How long
until you burn?

Direct hits on DNA

DNA bases absorb UVB directly. When two pyrimidines sit next to each other on the same strand — TT, TC, CC — the energy can fuse them into a cyclobutane pyrimidine dimer or a 6–4 photoproduct. The helix kinks. Replication machinery stalls or guesses.

The guesses have a fingerprint: C→T and CC→TT substitutions at dipyrimidine sites, found in the majority of skin cancers and almost nowhere else in the body. Pathologists can read sunlight off a tumour's genome.

UVB is only about 5% of the UV reaching the ground, and it does most of the burning.

Oxidative damage, deeper down

UVA is poorly absorbed by DNA but penetrates to the dermis. It works through intermediaries — chromophores that hand energy to oxygen, producing reactive oxygen species. Those oxidise guanine to 8-oxo-guanine, which pairs wrongly, and shred the collagen scaffold via matrix metalloproteinases.

UVA is 95% of ground-level UV, barely varies with season or time of day, and passes straight through window glass. It is the ageing wavelength, and it is not innocent of cancer either.

Damage that continues after dark

Melanin was supposed to be purely protective. Then a 2015 study showed that in pigmented cells, UV generates a slow chemical reaction in which melanin fragments transfer energy to DNA hours after exposure ends, creating so-called "dark" pyrimidine dimers in the evening.

Roughly half the CPDs measured in melanocytes formed after the lights went out. The exposure ends when you go inside. The chemistry takes longer to get the message.

Your repair crew is very good, and it is not perfect

Nucleotide excision repair finds distorted DNA, excises a ~30-base patch around the lesion and resynthesises it. Most dimers from a day at the beach are gone within 24 hours. The protein p53 supervises: pause the cell cycle, repair, or — if the damage is overwhelming — order the cell to kill itself.

Those suicides are what a sunburn is made of. The pink is vasodilation summoned by prostaglandins; the "sunburn cells" a pathologist sees are apoptotic keratinocytes. The redness isn't the injury. It's the cleanup. Which is why a dose that doesn't turn you pink is not automatically a dose that did nothing.

People born without working NER — xeroderma pigmentosum — develop their first skin cancers in childhood, at roughly a thousand times the normal rate. It's the clearest possible demonstration that the whole game is repair capacity versus dose rate.

How damage spreads: fields, not spots

When p53 itself is the gene that gets mutated, the cell loses its ability to order its own death — and gains a small growth advantage over its neighbours. It divides. Its descendants divide.

Sequencing of ordinary, healthy-looking sun-exposed skin found thousands of mutant clones per square centimetre, many carrying cancer-driver mutations in p53 and NOTCH1, in people with no skin cancer at all. Middle-aged eyelid skin is already a mosaic of competing pre-cancerous colonies.

This is field cancerization, and it explains a lot of clinical behaviour: why actinic keratoses arrive in crops rather than singly, why treating one lesion doesn't stop the next, and why sun protection is worth starting at any age. You're not preventing one tumour. You're slowing the expansion of a whole field.

The base-tan trade is a bad one

To acquire a tan worth roughly SPF 3, you have to absorb the DNA damage that ordered its production. There is no signalling pathway from "melanin, please" that doesn't run through "this cell has been hit." A tan is the receipt for damage already done, and the discount it gives on the next transaction is small.

Tanning beds make this worse, not better: the WHO's cancer agency classifies UV-emitting tanning devices as a Group 1 human carcinogen — the same tier as tobacco and asbestos — and first use before age 35 is associated with a substantially higher lifetime melanoma risk.

Red hair, freckles, and the MC1R problem

Some MC1R variants shift melanocytes toward pheomelanin — the reddish-yellow pigment — instead of the brown-black eumelanin. Pheomelanin absorbs UV poorly and, worse, appears to generate oxidative damage of its own. Mouse work suggests a pheomelanin background raises melanoma risk even with UV excluded entirely.

That's why type I skin isn't just "less tanned type III." It's running different chemistry, and it needs a different plan: shade and fabric first, sunscreen as the layer for what's left uncovered.

Why 30 and 50 are closer than they look — and further than they look

Read the left column and SPF 50 looks like a 1.3-point upgrade on SPF 30. Read the right column and it's letting through 40% less UV. The second reading is the one your DNA is doing. This is also why a higher label number is a useful buffer against under-application rather than an invitation to stay out longer.

SPF says nothing about UVA on its own

SPF is calibrated to erythema, and erythema is mostly a UVB phenomenon. A product could earn SPF 50 while letting through most of the UVA that drives photoageing and contributes to melanoma.

