Languages:
Home » Tooth Whiteners » Level 3 » Question 6

Tooth Whiteners & Oral Hygiene Products containing hydrogen peroxide

6. How safe are products containing hydrogen peroxide?

  • 6.1 How are hydrogen peroxide solutions classified and labelled?
  • 6.2 How safe are oral hygiene products and toothwhiteners?

6.1 How are hydrogen peroxide solutions classified and labelled?

The SCCP opinion states:

3.3.13.2. Regulations

IARC has concluded that there is “limited” evidence of carcinogenicity of hydrogen peroxide in experimental animals (IARC 1999).

No labelling is required in EU for hydrogen peroxide solutions of less than 5%. Solutions containing above 5% hydrogen peroxide are labelled harmful. In addition solutions containing: 5 – 8% hydrogen peroxide are labelled “Irritating to eyes” (R36), more than 8% are labelled "Harmful if swallowed" and “Risk of serious damage to eyes” (R22-41), more than 35% have an additional label “Irritating to respiratory system and skin”, higher concentrations are in addition labelled “Cases burn”.

According to Annex III of the Cosmetic Products Directive, oral hygiene products must not contain more than 0.1% hydrogen peroxide.

Source & ©: SCCP,  Opinion on Hydrogen peroxide, in its free form or when released, in oral hygiene products (2007), 3.3 Toxicological evaluation, 3.3.13. Safety evaluation, p.62

6.2 How safe are oral hygiene products and toothwhiteners?

The SCCP opinion states:

3.3.13. Safety evaluation (including calculation of the MoS)

3.3.13.1 Calculation of MOS

SCCP is of the opinion that the risk of systemic effects is low. This is supported by the fact that hydrogen peroxide which may enter into the bloodstream is rapidly metabolised. However, adverse effects have been observed in repeated dose studies in animals, allowing calculation of a MoS for systemic toxicity. Irritating effects both due to a direct effect in the oral cavity and in the gastrointestinal system after swallowing are of concern.

Toothpastes and mouth-rinses

Repeated dose toxicity

A NOAEL of 20 mg/kg bw/day of hydrogen peroxide has been obtained from a 100 days rat gavage study based on a significantly reduced plasma catalase level at higher dose levels

Estimated daily exposure (SCCP, 2007):

Toothpaste: 480 mg/day

Mouth-rinses:3000 mg/day

Concentration of hydrogen peroxide: 0.1%

Toothpaste: 0.48 mg/day, Systemic exposure (0.48/60) 0.008 mg/kg bw/d

MOS = (20/0.008) 2500

Mouth-rinse: 3.0 mg/d, Systemic exposure (3.0/60) 0.05 mg/kg bw/d

MOS = (20/0.05) 400

Conclusion

The calculated MOS for repeated dose toxicity is considered to give sufficient protection in relation to the use of 0.1% hydrogen peroxide in its free form or when released when used in oral hygiene products.

Tooth whitening products

Safety calculation of tooth whitening products due to hydrogen peroxide may be performed by MOS calculations based on the systemic exposure or by comparing the exposure in μg/cm2 caused by tooth whitening products with that causing an adverse effect.

MOS calculation

Estimated daily exposure from tooth whitening products containing 6% hydrogen peroxide is estimated to 0.2 mg/kg bw/d (see discussion)

Repeated dose toxicity

A NOAEL of 20 mg/kg bw/day of hydrogen peroxide has been obtained from a 100 days rat gavage study based on a significantly reduced plasma catalase level at higher dose levels

MOS = (20/0.2) 100

Conclusion

The calculated MOS for repeated dose toxicity is on the borderline of that considered to give sufficient protection in relation to the use of 6% hydrogen peroxide in its free form or when released when used in tooth whitening products. For hydrogen peroxide concentrations above 6% the MOS will be below 100, and thus not considered safe.

3.3.14. Discussion

Chemistry

Possible impurities in hydrogen peroxide and carbamide peroxide as well as the hydrogen peroxide releasing substances discussed in Appendix (sodium perborate, sodium percarbonate and peroxymonosulphate) are not known. No information on the stability of hydrogen peroxide and hydrogen peroxide releasing substances in oral hygiene products was submitted.

Acute toxicity of hydrogen peroxide

The oral and dermal LD50 in rats is higher than 600 mg/kg bw. The dermal LD50 in rabbits is 630 mg/kg bw.

A 16-month-old boy (body weight 11.6 kg) died after ingestion of about 600 mg/kg bw.

Irritation and corrosivity

Skin irritation in rabbits following 4 hour exposure to 10% hydrogen peroxide was slight. A 5% solution of hydrogen peroxide was slightly irritating to the eye while a 10% solution was highly irritating. The threshold of detection for irritation was about 0.1% when hydrogen peroxide was administered as drops directly to the human eye.

Stomach gavage of 15 mg/kg bw of carbamide peroxide (5.4 mg/kg bw of hydrogen peroxide) produced ulceration of gastric mucosa in rats observed after 1 hour; the lesions appeared to be healing after 24 hours. No effects were observed with 5 mg/kg bw of carbamide peroxide (1.8 mg/kg bw of hydrogen peroxide) (Dahl and Becher, 1995).

