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Skin Aging UV Protection



Sure skin aging is intrinsic, but the UV protection keeps skin looking younger for years.



Published November 9, 2005
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Skin Aging  UV Protection


Skin is a unique, continuous external covering that protects us from toxic environmental elements and disease. The skin is also part of the natural resistance of the body against invasion by microorganisms. Yet, despite its well-known barrier properties, skin itself must be protected.

Desquamation, normal flora, the fatty acids of sebum and lactic acid of sweat, are all natural defense mechanisms against microorganism invasion. Langerhans cells present in the epidermis have an antigen-presenting capacity and might play an important role in delayed hypersensitivity reactions. They also play a role in immuno-surveillance against viral infections.

Langerhans cells interact with neighboring keratinocytes, which secrete a number of cytokines and epidermotropic T-cells to form the skin's immune system. The skin is also a huge sensory receptor for heat, cold, pain and touch. Parts of the skin are considered erogenous zones.

The skin has great psychological importance at all ages. It is an organ of emotional expression and a site for the discharge of anxiety. Caressing aids in emotional development, learning and the growth of newborn infants. The skin is a vital part of the body's temperature regulation system, protecting us against hypothermia and hyperthermia; both of which can be fatal.

Like all the body's organs, the skin undergoes many changes during the normal aging process. Chronological aging or genetically programmed processes, takes place during normal life cycles.

Extrinsic Aging
The skin can also age prematurely as a result of prolonged exposure to outside aggressors such as UV radiation, environmental pollutants and heavy metals. Chronological aging primarily occurs in the dermis, the supportive element of the skin. Modifications take place in the extracellular matrix, qualitatively as well as quantitatively. They alter the dermis structure and the skin loses rigidity, elasticity and resilience. Such alterations to the extra cellular matrix eventually result in rough, leathery, wrinkled, yellowed and uneven pigmentation. Over time, facial skin becomes progressively lax, sagging along the jawbone and under the eyes.

UV radiation has a bigger impact on skin aging than any other environmental factor.

A network of dilated blood vessels may be visible on the cheeks and nose, imbuing the face with an unnatural ruddiness. Various blemishes, and visible precancerous and cancerous lesions can also pose a serious threat to the skin. The skin is also more fragile and may bruise or tear easily and take longer to heal. One or more benign lesions are present on the skin of virtually all individuals older than 65, and the incidence of skin cancer increases dramatically with age.

The sun is the chief culprit when it comes to extrinsic aging. Humans love light and the worship of the sun has been a fundamental tenet that many societies hold even today. The properties of the sun that have inspired such reverence include its light (visible radiation) and its warmth (infrared radiation). Additional portions of the solar spectrum that cannot be perceived directly by the senses (ultraviolet) are capable of evoking both physiologic and pathologic events in the skin.

Earth's rapid spin and molten nickel-iron core creates an extensive magnetic field, which, along with the atmosphere, shields us from nearly all of the harmful radiation coming from the sun and other stars. Sunlight is the ultimate source of energy and is vitally important to life. As already noted, the absorption of incident solar energy by components of the skin can cause a variety of pathological conditions.

Until the 20th century, the sun was the predominant source of human skin exposure to energy within the photobiologic action spectrum. More recently, artificial devices capable of mimicking the emission of some or the entire solar spectrum have been introduced, compounding the opportunities and risks of ultraviolet radiation. The most common sources of artificial UV exposure are various kinds of lamps that emit this form of energy. These lamps are used primarily for recreational tanning and phototherapy of skin diseases (e.g., psoriasis and cutaneous T-cell lymphoma (mycosis fungoides). UVR lamps can emit UVA, UVB, and/or UVC. Those lamps currently used for recreational tanning emit UVA primarily or exclusively. Some UVA lamps generate greater than five times the UVA per unit time than solar UVA radiation reaching the Earth's surface at the Equator.

At these doses, "pure UVA" is likely to have adverse biologic effects. However, UVB remains a potential problem with most of these sources. Even 1% UVB emission from a UVA source can cause a significant increase in the potential for skin cancer. The tanning industry is rapidly growing in the U.S. and Europe. Currently, more than one million people use commercial tanning facilities every day. The biggest categories of users are adolescents and young adults, especially women.

