causing chemicals can also trigger localized inflammation, which when chronic can promote initiated cells towards transformation.
Other chemicals found in sunscreen can directly act as promoters as well. An endocrine disruptor such as oxybenzone, a chemical found in sunscreen mimics natural estrogen. The link between melanoma and estrogen is particularly noted during pregnancy, where higher the levels of estrogen are associated with increased risk of melanoma progression and metastasis.
Finally, some chemicals in sunscreen exhibit both DNA damaging and endocrine disruption activities. Octinoxate is a chemical that when exposed to sunlight, degrades to from ROS thereby leading to oxidative stress and DNA damage but also happens to have a chemical structure similar to estrogen, thereby mimicking its effects.
A Rethink on Melanoma Prevention
So, if protecting ourselves from the sun is important—so is protecting ourselves from products that might be doing more harm than good. Perhaps sunscreen isn’t the fail-safe solution to melanoma prevention. In fact, this fear of sun exposure is leading to an epidemic of vitamin D deficiency.
So, what is the answer to melanoma prevention? The answer may lie in moving beyond one-size-fits-all public health campaigns to a more targeted approach. Rather than blanketing the population with sunscreen mandates, perhaps focusing on identifying those most at risk—people with pale skin, red hair, or a history of severe sunburns—and equipping them with tailored preventative strategies. For example, encouraging the use of natural mineral blockers that only contain zinc oxide, with no known carcinogenic effects maybe a better approach. In addition, interventions that reduce chronic inflammation could be considered.
At the same time, we need to re-evaluate, study, regulate, and even ban dangerous ingredients in sunscreens. The chemicals we’re slathering on our skin are doing more harm than good. Rigorous research is needed to determine what these products and chemicals are doing both genetically and epigenetically to our cells. Are these chemicals truly safe or are they inadvertently fueling the rise in melanoma rates?
The Vitamin D deficiency must be bigger than a lack of sun exposure, though. I sunbathe religiously, yet in a blood test, I was deficient in it. I can only speculate as to what else might be increasing our Vitamin D requirements.
Thanks for the information!