The Ingredients are Simple:
Zinc Oxide Powder, Organic Shea Butter, Beeswax Organic, Olive Oil, Organic Coconut Oil, and Fragrances derived from Essential Oils.
Fragrance Free available
We only source the best ingredients for all of our products. Organic and natural ingredients that are fair trade is what we strive for, and if it's available, rest assured it's in your sunscreen from Sun Worshiper Sunscreen.
Whats the BIG deal?
We use Sunscreen to keep from getting sunburn and to prevent skin cancer. Most brands (not ours) can actually cause Skin Cancer among other things we haven’t even discovered because of their ingredients like Oxybenzone, Octinoxate, Ethylhexyl, and Homosalate to name a few. Oxybenzone Acts like estrogen in the body; alters sperm production in animals; associated with endometriosis in women. These chemicals do not need to be on your skin or in your blood stream.
We use only the best ingredients available in all of our products(90% Organic). Sun Worshiper Sunscreen uses Pharmaceutical Cosmetic Grade Zinc Oxide Non-nano as its only active ingredient. Non-nano means it wont enter the blood stream. We also get SPF from the Organic Coconut Oil & Raw Shea Butter.
Our natural sunscreen has many benefits and once you try it you will feel the difference and the love that is put in to every bottle.
What are other companies putting in their Sunscreen?
What are other companies putting in their sunscreen, and why?
Most of the sunscreen companies put very harsh chemicals in their brands to propel them from an aerosol container, or to rub in nice so you can't even tell you're wearing sunscreen.
The fact is that those chemicals to make their products do that are killing us, even if we don't use those other brands, they leach into the water supply and are not filtered out by standard methods.
Feel confident wearing our sunscreen that you are doing the best for you, your family and our planet.
Found in other Companies sunscreen's, not ours!
Safety Measures/Side Effects:
According to the Environmental Working Group, there are several suspected dangers associated with Oxybenzone. Despite its sun protective abilities, it has been shown to penetrate the skin and cause photo-sensitivity. As a photocarcinogen, it has demonstrated an increase in the production of harmful free radicals and an ability to attack DNA cells; for this reason, it is believed to be a contributing factor in the recent rise of Melanoma cases with sunscreen users. Some studies have shown it to behave similarly to the hormone estrogen, suggesting that it may cause breast cancer. It has also been linked to contact eczema and allergies.
In addition, there exist many concerns regarding the human body’s percutaneous absorption of Oxybenzone. In one study, individuals applied a sunscreen with 4% Oxybenzone and submitted urine samples 5 days after topical application. All the subjects’ urine secretions were found to contain Oxybenzone, suggesting the body’s ability to store the substance (Source). In 2008, the US Centers for Disease Control & Prevention conducted a similar experiment on a national scale, and found the chemical compound to be present in 96.8% of the human urine samples surveyed (Source). As a result, it is recommended that parents keep their small children from using products containing the ingredient. This is based on the assertion that children under the age of 2 have not fully developed the enzymes that are required to break down derivatives of Oxybenzone. Source
Oxybenzone is produced by Friedel-Crafts reaction of benzoyl chloride with 3-methoxyphenol(3-hydroxyanisole).
Oxybenzone is used in plastics as an ultraviolet light absorber and stabilizer. It is used, along with other benzophenones, in sunscreens, hair sprays, and cosmetics because they help prevent potential damage from sunlight exposure. It is also found, in concentrations up to 1%, in nail polishes.Oxybenzone can also be used as a photostabilizer for synthetic resins. Benzophenones can leach from food packaging, and are widely used as photo-initiators used to start a chemical that dries ink faster.
As a sunscreen, it provides broad-spectrum ultraviolet coverage, including UVB and short-wave UVA rays. As a photoprotective agent, it has an absorption profile spanning from 270 to 350 nm with absorption peaks at 288 and 350 nm. It is one of the most widely used organic UVA filters in sunscreens today. It is also found in nail polish, fragrances, hairspray, and cosmetics as a photostabilizer. Despite its photoprotective qualities, much controversy surrounds oxybenzone because of its possible hormonal and photoallergenic effects, leading many countries to regulate its use.
Safety and controversy:
Some debate focuses on the potential of oxybenzone as an endocrine disruptor. According to the Environmental Working Group (EWG) oxybenzone is ineffective and harmful. Similar concerns have been expressed for related products including avobenzone, octisalate, octocrylene, homosalate, and octinoxate. Due to the advent of PABA-free sunscreens, oxybenzone is now the most common allergen found in sunscreens.
In vivo studies
Among common sunscreen chemicals, oxybenzone is associated with allergic reactions triggered by sun exposure. In a study of 82 patients with photoallergic contact dermatitis, over one quarter showed photoallergic reactions to oxybenzone.
In a 2008 study of participants ages 6 and up, oxybenzone was detected in 96.8% of urine samples. Humans can absorb anywhere from 0.4% to 8.7% of oxybenzone after one topical application of sunscreen, as measured in urine excretions. This number can increase after multiple applications over the same period of time. Oxybenzone is particularly penetrative because it is the most lipophilic of the three most common UV filters.