The use of artificial ultraviolet sources for the phototherapy of dermatological disease has increased substantially in recent years and has exposed a group of people to markedly increased doses of UVR. Epidemiological studies of these patients have shown an unequivocal dose-dependent increase in the incidence of non-melanoma skin cancer (NMSC), especially squamous cell carcinoma (SCC).

Another potential, but as yet unexplored, source of artificial UVR is unshielded fluorescent bulbs used for illumination. An unresolved issue has been the amount of UVA emitted by such sources and the long-term effects of this exposure. More research is needed to clarify these problems.

The skin plays an important role in calcium homeostasis by contributing to the body's supply of vitamin D. Vitamin D3 (cholecalciferol) is produced in the skin by the action of ultraviolet light on dehydrocholestrol which is then hydroxylated in the liver and kidneys (which needs parathyroid hormone to activate alpha-hydroxylase) to 1,25 dihydroxycholecalciferol, the active form of vitamin D. This anti-rachitic vitamin acts on the intestine increasing calcium absorption through stimulation of synthesis of calcium-binding proteins in the mucosal cells of the intestine, as well as on the kidneys promoting calcium absorption.

A Lifetime of Damage
Despite the undeniable importance of cutaneous exposure to ultraviolet radiation for vitamin D homeostasis, there is little evidence to indicate that there are additional beneficial effects of such exposure. Indeed, overwhelming evidence exists to support the concept that the skin is damaged in many different ways by its direct exposure to natural or artificial ultraviolet radiation. Some exposure is virtually unavoidable over a lifetime and is dramatically dissimilar in different populations depending upon climate, geography, occupation and recreational activities. The consequences of this exposure are also influenced by factors such as the degree of melanin pigmentation.

The effects of UV radiation can be divided into two general types, acute and chronic. Acute effects include sunburn, and chronic effects include, among others, the development of certain forms of skin cancer. In addition, the skin is a major site of immunologic activity, and UV radiation is capable of affecting the immune system via its effects on the skin. The skin is also susceptible to degenerative changes evoked by chronic UV radiation. These changes are a major component of the constellation of physical changes perceived as skin aging but which in reality, are due to chronic photo damage.

It is now possible to measure the effects of solar radiation on the skin. Epidemiological studies from around the world have provided important new knowledge concerning the risks and benefits of exposure to sunlight and ultraviolet radiation. Considerable controversy remains concerning the specific adverse effects caused by various wavelengths of UV radiation, the magnitude of the adverse effects and potential strategies for their prevention and treatment.
With all the rhetoric, avoiding the sun altogether is not possible. Scientists have been studying the effects of the sun's rays for decades. Expanding knowledge about the hazards of exposure to sunlight and ultraviolet radiation has been accompanied by improved approaches to photoprotection, including the development of more effective skin care and sunscreen formulations.

The sun emits a wide variety of electromagnetic radiation, including infrared, visible, ultraviolet A (UVA; 320-420nm), ultraviolet B (UVB; 290-320nm) and ultraviolet C (UVC; 10-290nm). The only ultraviolet radiation (UVR) wavelength that reaches the earth's surface is UVA and UVB. UVA radiation is 1000-fold less effective than UVB in producing skin redness. However, its predominance in the solar energy reaching the Earth's surface (tenfold to one hundredfold more than UVB) permits UVA to play a far more important role in contributing to the harmful effects of sun exposure than previously suspected.

The right UV protection is critical when it comes to maintaining healthy-looking skin.

There is greater UV exposure with decreasing latitude. Residing at higher altitude results in a greater UV exposure such that for every 1000 feet above sea level, there is a compounded 4% increase in UV exposure. UV exposure increases with decreased stratospheric ozone. Other factors that influence exposure to UV include heat, wind, humidity, pollutants, cloud cover, snow, season and time of day. Solar flares (sunspots) also alter the amount of UV reaching the earth. Solar flares increase ozone concentration in the stratosphere (above 50 km), thereby reducing the amount of surface UVB.

This 11-year cycle of solar flares causes as much as a 400% variation in UVB at 300 nm reaching the earth. When solar flares are inactive, there is a decrease in the ozone concentration, allowing increased UVB to penetrate to the Earth's surface.

