The promotion surrounding sunscreens has been the promise that they protect from both skin cancers and photoaging of the skin. However, readily available evidence reveals that sunscreens not only increase the risk of skin cancers, including melanomas, but also leave the skin exposed to a higher percentage of the solar rays that actually break down collagen and elastin, resulting in greater photoaging of the skin than without sunscreen use.*

Skin Cancers Increasing in Epidemic Proportions
Melanoma
Over last few decades, the admonition to use sunscreen whenever going outdoors has taken over the headlines, yet melanomas have shown a consistent rise in incidence rate since sunscreens were first introduced. Figure 1 shows the increasing incidence of melanomas in the US, and this rise is reflected throughout the world.¹

Figure 1: Melanoma - U.S. Incident Rates

Basal Cell and Squamous Cell Carcinomas
The US National Institutes of Health does not keep track of the numbers of skin cancers that are caused by basal cell or squamous cell carcinomas as it does for melanomas. Therefore, retrospective (historic) case reviews and statistical analyses on pooled data bases need to be utilized to determine the prevalence of these skin cancers. In a Journal of the American Medical Association (JAMA) study published in 2005, doctors stated that they found that the number of women under age 40 diagnosed with basal cell carcinoma had more than doubled in the previous 27 years. The incidence rose from 13.4/100,000 to 31.6/100,000.²  They also stated that, during this same time, the squamous cell carcinoma rate for women also increased significantly.

An analysis published in Archives of Dermatology in 2010 showed that in the 14 years between 1992 and 2006, the total number of procedures for skin cancer in the Medicare (fee-for-service) population increased by 76.9%. The number treated per year rose during this time from 1,158,298 in 1992 to 2,048,517 in 2006. With totals of skin cancer diagnoses and number of patients in the US population much higher than previous estimates, the researchers concluded: "… these data give the most complete evaluation to date of the under recognized epidemic of skin cancer in the United States."³

Our skin is designed to use antioxidants to neutralize the solar radiation as well as increase melanin in the skin as part of its natural protection. Melanin, the brown pigment made by the melanocytes in the basal layer of the skin, is the body's own built-in protective defense, as it effectively absorbs the energy of the UV radiation.⁴ The use of sunscreens stops the body's natural process of creating more melanin to protect the cells. Sunscreen use also prevents our built-in red warning light – painful sunburn on the skin – from signaling us to get out of the sun. Staying in the sun 10, 20, 30, or 50 times longer than people normally would because a sunscreen chemical is preventing the sunburn consumes the skin's store of antioxidants, leaving the skin open to damage from the radiation. The result has been increased skin cancers paralleling the increased use of sunscreens. One of the reasons that this has occurred is that the first sunscreens only blocked the UVB sunburning rays, and did not block the UVA portion of the solar spectrum. The UVA rays penetrate much deeper than UVB and create reactive oxygen species (ROS) that cause damage at the cellular level, damage that leads to both skin cancers and photoaging.

Combining Sunscreen Chemicals to Create 'Broad-Spectrum' Coverage
Even though this problem was soon recognized, it was not until 2011 that the US Food and Drug Administration (FDA) issued new guidelines mandating that a sunscreen must filter both UVA and UVB radiation in order for manufacturers to put a SPF (sun protection factor) rating on their labels.⁵ These newer formulated sunscreens are termed "broad spectrum," as they are now required to filter both UVB and UVA solar rays. Since each chemical covers only a specific portion of the solar spectrum, several chemicals must be combined to assure that more of the solar spectrum is filtered. This combining creates diverse problems.
 
Accelerated Photodegradation: Some of the chemicals or metals used as sun filters actually become inactivated upon exposure to sunlight, a photodegradation that prevents them from being capable of protecting the skin from solar radiation. This photodegradation can occur even more rapidly when chemicals are combined, compared with when they are used by themselves.⁶

Increased Toxicity: Even more important, research studies have been identifying that chemicals may not be "too toxic" when used individually, but low concentrations of several in combination create new harmful chemical complexes that result in a much more toxic formula. Articles end with the recommendation that all future research on possible toxic effects of sunscreen chemicals has to look at these chemicals in combinations, the way they are now being required to be sold.⁷

