Sunburn is a form of radiation burn caused by excessive exposure to ultraviolet (UV) radiation from the sun. This overexposure triggers a complex biological response within the skin. The sensation of heat associated with sunburn is a direct result of these underlying scientific processes, signaling the body’s efforts to repair the damage.
Sunburn: More Than Just Red Skin
Excessive UV radiation, particularly UVB rays, directly damages the DNA within skin cells, primarily keratinocytes. If the DNA damage is extensive and cannot be repaired, these cells undergo programmed cell death (apoptosis) to prevent the proliferation of mutated cells. This cellular death is part of the body’s protective mechanism against skin cancer.
Melanin, the pigment responsible for skin color, offers a natural defense by absorbing and scattering UV radiation. However, melanin’s protective capacity has limits and can be overwhelmed by prolonged or intense UV exposure. When this natural shield is insufficient, UV rays penetrate deeper, causing widespread cellular harm that initiates the visible and palpable signs of sunburn.
The Body’s Inflammatory Response
Following UV-induced cellular damage, the body initiates an immediate biological response to begin the repair process. Damaged skin cells release chemical messengers, including prostaglandins, histamine, and cytokines. These substances signal the immune system, initiating an inflammatory cascade.
This inflammatory response involves vasodilation, the widening of blood vessels in the affected area. Increased blood flow delivers immune cells, such as neutrophils and T lymphocytes, to clear away damaged cells and facilitate healing. The influx of these cells and associated biochemical changes contribute to the redness and swelling characteristic of sunburn.
The Science of Sunburn’s Heat
The sensation of heat from sunburned skin stems from physiological changes driven by the inflammatory response. The increased blood flow due to vasodilation brings a greater volume of warm blood from the body’s core to the skin’s surface. This elevates the surface temperature of the skin, making it feel hot to the touch. This physical increase in temperature is a primary reason for the warmth experienced.
Chemical mediators released during inflammation, particularly prostaglandins and bradykinin, sensitize nerve endings in the skin. These specialized nerve receptors, known as nociceptors, detect potentially damaging stimuli, including extreme temperatures and pain. When sensitized, these nerves become more responsive to heat and pressure, sending amplified “hot” and “pain” signals to the brain.
Heightened cellular activity involved in the immune response and tissue repair also generates localized metabolic heat. This combination of increased surface temperature from enhanced blood flow, along with the heightened sensitivity of nerve endings, collectively leads to the feeling of heat associated with sunburn.