Light Sensitivity Part One: The Light Spectrum:


Light sensitivity is a broad and technical subject and our goal is to< provide you with a lot of very important key information. Please be< aware that this subject is isolated into four separate pages as noted< here: Light Spectrum (Part One) | Causes Of (Part Two) | Conditions Of< (Part Three) | Prescriptions And…(Part Four) (****please add the< links to these when you are done adding the info there are 4 separate< parts to the information .)******

Ultraviolet C (UVC) – (100-280nm)

UVC wavelengths are the shortest ultraviolet rays and are recognized< as the most carcinogenic. UVC is severely photo damaging to the skin,< resulting in skin burn with exposure. These wavelengths can very< efficiently kill germs, giving rise to their common name, “germicidal< waves.”

Fortunately, virtually all UVC generated by the sun is screened from< reaching us by the protective ozone layer. Unfortunately, pollution< damage to the ozone layer is undermining its protective ability, and< UVC may become increasingly problematic for those living at high< altitudes. If ozone depletion persists, the consequences will threaten< life on a large-scale. Artificial sources such as some mercury< arc-welding units and germicidal lamps also emit UVC.

Ultraviolet B (UVB) – (280-315nm)

UVB is the intermediate wavelength of ultraviolet rays and causes the< initial appearance of erythema, commonly called “sunburn.” UVB< primarily damages the epidermis (the outer most layer of the skin).< The immediate result is skin redness and thickening of the stratum< corneum, which is the body’s attempt to reduce UVB ‘s impact on the< epidermis. The superficial redness and painful irritation caused by< UVB subsides after a relatively short period of time, but the< underlying damage remains and accumulates, potentially resulting in< basal cell and squamous cell cancers. Excessive exposure to UVB is the< foremost promoter of premature aging of the skin. UVB also has< significant immunosuppressive effects.

In addition to staying out of the sun between 10 a.m. and 4 p.m. when< UV rays are strongest, we can protect ourselves from UVB by applying< sunscreen, wearing protective clothing and sunglasses. The SPF rating< assigned to a sun protection product is an indicator of its ability to< protect against the UVB wavelength of light and is determined based on< acute erythemal reaction, i.e. sunburn.

IMPORTANT NOTE: Choosing a sun protection based solely on SPF is not< enough. The common rule of thumb to “use SPF 30 or above” to protect< your skin from sun damage is outdated, misleading and can be< dangerous. SPF ratings pertain to UVB radiation only. UVB is not the< only ultraviolet wavelength that damages the skin. SPF is not a< sufficient or reliable indicator of the level of protection against< any biological damage other than sunburn. As our understanding of< light’s impact on skin has evolved, it has become clear that UVA< adversely affects the deep dermis far more than the superficial< “sunburn” caused by UVB rays, and mounting evidence suggests that UVA< plays a relatively greater role in long-term photodamage.

Ultraviolet A (UVA) – (315-400nm)

UVA are longest of the ultraviolet wavelengths. While energy from the< shorter UVB wavelength is absorbed in greater amounts in the epidermis< and in keratinocyte DNA, energy from UVA penetrates more deeply into< the dermis.  Once thought of as essentially harmless, UVA causes the< pigmentation changes associated with what we misguidedly refer to as a< “healthy tan.”  Scientific evidence now indicates that UVA is anything< but harmless. In addition to skin darkening (tanning), UVA induces< cutaneous photodamage, usually seen as dryness, uneven pigmentation,< inflammation, fine wrinkles, and skin cancer.  Even a low dose of UVA< can cause photodamage leading to wrinkles and sagging skin. UVA< adversely affects the deep dermis resulting in a loss of the elastic< quality of its supportive collagen, causing premature aging. UVA< exposure has been linked to the development of basal and squamous cell< cancers, as well as pre-cancerous lesions.  It has recently been< reported that depletion of Vitamin A in the skin caused by UVA< exposure may contribute to both photoaging and cancers of the skin.< Tissue damage from UVA rays is cumulative, and generally, the effects< will not appear until after years of exposure.

Several studies have demonstrated UVA’s involvement in tumor< development and depression of immune function. Skin’s upper layers< present a weak resistance to UVA penetration and are not equipped to< counteract photons that impact immune functions. While UVA and UVB are< immunosuppressive, UVA radiation is generally not considered to< directly impact nuclear DNA at a significant level, but rather produce< radical oxidative species (ROS) triggering genotoxic effects.< Epidermal pigment cells have been used in order to investigate the< induction of DNA breaks due to UVA. What was determined is that with< relatively low doses of UVA significant DNA breaks were found< UVA represents 90-95% of terrestrial UV radiation. It is estimated< that 10 to 12 times more UVA than UVB reaches the earth’s surface at< sea level.  Unlike the shorter UVB wavelengths, UVA easily penetrates< window glass and retains essentially the same energy level all day< long, every day of the year, presenting the same damaging effects at 9< a.m. in December as it does at the 4 p.m. in July.

As with UVB, our protection against UVA includes staying out of the< sun, sunscreen, protective clothing and sunglasses. Products that< address this wavelength specify “UVA Protection” or “Broad-Spectrum< Protection” on the label. However, broad spectrum is not total< spectrum protection. The SPF rating system used does not predict< ability to block UVA. Unfortunately, there is presently no< standardized indicator, numerical or otherwise, to signify the level< of protection against UVA. Safely maintaining unaltered essential< biological functions can only be achieved by well-balanced,< photostable sunscreens that protect against the entire spectrum of UV< radiation. Sunscreens containing titanium dioxide and zinc oxide will< protect against UVA radiation.

Visible Light (400nm – 780nm)

As the name describes, visible light are the wavelengths that humans< can see (violet, indigo, blue, green, yellow, orange, and red.).< Nearly 50% of the sun’s radiation reaching us at sea level is within< the visible range. The energy level of visible light is lower than< that of the ultraviolet wavelength, but it is a misconception to think< of visible light as harmless to human skin. This lower energy has the< ability to penetrate deeper into the skin than UVA, reaching down< within the dermis, and create adverse skin reactions. Prestigious< journals such as the “Journal of Investigative Dermatology”, “Cancer< Research”, and the “British Journal of Dermatology” have published< reports showing that visible light is capable of precipitating< phototoxic reactions, promoting DNA cross-linking and enhancing tumor< growth. Visible light’s significance as an active wavelength is< evidenced by its current role in multiple Photo Dynamic Therapies (PDTs), some of which are used for the treatment of esophageal cancer, certain lung cancers and premalignant skin cancer.

Infrared- “IR” (greater than 780-1,000,000nm)

Infrared goes from above 780nm to infinity, but most of the energy is in the 780nm to about 1800nm range. It comprises more than 40% of the sun’s rays that reach us at sea level.  These wavelengths warm us when we stand in the sun (perceived as deeply penetrating heat) and are emitted by stoves, furnaces, light bulbs, heat lamps, ovens, and space heaters.  A number of studies have implicated infrared waves as photodamaging. Chronic exposure to infrared light leads to mottled pigmentation, loss of elastin (elastosis) and the typical characteristics seen in photo-aged skin (wrinkling, sagging, leathery-feel). Infrared has also been known to cause cancer, such as Kang Cancer in China, Kangri in Kashmir, Kairo in Japan, and Peat Fire Cancer in Ireland.