Is Broad Spectrum UV Coverage Really an Answer?
Only 4% of the Solar Radiation that Reaches Our Skin Is UV
With the realization that UVA is more damaging, the promotion currently is: as long as we are using the "broad spectrum" sun filters, we are safe. However, the entire UVA and UVB spectrum makes up only 4% of the total solar radiation that reaches us through the earth's atmosphere. This is another reason why skin cancers have increased with sunscreen use. The far greater amount of radiation that our skin is exposed to is the near infrared radiation (NIR), and NIR constitutes 47% of the solar radiation penetrating our atmosphere and thereby reaching our skin.⁸ These rays penetrate even deeper than the UVA rays. They go deep into subcellular structures, including the mitochondria, where they create ROS, and that is where the blocking of damaging radiation needs to take place.⁹ Many new methods have been researched to prevent ROS damage at the mitochondrial level, but no satisfactory solutions have been found to stop the NIR damage – damage that can lead to skin cancers, as well as photoaging of the skin because NIR leads to the destruction of both collagen and elastin.¹⁰

Some researchers are investigating an agent called mitoquinone (MitoQ), a quinone similar to coenzyme Q10 (CoQ10) that would work on preventing IR from producing ROS in the mitochondria. Preliminary studies are indicating that it does.¹¹

Sunscreen Chemicals are Potent Endocrine-Disrupting Chemicals
Not only are sunscreens doing the opposite of what they have been promoted for, many journal articles published today are revealing that these chemicals also lead to damaging changes in the species of life that have been tested. Classified as endocrine-disrupting chemicals (EDCs), many of the sunscreen chemicals used are potent estrogens, antiestrogens, testosterones, and antitestosterones.¹² In fact, the very commonly used benzophenones and salicylates demonstrate more antiandrogenic activity than that of flutamide, the antiandrogen drug given to prostate cancer patients to stop the influence of testosterone in the effort to slow prostate cancer growth.¹³

One chemical that is almost universally used in sunscreens is benzophenone-3 (BP3). A generational study on mice showed that it results in both general as well as reproductive toxicity, as shown in Table 1.

These results demonstrate that this common sunscreen chemical affects the entire body, including the liver and kidneys, as well as disrupts normal reproductive development in subsequent generations.¹⁴

Benzophenone  is Found In 97% of Humans Tested
Due to such excessive use as has been promoted by both sunscreen manufacturers and the medical community, the chemicals are now so ubiquitous in the environment that they are in the bloodstreams of 97% of Americans who were tested, including 90% of Americans who stated that they had never used sunscreens.¹⁵

Sunscreen chemicals are also found in household dust, which means that we are breathing them into our lungs, giving them even greater access to the bloodstream.¹⁶

In addition, 85% of nursing mothers' milk samples now test positive for sunscreen chemicals, resulting in our children's drinking potent hormones during crucial early development.¹⁷

An even bigger problem is that many ingredients belong to a chemical family known as phenols. Bisphenol A (BPA) is a commonly known phenol, which as of 2011 in California and 10 other states is outlawed in baby bottles and baby items such as pacifiers.¹⁸

Phenols can pass through the placenta and enter the fetus.¹⁹ The fact that offspring of mice and rats exposed to sunscreen chemicals show general, thyroid, and reproductive toxicity means that these chemicals can cause the same harmful changes in our human offspring.²⁰

The Vitamin D Deficiency Pandemic
The promotion of using sunscreens in epidemic proportions has led to what is being described as a worldwide pandemic of vitamin D deficiency, so extreme that there has been a reemergence of rickets, the "17th century disease," in some parts of the world, including America.²¹ Rickets was given that title as it was rampant when people congregated in cities which became so large that they did not have exposure to sunlight. The vitamin D produced in the skin – our own built-in vitamin D manufacturing plant – in response to solar radiation is a crucial part of our overall health. Adequate vitamin D levels are essential to absorb calcium from the foods that we eat. With low levels of vitamin D, the body cannot adequately regulate calcium or phosphate levels for proper bone formation. This results in soft bones in newborns and toddlers. The children become bowlegged or knock-kneed and are diagnosed with rickets.²² Low vitamin D also results in the body's using parathyroid hormone to pull calcium from the bones for necessary muscle contraction and nerve conduction, which weakens bones even further, rather than building them. Back in the 17th century, once it was realized that lack of sun and therefore diminished levels of vitamin D in the body led to the development of rickets, sun exposure was actively encouraged, including putting babies and toddlers out in the sun, as well as fortifying foods with vitamin D. These practices wiped out that last pandemic.

Today, the message to fear the sunlight, along with the warning to never go in the sun without sunscreen, has led not only to a reemergence of rickets in the 21st century, but also to an increase in the many disease states that develop from low vitamin D levels, including osteoporosis.