There has been also a serious concern about depletion of stratosphere ozone by man-made chlorofluorocarbon (CFC). The U.S. Environmental Protection Agency (EPA) has been charged with estimating the effects on health associated with changes in stratospheric ozone levels. In a recent risk assessment document, EPA predicted that without controls on CFC production, there would be a 40% depletion of ozone by 2075. EPA further concluded that for every 1% decrease in ozone, there is a compounded 2% increase in the more damaging shorter UVB wavelengths reaching the earth's surface. Such an increase in UVB penetration to the earth is predicted to result in an additional 1-3% increase a year in non-melanoma skin cancer (NMSC).

Recent satellite measurements already indicate a worldwide decrease in stratospheric ozone during the past decade. Both satellite and land-based measurements have revealed a seasonal hole in the ozone layer over the Antarctic secondary to its destruction by CFCs. Although increased surface UVB has been measured in the Antarctic, there has not yet been a measurable change in UVB as a consequence of CFCs in the stratosphere.

During the past several decades, the average American's exposure to UVB has increased considerably due to changing lifestyles-more outdoor recreational activities, more emphasis on tanning, scantier clothing and a population shift to the southwestern U.S.

UV Effects on Skin

Marked morphologic changes in all parts of the skin, except perhaps the subcutaneous tissue, are recognized as consequences of exposure to UV radiation. These changes underlie the clinically observed sagging, wrinkling, leathery texture, and blotchy discoloration of skin typically associated with actinic damage. It is unclear how much exposure is required to make these changes, although it is evident that clinically normal appearing skin can show pathologic signs of sun damage upon histological and ultra structural examination. It is known that individuals with fair complexions are more susceptible to this damage.

In the epidermis, UV-induced changes include aberrant tissue architecture and alterations in keratinocytes and melanocytes and functional changes in Langerhans cells. Sun-exposed epidermis becomes thickened as much as twofold compared to sun-protected skin and is disorganized, showing evidence of hyperkeratosis, parakeratosis, and acanthosis.

Keratinocytes lose their typical alignment and progressive flattening, show inclusions in the nucleus and accumulate excessive amounts of melanosome complexes above the nucleus (capping). At the ultra structural level, clumped keratin filaments and alterations in electron density of some basal cells are characteristic. Keratinocytes of the more differentiated epidermal layers (upper spinous, granular and cornified) show few, if any, cytologic changes.

Despite evidence of morphologic change, there is no data indicating that altered keratinocyte differentiation is a result of sun exposure. Further, it is not known how UVR interactions with light-absorbing molecules within the keratinocytes (e.g., DNA, keratins and lipids) correlate with the changes in morphology. Two other cells of the epidermis are also affected by UVR.

The melanocyte, with its melanin pigment-containing melanosomes, is the primary cell involved in photoprotection of the skin. In a sun-damaged epidermis, these cells enlarge, increase in number and migrate to higher levels of the epidermis. The other cells affect the Langerhans cells in both animal and human skin by altering their immunological functions. Even low doses of UVB can reduce their antigen-presenting capability, block the normal pathway and evoke an abnormal response by activating T- suppressor networks. It is unclear whether UVR affects Langerhans cells both directly and indirectly through soluble factors released by damaged keratinocytes.

The dermal-epidermal junction loses its rete ridges and forms a flattened interface between the epidermis and dermis. This abutment is more susceptible to shearing forces than normal interlocked system of epidermal rete ridges and dermal papillae. At the ultra structural level, regions of reduplicated lamina densa are evident. This change is not unique to photo damage but is characteristic of trauma to the epidermis by wounding and/or by disease. UVR also causes unique dermal damage such as alterations in architecture, matrix composition, vascular structure and function and cellular activities.

The connective tissue immediately beneath the epidermis (Grenz zone) contains large bundles of densely packed, normal-appearing collagen fibrils. Beneath this region, a broad zone of electron-dense elastotic material is evident. There is no data that demonstrates how newly synthesized or degraded previously existing elastic fibers contribute to this material. Abnormal collagen fibrils can be admixed with the elastotic substance. Other studies show changes in the type 111:1 collagen ratio and an increase in glycosaminoglycans. Fibroblasts appear to be metabolically active. It is not clear whether this is a transient response to the UVR or whether there is a change in cell phenotype that can be retained in vitro.

The mechanisms for the altered connective tissue responses are not understood. Dermal vessels become dilated, leaky and accumulate excessive basement membrane-like material. Inflammatory cells collect around the vessels; mast cells are increased and may show evidences of degranulation and apparent physical association with fibroblasts. Although the nature of this relationship is unknown, it is a common observation in other disorders in which fibrosis occurs.