When applied topically UV filters, such as oxybenzone, are absorbed through the skin, metabolized, and excreted primarily through the urine. The method of biotransformation, the process by which a foreign compound is chemically transformed to form a metabolite, was determined by Okereke and colleagues through oral and dermal administration of oxybenzone to rats. The scientists analyzed blood, urine, feces, and tissue samples and found three metabolites: 2,4-dihydroxybenzophenone(DHB), 2,2-dihydroxy-4-methoxybenzophenone (DHMB) and 2,3,4-trihydroxybenzophenone (THB). To form DHB the methoxy functional group undergoes o-dealkylation; to form THB the same ring is hydroxylated.Ring B in oxybenzone is hydroxylated to form DHMB.
A study done in 2004 measured the levels of oxybenzone and its metabolites in urine. After topical application to human volunteers, results revealed that up to 1% of the applied dose was found in the urine. The major metabolite detected was DHB and very small amounts of THB were found. By utilizing the Ames test in Salmonella typhimurium strains, DHB was determinted to be nonmutagenic. Source
Widespread usage; best UVA protection of chemical filters Very limited skin penetration No evidence of hormone disruption Relatively high rates of skin allergy
Avobenzone appears to be relatively non-toxic and non-irritating to the skin. However, because it is often used in conjunction with photo-stabilizers, there is a greater risk for skin irritation and low-level toxicity. Furthermore, some studies have demonstrated it to be absorbed by the body and secreted into urine, and is therefore not recommended to use on children or pregnant women. Some skin specialists believe it to be just as harmful as PABA, and certain studies suggest that the ingredient behaves similarly to the hormone estrogen; however, the SCCNFP has gone on to negate the latter mentioned claim for chemical sunscreen actives in general.
Titanium dioxide is the subject of new controversy, yet it is a substance as old as the earth itself. It is one of the top fifty chemicals produced worldwide. It is a white, opaque and naturally- occurring mineral found in two main forms: rutile and anatase. Both forms contain pure titanium dioxide that is bound to impurities. Titanium dioxide is chemically processed to remove these impurities, leaving the pure, white pigment available for use. Titanium dioxide has a variety of uses, as it is odorless and absorbent. This mineral can be found in many products, ranging from paint to food to cosmetics. In cosmetics, it serves several purposes. It is a white pigment, an opacifier and a sunscreen. Concern has arisen from studies that have pointed to titanium dioxide as a carcinogen and photocatalyst, thus creating fear in consumers. But are these claims true? What does the research on these allegations bear out? Would we as consumers benefit from avoiding this mineral to preserve our long-term health?
A carcinogen is a substance that causes a cellular malfunction, causing the cell to become cancerous and thus potentially lethal to the surrounding tissue and ultimately the body as these rapidly growing mutated cells take over. With the surge in cancer rates among all segments of the population, many people are attempting to reduce or eliminate their exposure to carcinogens. Titanium dioxide is regarded as an inert, non-toxic substance according to its Material Safety Data Sheet (MSDS)
One form of mineral or mineral extract, including titanium dioxide, that we should be concerned about is ultrafine or nano particles. As technology has advanced, so has its ability to take normal sized particles of minerals and reduce them to sizes never before imagined. While many are praising this new technology, others are warning of its inherent dangers to our bodies.
The smaller the particle size, the more toxic it is (see Table 2). This conclusion is relevant to the consumer because of the cosmetics industry's increasing use of micronized pigments in sunscreens and colour cosmetics. Nanoparticles of titanium dioxide are used in sunscreens because they are colourless at that size and still absorb ultraviolet light. Many cosmetic companies are capitalizing on metal oxide nanoparticles. We have seen, however, that if titanium dioxide particles used to act as a sunscreen are small enough, they can penetrate the cells, leading to photocatalysis within the cell, causing DNA damage after exposure to sunlight (Powell, et. al. 1996) The fear is that this could lead to cancer in the skin.
With the multitude of cosmetics and chemicals available to us, it is in our best interest to become informed as consumers and make pure, natural and simple choices to protect our health and longevity.
Human endocrine disruptor - strong evidence European Commission on Endocrine Disruption
One or more studies show significant wildlife and the environment disruption
Produces excess reactive oxygen species that can interfere with cellular signaling, cause mutations, lead to cell death and may be implicated in cardiovascular disease.
