UVA rays are the longest-wavelength form of ultraviolet radiation from the sun, spanning 315 to 400 nanometers. They make up roughly 95% of all UV radiation that reaches the Earth’s surface, with UVB accounting for the remaining 5%. What makes UVA distinctive, and worth understanding, is how deeply it penetrates your skin and how quietly it causes damage you won’t notice for years.
How UVA Differs From UVB
Ultraviolet radiation falls into three bands: UVC (100 to 280 nm), UVB (280 to 315 nm), and UVA (315 to 400 nm). UVC is completely absorbed by the atmosphere and never reaches your skin. UVB hits the outer layer of skin (the epidermis), causes sunburns, and directly damages DNA in skin cells. UVA passes through the epidermis and penetrates into the dermis, the thicker layer underneath that contains collagen, elastin, and blood vessels. Some UVA wavelengths reach even deeper, into the hypodermis.
Because UVB is the radiation that turns you red, people often assume it’s the only UV worth worrying about. But UVA’s deeper penetration means it affects structures that UVB can’t easily reach, and its sheer volume (19 times more UVA hits your skin than UVB at midday) means your cumulative lifetime exposure is enormous.
UVA1 and UVA2: Two Sub-Bands
UVA is further divided into two ranges. UVA2 spans 320 to 340 nm and behaves somewhat like a bridge between UVB and longer-wave UVA. UVA1, from 340 to 400 nm, makes up the majority of UV radiation reaching the Earth’s surface. UVA1 is the primary driver of immediate skin darkening, photoaging, immune suppression in the skin, and contributes to cancer risk. It also generates reactive oxygen species and causes cell death in fibroblasts, the cells responsible for producing collagen.
How UVA Damages Skin Cells
UVB and UVA damage your DNA through completely different mechanisms. UVB is absorbed directly by the DNA in your cells, causing immediate structural damage to the genetic code. UVA works indirectly. It interacts with light-absorbing molecules already present inside your cells, which then generate reactive oxygen species: unstable molecules that attack DNA, proteins, and fats throughout the cell.
This oxidative damage is harder for your body to repair cleanly, and it accumulates over time. Certain medications, including some widely prescribed drugs, can act as additional light-absorbing molecules in the skin, amplifying this process and increasing the risk of sun-related cancer. The indirect nature of UVA damage is part of why it was underestimated for decades. It doesn’t leave the obvious calling card of a sunburn, but it contributes meaningfully to skin cancer risk.
UVA and Premature Aging
The dermis gives skin its firmness and elasticity through a network of collagen and elastin fibers. UVA radiation breaks this network down through two simultaneous processes: it triggers enzymes that chew through existing collagen, and it suppresses the production of new collagen to replace what’s lost.
Specifically, UVA exposure ramps up the activity of protein-breaking enzymes in the skin. These enzymes degrade collagen fibers and, separately, break down elastin, the protein that lets skin snap back into place. Research on reconstructed skin models found that UVA exposure increased the activity of elastin-degrading enzymes by 400% and boosted elastase activity by 500% within 48 hours. At the same time, the skin overproduced a precursor to elastin (tropoelastin) by 500%, a disorganized repair response that leads to the leathery, thickened texture characteristic of sun-damaged skin. Dermatologists call this solar elastosis.
The oxidative stress from UVA also creates chemical cross-links in collagen, making fibers stiff and brittle rather than flexible. When this process combines with glycation (a natural sugar-related aging process), the damage compounds. The result is what most people recognize as photoaging: deep wrinkles, sagging, uneven texture, and age spots that appear years or decades before they would from chronological aging alone.
The Tanning Response
UVA is responsible for a phenomenon called immediate pigment darkening, a visible tan that appears within minutes of sun exposure. Unlike a delayed tan (which takes one to three days and involves new melanin production), immediate darkening happens because UVA chemically modifies melanin pigment already present in your skin cells and causes structural changes in both melanocytes and the surrounding cells.
This darkening peaks right after exposure and fades relatively quickly. The wavelength most efficient at triggering it is around 340 nm, squarely in the UVA1 range. How strongly you experience it depends on your skin type and how much melanin you naturally carry. Importantly, this immediate tan provides little to no protection against further UV damage. It’s a cosmetic change, not a shield.
UVA Exposure Is Hard to Avoid
One of the most practical things to understand about UVA is how consistently it reaches your skin compared to UVB. UVA intensity does vary by season. Measurements have shown that peak UVA levels (in late summer) can be roughly 5.6 times higher than the yearly minimum (in early spring). But even at its lowest, UVA is present during all daylight hours, year-round.
Standard window glass blocks most UVB but transmits a significant portion of UVA. This means you can accumulate UVA exposure while driving, sitting near windows at work, or in any indoor space with natural light. Cloud cover reduces UVA somewhat, but far less than most people assume. Overcast skies can still transmit the majority of UVA to the ground. This is why dermatologists emphasize daily sun protection even when you don’t plan to be outdoors for extended periods.
What UVA Protection Looks Like in Sunscreen
SPF, the number on every sunscreen bottle, measures protection against UVB almost exclusively. It tells you very little about UVA defense. For UVA, look for one of two rating systems depending on where the product is sold.
The PA system, common on Asian and some European sunscreens, is based on a measurement called persistent pigment darkening (PPD), which tests how much UVA exposure is needed to darken the skin with and without the product applied. The scale works like this:
- PA+: PPD of 2 to 4 (some UVA protection)
- PA++: PPD of 4 to 8 (moderate protection)
- PA+++: PPD of 8 to 16 (high protection)
- PA++++: PPD of 16 or above (highest available protection)
In the U.S., there’s no numerical UVA rating. Instead, sunscreens that pass a critical wavelength test of 370 nm can be labeled “broad spectrum,” meaning they offer some level of UVA coverage. This is a lower bar than PA++++, so if strong UVA protection matters to you, checking for a PA rating or looking at the active ingredients (mineral filters like zinc oxide cover the full UVA range) gives you more information than “broad spectrum” alone.
Why UVA Matters More Than People Think
For most of the 20th century, UVB got nearly all the attention in skin cancer research and sunscreen development because it causes the visible, immediate damage of sunburn. UVA was considered relatively harmless. That understanding has shifted substantially. UVA’s ability to generate reactive oxygen species, damage DNA indirectly, degrade the structural proteins of the skin, and suppress local immune responses makes it a significant contributor to both skin cancer and the cosmetic damage most people associate with aging. The fact that it arrives in 19 times the quantity of UVB, passes through glass, and persists through clouds and across seasons means your cumulative exposure is far higher than most people realize.