What Causes Sunburn?
Sunburn is UVR-induced erythema of the skin caused by vasodilatation of dermal vessels. This may be mediated through cyclooxygenase and lipooxygenase products of arachidonic acid. Generation of the prostaglandins associated with UVB erythema produced within the first 6-12 hours can be blocked by topical non-steroidal anti-inflammatory agents such as indomethacin. These anti-inflammatory agents, however, cannot inhibit the delayed, post 24-hour erythema that is modulated by lipoxygenase products. The time-dependent release of varying mediators during the UV-induced inflammatory process underscores the need for further exploration into selective inhibitors of both the cyclo-oxygenase and lipoxygenase pathways in the prevention and treatment of sunburn erythema.

Also associated with UV irradiation of human skin is the appearance of dyskeratotic keratinocytes, known as sunburn cells, in the superficial layers of the epidermis. The mechanisms of the development of these cells are still unclear and warrant further exploration.

Tanning refers to the increase in melanin pigmentation following UVR exposure. It is mediated by a combination of immediate pigment darkening (IPD) and delayed pigment darkening (DPD). IPD is caused by UVA and is due to photo-oxidation of preformed melanin. It is not protective against UVB erythema. DPD occurs about 72 hours after UVR exposure and does not offer much protection against UVB erythema and pyrimidine dimer formation. It is accompanied by an increase in the number of DOPA-positive melanocytes, an increase in the number and melanization of melanosomes and an increase in dendricity of melanocytes.

The degree of protection afforded by melanin is not clear. Individuals with dark complexions are still susceptible to UVR-induced photo damage. UVR also increases the transfer of melanosomes from melanocytes to keratinocytes. Following UVR, melanosomes that are diffused within keratinocytes cluster above the nucleus, forming a cap. DPD occurs with either UVB or UVA. DPD induced by UVB is more protective against UVB erythema than is DPD induced by UVA. Both UVB- and UVA-induced DPD protect equally well against UVB dimer formation.

In addition to certain genetic and metabolic disorders that are precipitated by UVR, there are many photosensitive diseases of unknown cause. These include lupus erythematosus and polymorphous light eruption, which are elicited by certain wavelengths of the UVR spectrum. Photosensitivity disorders may also occur due to the interaction of UVR with many commonly used drugs including those used in cosmetics and consumer products.

UVR modifies local and systemic immune responses, alters Langerhans cell function and activates the T-cell suppressor pathway. Soluble factors released from UV-irradiated epidermal cells also may be responsible for this altered immune response. In certain experiments, UVR-induced tumors transplanted into genetically identical animals are normally rejected. If these host animals are UV-irradiated before transplantation, the tumor will be accepted.
UVR's role in the immunobiology of human skin cancer and particularly, in susceptibility against certain cutaneous infectious diseases, is unknown. More studies on the effect of UVR on human neoplastic and infectious disease are warranted.

There is extensive epidemiological evidence supporting the direct role sunlight plays in human skin cancer. Basal cell carcinomas (BCC), the most common skin cancers in Caucasians, are found primarily on sun-exposed areas such as the head and neck where a dose-response relationship exists. Furthermore, cancer-damaged skin generally has decreased melanin pigmentation and associated photoprotection; people with light complexions and who sunburn easily have a higher incidence of tumors. There is even stronger evidence for the role of sunlight in causing squamous cell carcinoma (SCCs).

Although both BCCs and SCCs are more prevalent in geographic areas of high sun exposure, there is a much greater increase in SCC with decreasing latitude and increasing sun exposure. A reasonable correlation exists between sunlight exposure and melanomas, but the relationship is not as clear as with non-melanoma skin cancer (NMSC). It should be emphasized that the incidence of NMSC and melanomas has been steadily increasing. Unlike NMSC, melanomas occur most frequently on the upper back in males and lower extremities in females. Melanoma incidence does not follow a pattern of increased risk with cumulative UVR exposure whereas the incidence of NMSC does.