Vitamin D plays such numerous roles in most body systems that our entire population is at risk for the many disease states that arise when levels of vitamin D are deficient due to slathering on sunscreen before going outdoors. Newborn infants are at risk for seizures because of low calcium levels caused by low vitamin D.²³ Owing to its involvement in glucose metabolism, type 2 diabetes in adults is shown to be associated with low vitamin D levels, and low levels during pregnancy can result in newborns and children developing type 1 diabetes.²⁴ Many autoimmune diseases such as Hashimoto's thyroiditis as well as bowel disorders like Crohn's disease can arise.²⁵

Important in muscle metabolism, vitamin D levels when deficient can lead to fibromyalgia.²⁶ The weakened muscles also can result in bladder incontinence and weak pelvic floors in women, which is linked to an increase in the number of caesarean deliveries that are necessary.²⁷

Part 2 is also online

Dr. Elizabeth Plourde
elizabeth@newvoice.net
P.O. Box 14133
Irvine, California 92623-4133

Notes
1.  World Health Organization Website: The World Health Organization recommends that no person under 18 should use a sunbed. Available at: www.who.int/mediacentre/news/notes/2005/np07/en/index.html. Accessed June 1, 2011.
2.  Christenson LJ, Borrowman TA, Vachon CM, et al. Incidence of basal cell and squamous cell carcinomas in a population younger than 40 years. JAMA. 2005;294(6):681–690.
3.  Rogers HW, Weinstock MA, Harris AR, et. al. Incidence estimate of nonmelanoma skin cancer in the United States, 2006. Arch Drematol. 2010;146(3):283–287.
4.  eMedicine Website. Amirlak B. Skin anatomy. Available at: http://emedicine.medscape.com/article/1294744-overview#aw2aab6b3. Accessed 5/27/10.
5.  US Dept. of Health and Human Services Website. Question and Answers: FDA announces new requirements for over-the-counter (OTC) sunscreen products marketed in the U.S. Available at: www.fda.gov/Drugs/ResourcesForYou/Consumers/BuyingUsingMedicineSafely/UnderstandingOver-the-CounterMedicines/ucm258468.htm. Updated 06/24/2011. Accessed October 28, 2011.
6.  Nguyen U, Scholossman D. Stability Study of Avobenzone with Inorganic Sunscreens. www.koboproductsinc.com/Downloads/NYSCC-Avobenzone.pdf. Accessed March 20, 2011.
7.  Schlumpf M, Schmid P, Durrer S, et. al. Endocrine activity and developmental toxicity of cosmetic UV filters–an update. Toxicology. 2004;205:113–122.
8.  Escobedo João F, et al., Ratios of UV, PAR and NIR components to global solar radiation measured at Botucatu site in Brazil, Renewable Energy. 2010. doi:10.1016/j.renene.2010.06.018 (Article in Press).
9.  Bachem A, Reed CI. The penetration of radiation through human skin. Am J Physiol. 1931;97: 86–91. Cited in Schieke SM, Schroeder P, Krutmann J. Cutaneous effects of infrared radiation: from clinical observations to molecular response mechanisms. Photodermatol Photoimmunol Photomed. 2003;19(5):228–234.
10.Kligman LH. Full spectrum solar radiation as a cause of dermal photodamage: UVB to infrared. Acta Derm Venereol Suppl (Stockh). 1987;134:53–61.
     Schroeder P, Haendeler J, Krutmann J. The role of near infrared radiation in photoaging of the skin. Exp Gerontol. 2008. 43(7):629–632. Epub 2008 Apr 27.
11.Schroeder P, Pohl C, Calles C, et.al. Cellular response to infrared radiation involves retrograde mitochondrial signaling. Free Radical Biology and Medicine. 2007;43(1):128–135.
12.Fent K, Kunz PY, Gomez E. UV filters in the aquatic environment induce hormonal effects and affect fertility and reproduction in fish. Endocrine disruptors: natural waters and fishes. Chimia. 2008;62(5):368–375.
Kunz PY. Fent K. Multiple hormonal activities of UV filters and comparison of in vivo and in vitro estrogenic activity of ethyl-4-aminobenzoate in fish. Aquat Toxicol. 2006;79:305.
13.Kunz PY, Fent K. Multiple hormonal activities of UV filters and comparison of in vivo and in vitro estrogenic activity of ethyl-4-aminobenzoate in fish. Aquat Toxicol. 2006;79(4):305–324. Epub 2006 Jun 30.
14.Chapin R, Gulati D, Mounce R. 2-Hydroxy-4-methoxybenzophenone. Environ Health Perspect. 1997;105(Supplement 1):313–314. Available at: www.ncbi.nlm.nih.gov/pmc/articles/PMC1470294/pdf/envhper00326-0308.pdf.