One or more human case studies show possible photoallergic or allergenic effects
One or more animal studies show reproductive effects at moderate doses
Ingredient is suspected or measured to accumulate in people
Wildlife and environmental toxicity
Enhanced Skin Absorption Penetration enhancer
Similar to other UV filter compounds, more homosalate is absorbed into the stratum corneum of the face (25% of applied dose) versus back of volunteers. Homosalate has been identified as an antiandrogen in vitro, as well as having estrogenic activity toward estrogen receptors α, and general in vitro estrogenic activity. Homosalate has been shown to be an antagonist toward androgen and estrogen receptors in vitro. There is also heavy evidence that homosalate, (and other UV filters) can break down into more toxic products
Found in mothers’ milk; skin penetration less than 1% in human and laboratory studies
Widespread; stabilizes avobenzone, Skin penetration in lab studies. Rarely reported skin allergy This organic compound can penetrate into the skin where it acts as a photosensitizer. This results in an increased production of free radicals under illumination. Free radicals are known to induce indirect DNA damage, and an increased concentration of free radicals might have contributed to the increased incidence of malignant melanoma in sunscreen-users compared to non-users Source
Widespread usage, Found in mothers’ milk; skin penetration in lab studies Relatively high rates of skin allergy Octisalate's safety record seems to be fairly good although it has been linked to contact dermatitis.
The acute toxicity of DEHP is low in animal models: 30 g/kg in rats (oral) and 24 g/kg in rabbits (dermal). Concerns instead focus on its potential as an endocrine disruptor.
DEHP, along with other Phthalates, is believed to cause endocrine disruption in males through its action as an androgen antagonist, and may have lasting effects on reproductive function both for childhood and adult exposures. Prenatal phthalate exposure has been shown to be associated with lower levels of reproductive function in adolescent men. In another study, airborne concentrations of DEHP at a PVC pellet plant were significantly associated with a reduction in sperm motility and chromatin DNA integrity. Additionally, the authors noted that the daily intake estimates for DEHP were comparable to the general population, indicating that a “high percentage of men are exposed to levels of DEHP that may affect sperm motility and chromatin DNA integrity”.
In one study, the level of phthalates and DEHP metabolites in the blood of pregnant women was significantly correlated with decreased penis width, shorter anogenital distance, and incomplete descent of testes of their newborn sons, replicating effects identified in animals. Approximately 25% of US women have phthalate levels similar to those in the study. However, the study author cautioned that replication of these results are needed to strengthen any links between phthalates and adverse health outcomes in humans.
Numerous studies of DEHP have shown changes in sexual function and development in mice and rats. DEHP exposure during pregnancy has been shown to disrupt placental growth and development in mice, resulting in higher rates of low birthweight, premature birth, and fetal loss. In a separate study, exposure of neonatal mice to DEHP through lactation caused hypertrophy of the adrenal glands and higher levels of anxiety during puberty. In another study, pubertal administration of higher-dose DEHP delayed puberty in rats, reduced testosterone production, and inhibited androgen-dependent development; low doses showed no effect.
When DEHP is ingested intestinal lipases convert it to MEHP, which then is absorbed. MEHP is suspected to have an obesogenic effect. Rodent studies and human studies have shown DEHP to be a possible disruptor of thyroid function, which plays a key role in energy balance and metabolism. Exposure to DEHP has been associated with lower plasma thyroxine levels and decreased uptake of iodine in thyroid follicular cells. Previous studies have shown that slight changes in thyroxine levels can have dramatic effects on resting energy expenditure, similar to that of patients with hypothyroidism, which has been shown to cause increased weight gain in those study populations.
A clinically relevant dose and duration of exposure to DEHP has been shown to have a significant impact on the behavior of cardiac cells in culture. This includes an uncoupling effect that leads to irregular rhythms in vitro. Untreated cells had fast conduction velocity, along with homogenous activation wave fronts and synchronized beating. Cells treated with DEHP exhibited fractured wave fronts with slow propagation speeds. This is observed in conjunction with a significant decrease in the amount of expression and instability of gap junctional connexin proteins, specifically connexin-43, in cardiomyocytes treated with DEHP.
The decrease in expression and instability of connexin-43 may be due to the down regulation of tubulin and kinesin genes, and the alteration of microtubule structure, caused by DEHP; all of which are responsible for the transport of protein products. Also, DEHP caused down regulation of several growth factors, such as angiotensinogen, transforming growth factor-beta, vascular endothelial growth factor C and A, and endothelial-1. The DEHP-induced down regulation of these growth factors may also contribute to the reduced expression and instability of connexin-43.
DEHP has also been shown, in vitro using cardiac muscle cells, to cause activation of PPAR-alpha gene, which is a key regulator in lipid metabolism and peroxisome proliferation; both of which can be involved in atherosclerosis and hyperlipidemia, which are precursors of cardio vascular disease.
Other health effects
Studies in mice have shown other adverse health effects due to DEHP exposure. Ingestion of 0.01% DEHP caused damage to the blood-testis barrier as well as induction of experimental autoimmune orchitis. There is also a correlation between DEHP plasma levels in women and endometriosis.
DEHP is also a possible cancer causing agent in humans, although human studies remain inconclusive, due to the exposure of multiple elements and limited research. In vitro and rodent studies indicate that DEHP is involved in many molecular events, including increased cell proliferation, decreased apoptosis, oxidative damage, and selective clonal expansion of the initiated cells; all of which take place in multiple sites of the human body.