However, extensive data exist concerning UVR-induced skin cancer in experimental animal studies which indicate that UVB is much more effective than UVA in causing NMSC. Nevertheless, UVA can induce DNA damage, erythema and SCC in both pigmented and albino mice and guinea pigs. Recent evidence suggests that the longer UVA wavelengths (UVA I: 340-400 nm) of the UVA spectrum are less damaging than the shorter UVA wavelengths (UVA II: 320-340 nm), but further research is needed to confirm this distinction.

The exposure of skin to UVB is essential for the endogenous production of vitamin D. In areas of the world where there are inadequate levels of nutritionally available vitamin D, UVB is the only source. The relationship of sunshine to vitamin D and the normal growth and development of the skeleton is well known. Exposure of skin to UVR in the region of 290 to 315 nm is essential for the formation of vitamin D in the epidermis. There is evidence that vitamin D synthesis is inhibited by the use of sunscreens. However, vitamin D supplementation can overcome this deficiency.

Significant factors that influence susceptibility to UVR damage include race, ethnicity, eye and hair color, and the tendency toward formation of freckles and birthmarks. One approach to categorizing humans in terms of susceptibility to UVR is distinguishing them according to their histories of sunburning and tanning. Two skin types have been defined: Type I individuals always burn and never tan and type II individuals always tan and never burn. The age of an individual may be correlated with factors that influence the susceptibility to UVR. These may include age-related structural differences in the skin, behavioral differences (e.g., adolescent risk-taking) and, hypothetically, age-related immunological differences.

Numerous systemic medications may also augment UVR susceptibility. Increased UVR damage may occur with the use of oral antibiotics, anti-hypertensives, psoralens, immunosuppressive agents, non-steroidal anti-inflammatory drugs and numerous other medications. In addition, a number of topical medications and industrial chemicals may increase the susceptibility to damage by sunlight. These include topical psoralens, tretinoin and other photosensitizing and depigmenting agents.

The Impact of Aging
As a result of prolonged exposure to ultraviolet (UV) radiation emanating from the sun or artificial sources, the skin ages prematurely. Both UVA and UVB rays cause damage leading to wrinkles, lower immunity against infection, aging skin disorders, and cancer. Even small amounts of UV radiation damage collagen fibers (the major structural protein in the skin) and cause accumulation of abnormal elastin (the protein that causes tissue to stretch), during the process, large amounts of enzymes called metalloproteinase are produced.

The normal function of these enzymes is to remodel the sun-injured tissue by synthesizing and reforming collagen. This is an imperfect process, however, and to achieve it, some of these enzymes actually degrade collagen. The result is an uneven formation (matrix) of disorganized collagen fibers called solar scars. Wrinkles will form if this process of imperfect skin rebuilding occurs again and again. One study indicated when people with light to moderate skin color are exposed to sunlight for just 5-15 minutes, metalloproteinases remain elevated for about a week. It should be noted, however, that some studies indicate that metalloproteinases may also have factors that protect against melanoma.1

Despite the damage caused by UVR, good skin care habits can help and sunscreen products are the first line of defense. The use of sunscreens, especially on the face is critical. Consumers 30 and older should use a moisturizing sunscreen product. To increase awareness of the damaging potential of UV radiation, the EPA and the National Weather Service developed the UV Index. Besides skin cancer, UV radiation also increases the risk of cataracts and certain other eye problems and can suppress the immune system. The UV Index number, ranging from 0 to 10+, indicates the amount of UV radiation reaching the earth's surface at noon for an hour. The UV Index is valid only for about a 30-mile radius from the city, and, as with any forecast, local variability in cloud cover and other factors may affect actual levels. But it serves as a reminder to take precautions against UV exposure.

Two types of UV radiation reach the earth, UVA and UVB. Both contribute to skin damage, including skin cancer. There are no "safe" UV rays, but the SPF numbering system was devised as a guide to protect against sunburn, which is caused mostly by UVB. SPF (Sun Protection Factor) indicates the strength of sunscreens to block out the sun's UV rays. It ranges from 2 to SPF 60. For example, if a person gets a burn under the sun after 20 minutes, then with a sunscreen of SPF 30 it would need 30 times of the 20 minutes to get a burn. The use of sunscreen product has a dual purpose, staving off wrinkles and reducing risks of skin cancer.

The correct use of skin care products can do wonders to minimize lines and creases. Moisturizers do not actually prevent aging, but they can keep drier skin from looking parched. Some skin care products can also smooth skin.