15.Calafat AM, Wong LY, Ye X, Reidy JA, Needham LL. Concentrations of the sunscreen agent benzophenone-3 in residents of the United States: National Health and Nutrition Examination Survey 2003–2004. Environ Health Perspect. 2008;116(7):893–897. Available at: www.medscape.com/viewarticle/577046.
16.Negreira N, Rodríguez I, Rubí E, Cela R. Determination of selected UV filters in indoor dust by matrix solid-phase dispersion and gas chromatography–tandem mass spectrometry. J Chromatogr A. 2009;1216(31):5895–5902. Epub 2009 Jun 10.
17.Schlumpf M, Kypke K, Wittassek M, et. al. Exposure patterns of UV filters, fragrances, parabens, phthalates, organochlor pesticides, PBDEs, and PCBs in human milk: Correlation of UV filters with use of cosmetics. Chemosphere. 2010;81(10):1171–1183. Epub 2010 Oct 27.
18.United Press International Website. California bans BPA in baby bottles. www.upi.com/Science_News/2011/10/05/California-bans-BPA-in-baby-bottles/UPI-67921317866619/. Updated October 5, 2011. Accessed October 28, 2011.
19.Nishikawa M, Iwano H, Yanagisawa R, Koike N, Inoue H, Yokota H. Placental transfer of conjugated bisphenol A and subsequent reactivation in the rat fetus. Environ Health Perspect. 2010;118(9):1196–1203. Epub 2010 Apr 9.
Balakrishnan B, Henare K, Thorstensen EB, Ponnampalam AP, Mitchell MD. Transfer of bisphenol A across the human placenta. Am J Obstet Gynecol. 2010;202(4):393.e1-7.
20.Schmutzler C, Bacinski A, Gotthardt I, et. al. The ultraviolet filter benzophenone 2 interferes with the thyroid hormone axis in rats and is a potent in vitro inhibitor of human recombinant thyroid peroxidase. Endocrinology. 2007;148(6):2835–2844. Epub 2007 Mar 22.
Boas M, Feldt-Rasmussen U, Skakkebaek NE, Main KM. Environmental chemicals and thyroid function. Eur J Endocrinol. 2006;154(5):599–611.
21.Holick MF, Chen TC. Vitamin D deficiency: a worldwide problem with health consequences. Am J Clin Nutr. 2008;87(4):1080S–1086S.
Alleyne R. Vitamin D health warning for the children who shun the sun. www.telegraph.co.uk/health/healthnews/7995128/Vitamin-D-health-warning-for-the-children-who-shun-the-sun.html#disqus_thread. Accessed February 2, 2011.
Medscape Today Website. Rickets Reemerging In United States. www.medscape.com/viewarticle/412104. Accessed February 2, 2011.
Medline Plus Website. Rickets. Available at: www.nlm.nih.gov/medlineplus/ency/article/000344.htm. Accessed November 26, 2011.
Office of Dietary Supplements (NIH) Website. Dietary supplement fact sheet: vitamin D. Available at: http://ods.od.nih.gov/factsheets/VitaminD/. Accessed November 26, 2011.
23.Alleyne R. Vitamin D health warning for the children who shun the sun. www.telegraph.co.uk/health/healthnews/7995128/Vitamin-D-health-warning-for-the-children-who-shun-the-sun.html#disqus_thread. Accessed February 2, 2011.
24.Ozfirat Z, Chowdhury T. Vitamin D deficiency and type 2 diabetes. Postgrad Med J 2010; 86:18-25. doi:10.1136/pgmj.2009.078626.
Mohr SB, Garland CF, Gorham ED, Garland FC. The association between ultraviolet B irradiance, vitamin D status and incidence rates of type 1 diabetes in 51 regions worldwide. Diabetologia. 2008;51(8):1391–1398. Epub 2008 Jun 12.
Hyppönen E, Laara E, Reunanen A, Jarvelin M-R, Virtanen SM. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet. 2001;358(9292):1500–1503.
25.Kivity S, Agmon-Levin N, Zisappl M, et al. Vitamin D and autoimmune thyroid diseases. Cell Mol Immunol. 2011;8(3):243–247. Epub 2011 Jan 31.
Hewison M. Vitamin D and immune function: an overview. Proc Nutr Soc. 2011;18:1–12. [Epub ahead of print]
26.Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain. Mayo Clin Proc. 2003;78(12):1463–1470.
27.Schubert L, DeLuca HF. Hypophosphatemia is responsible for skeletal muscle weakness of vitamin D deficiency. Arch Biochem Biophys. 2010;500(2):157–161. Epub 2010 May 31.
Barclay L. Higher Vitamin D Levels Linked to Lower Risk for Female Pelvic Floor Disorders? www.medscape.com/viewarticle/719592. Accessed February 2, 2011.
Barclay L. Vitamin D Deficiency Linked to Greater Risk for Primary Cesarean Delivery. www.medscape.com/viewarticle/585864. Accessed February 2, 2011.