That's what the extra marks are for. In the US, "broad spectrum" means the critical wavelength is at least 370 nm. In the EU, the circled UVA seal means UVA protection is at least one third of the labelled SPF. In much of Asia, PA+ to PA++++ grades persistent pigment darkening. Any one of them is a signal that someone measured the long wavelengths. A bare SPF number is not.

Filters differ too: zinc oxide and titanium dioxide are broad and photostable; avobenzone covers UVA well but degrades in light unless stabilised (octocrylene usually does that job). Several excellent modern filters — Tinosorb, Uvinul A Plus, Mexoryl — are routine in Europe, Japan and Australia and still not approved in the United States, where sunscreens are regulated as over-the-counter drugs.

How much, and how often

Reapplication isn't topping up a reservoir. The film is being physically removed by sweat, towels, sand and clothing, and some filters degrade photochemically while doing their job. Two hours in, an unrefreshed layer is a fraction of what you put on.

The map of places people miss

Fluorescence photography of people who have just "finished" applying sunscreen reliably shows the same gaps. Most of them are high-incidence sites for skin cancer, which is not a coincidence — they're the places sunlight lands most directly.

Eyelids get skipped for obvious reasons and are a common site for basal cell carcinoma; sunglasses that wrap and block UV400 cover them, and also protect the lens and retina from cataract and ocular melanoma risk. Lips need a balm with a filter — lower-lip actinic damage is a genuinely under-recognised precursor lesion.

Sunscreen is the last layer, not the first. Shade, timing, a wide brim and UPF fabric all beat it on reliability, because none of them depends on you having spread 30 mL evenly and remembered to do it again at 1:40 p.m.

Basal cell carcinoma

Cell of origin: basal keratinocytes and hair-follicle stem cells. Driven overwhelmingly by loss of PTCH1 and runaway Hedgehog signalling — a pathway that should be quiet in adult skin.

Exposure pattern: both chronic accumulation and intense intermittent burns. Head, neck and upper trunk dominate.

Looks like: a pearly or translucent papule with fine surface vessels and a rolled border, sometimes a scab that keeps returning to the same spot for months. Left long enough, it ulcerates — the old term was rodent ulcer.

Behaviour: metastasis is rare, but it invades locally and can be genuinely destructive around the eye, nose and ear. About four in five skin cancers.

Squamous cell carcinoma

Cell of origin: keratinocytes of the upper epidermis, usually via a p53-mutant clone that expanded over decades.

Exposure pattern: total lifetime dose. It's the cancer of outdoor work, of the left forearm and the driving-side cheek, and of bald scalps.

Looks like: a firm, scaly, tender papule or plaque, often with a keratin crust or horn; it may ulcerate. It frequently emerges from an existing actinic keratosis or from squamous cell carcinoma in situ (Bowen's disease).

Behaviour: metastasises in a few percent of cases, more from the lip and ear, from large or poorly differentiated tumours, and dramatically more in organ transplant recipients — whose SCC risk runs 65 to 100 times the general population.

Melanoma

Cell of origin: melanocytes. Common drivers include BRAF V600E, NRAS and loss of CDKN2A; UV-signature mutation burdens are among the highest of any tumour type.

Exposure pattern: intense intermittent exposure and blistering sunburns, especially early in life — a different pattern from the keratinocyte cancers, and the reason melanoma is not simply a disease of outdoor workers.

Looks like: ABCDE, below. But also trust the ugly duckling sign — most of a person's moles resemble each other, so the one that doesn't belong deserves attention regardless of its measurements.

Behaviour: prognosis hinges on Breslow depth, the millimetres of vertical invasion at the moment of excision. Thin melanomas are usually cured by surgery alone. This is the entire argument for looking early and often.

Merkel cell carcinoma

A neuroendocrine tumour of sun-exposed skin in older and immunosuppressed people, arising either from Merkel cell polyomavirus integration or from very heavy UV mutation load. It grows fast and metastasises early.

The mnemonic is AEIOU: asymptomatic, expanding rapidly, immunosuppression, older than 50, UV-exposed fair skin. A painless, fast-growing red-violet nodule on the head or neck of an older patient is a same-week referral.

Darker skin is lower-risk, not no-risk

Deeply pigmented skin carries a native SPF in the range of 8–14 against erythema, and melanoma incidence is far lower. But outcomes are consistently worse, because diagnosis comes later.

Part of that is a subtype difference: acral lentiginous melanoma — palms, soles, nail beds — occurs at similar absolute rates across ethnic groups and is largely UV-independent, so it makes up a much larger share of melanoma in Black, Asian and Hispanic patients. It hides where nobody is looking and where sun advice doesn't apply.

Practical translation: everyone checks soles, palms, and nail beds. A new pigmented streak in a single nail — especially one that widens or spreads onto the surrounding skin — gets examined, not watched.