UVR Effects on Hair

Scalp hair is a major social and visual display feature of the human body. Hair that is short or long, curly or straight, shimmering with health and vitality complements personal appearance. Hair is similar to the epidermis and is made up of dead cells pushed upward by new living cells in the hair follicle. Like the skin's surface, the cells that make up a strand of hair contain keratin. Sebaceous glands attached to the hair follicles produce and secrete the oily substance sebum, which lubricates and smoothes the hair strands as they move toward the surface. Between 100,000 and 200,000 hair follicles produce hair on the scalp.

The most important feature of hair follicles is that their activity is intermittent (cyclical). As the hair reaches a certain length, it is shed and replaced with a new hair. The main part of each hair fiber is the cortex, which is composed of keratinized spindle-shaped cells. Terminal hairs have a central core known as the medulla consisting of specialized cells, which contain air spaces. Covering the cortex is the cuticle, a thin layer of cells overlapping like the tiles on a roof, with the free margins of the cells pointing toward the tip of the hair. The color of hair is governed by melanin. Less melanin is produced as we grow older, causing gray hair. The average rate of growth of human scalp hair is 0.37mm a day.

A woman's scalp hair grows faster than a man's, but a woman's body hair grows more slowly. Hair growth is undoubtedly increased by androgens, since it can be reduced by treatment with anti-androgenic steroids. The texture of hair is determined by the diameter of each hair strand. A strand of coarse hair is relatively large in diameter, while a strand of fine hair is relatively small in diameter.

To help reduce hair damage, heat and sun should be avoided. UVR, blow dryers and styling appliances damage hair by drying it out and making it brittle.

Skin isn't the only part of our body that needs protection from UVR. Hair is also subject to UVR exposure and photo damage to hair takes the form of texture changes, excessive drying, loss of elastic strength and photo fading of (natural or artificial) color. The inclusions of "photo filters" in shampoos and conditioners have been shown to significantly decrease photo damage.

Photo filters come in a variety of forms and are included in different products. Non-substantive UV absorbers including salicylic acid derivatives, octylmethoxycinnamate and benzophenone derivatives, make up the majority of photo filters in hair products. Relying on a Fluorolog instrument, Janusz Jachowitz demonstrated the effectiveness of a substantive UV photo filter commercially known as Escalol HP610.

This material, dodecyl dimethylaminobenzamidopropyl-dimethyl ammonium tosylate (DDABDT), has demonstrated a significant decrease in fluorescence intensity, which is caused by a decomposition of tryptophan, an amino acid naturally occurring in human hair on account of photo damage. 2

Catezomes are substantive, non-penetrating, non-phospholipid liposomes.3 Two types are available, Catezomes OMC (ethylhexyl methoxycinnamate (and) stearamidopropyl dimethylamine stearate) and Catezomes P-1789 (octyldodecyl neopentanoate (and) avobenzone (and) stearamidopropyl dimethylamine stearate). Due to their cationic surface charge, Catezomes are highly substantive to the skin and hair. This property enables the delivery of active ingredients in a capsule that is both protective and provides greater concentrations at the intended site of action.

Catezomes SI, a liposome product consisting of 0.25 % dimethicone 200 cts, and behenamidopropyl dimethyl-amine behenate, was compared to the standard conditioning agent 0.5 % cetrimonium chloride in both objective and subjective studies for combability, static reduction and the feel of hair. Catezomes SI was found to be the winner in all the aforementioned effects.4

UVR exposure causes wrinkles and premature aging of the skin. Recent studies have also shown the effect that UVR has on hair including texture changes, excessive drying, loss of elastic strength and photo fading of natural or artificial color. In this respect, the cosmetic industry should bear the major responsibility of educating the public while selling its cosmetic products. The trend in the cosmetic industry has been to develop more skin care and sun care products with increasingly higher sun protection factors (SPF). The next generations of products that include either physical sun blockers or chemical sunscreens should be elegant, long-lasting and result-oriented in addition to skin-friendly and environmentally-safe.

References
1. Sunlight, Ultraviolet Radiation, And The Skin, Conference Statement, May 1989     text.nlm.nih.gov/nih/cdc /www/74txt.html
2. International Specialty Products, Wayne, NJ.
3. www.Jyinc.Co/fluor/ap and tc/sscreen.htm
4. Collaborative Laboratories, Stony Brook, NY.



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