Solutions containing more than 5 % hydrogen peroxide are in EU labelled harmful due to eye and skin irritation.

Skin sensitisation

Hydrogen peroxide is not considered to cause skin sensitisation.

Dermal / percutaneous absorption

Biological membranes are highly permeable to hydrogen peroxide. Thus, hydrogen peroxide is expected to be readily taken up by the cells constituting the absorption surfaces, but at the same time it is effectively metabolised, and it is uncertain to what extent the unchanged substance may enter into blood circulation. Moreover, in the red blood cells have an immense metabolic capacity to degrade hydrogen peroxide.

Repeated dose toxicity

In a 90 day study in mice with hydrogen peroxide in the drinking , a NOAEL of 100 ppm was found based on dose-related reductions in food and water consumption, and on the observation of duodenal mucosal hyperplasia. This corresponds to 26 and 37 mg/kg bw/day for males and females, respectively. In a 100 days rat gavage study a NOAEL of 20 mg/kg bw/day was found based a significantly reduced plasma catalase level at higher dos levels.

A NOAEL of 20 mg/kg bw/day of hydrogen peroxide may be used for calculation of MOS for repeated dose toxicity.

Mutagenicity / Genotoxicity

Hydrogen peroxide is a mutagen and genotoxicant in a variety of in vitro test systems. The responses observed were modified by the presence of degrading enzymes (catalase), the extent of formation of hydroxyl radicals by Fenton reaction, and the cells repair abilities.

The available studies are not in support of a significant genotoxicity/mutagenicity for hydrogen peroxide under in vivo conditions. Further studies of genotoxicity and mutagenicity tissues in direct contact with hydrogen peroxide are needed. Mechanistic studies suggest that cells are adapted to repair DNA damage caused by oxidants; on the other hand there is some evidence that hydrogen peroxide may inhibit the repair of DNA lesions inflicted by other types of reactive chemicals.

Carcinogenicity

A drinking water study in mice showed that hydrogen peroxide caused duodenal hyperplasia at a high frequency and localised duodenal carcinomas at a low frequency. A subsequent study with different strains of mice showed a strong negative correlation between incidence of duodenal tumours and catalase activity in duodenal mucosa. In one study with rats a high incidence of forestomach papillomas were found after receiving 1% hydrogen peroxide in the drinking water. While humans do not have a forestomach, they do have comparable squamous epithelium tissues in the oral cavity and the upper 2-3 part of the oesophagus. Thus, in principle, carcinogens targeting the forestomach squamous epithelium rodents are relevant for humans. Also, the target tissues for carcinogens may differ between experimental animals and humans and a forestomach carcinogen in rodent may target a different tissue in humans. Some tumour promotion studies indicate that hydrogen peroxide may act as a promoter.

Hydrogen peroxide has a weak potential to induce local carcinogenic effects. The mechanism is unclear, but a genotoxic mechanism cannot be excluded. As regard to tumour promotion, several mechanisms might be operative; direct genotoxicity, impairment of DNA repair, and chronic inflammation.

Reproductive toxicity

No appropriate animal studies were available for a complete evaluation of reproductive and developmental toxicity. Limited studies with mice and rats exposed to hydrogen peroxide in drinking water suggested no grave disturbances on the male or female reproductive functions.

Toxicokinetics

Hydrogen peroxide is a normal metabolite in the aerobic cells. It is produced from superoxide anion spontaneously or as a result of the activity of superoxide dismutase (SOD). Hydrogen peroxide occurs under most conditions at submicromolar concentrations in the organism. Because hydrogen peroxide reacts slowly with organic substrates, it can diffuse considerable distances in biological systems. There are two main hydrogen peroxide metabolising enzymes, catalase and glutathione peroxidase which control the hydrogen peroxide concentration. Catalase deals with large amounts of H2O2 that may be generated in peroxisomes. Glutathione peroxidase (GSH peroxidase) metabolises H2O2 in both the cytosolic and mitochondrial compartments. Significant amounts of topically applied hydrogen peroxide can penetrate the epidermis or mucous membranes followed by rapid spontaneous or enzyme-catalysed decomposition to oxygen and water in the underlying tissue. The local spontaneous or enzymatic-catalysed breakdown prevents it to enter the general circulation and thus its systemic distribution.

In the presence of traces of transition metal ions, superoxide anion and hydrogen peroxide undergo the so-called iron-catalyzed Haber-Weiss reaction which results in OH· formation. The hydroxyl radical is highly reactive and oxidises all organic chemicals, including biomolecules, when present in very close proximity to the place where the hydroxyl radical is formed. Superoxide and H2O2 are less reactive and can diffuse away from their site of formation, leading to OH· generation whenever they meet a “spare” transition metal ion.

Acatalasemic individuals are more susceptible to hydrogen peroxide exposure because of a hereditary disorder in their hydrogen peroxide metabolising enzymes, i.e. the blood catalase activity level is below normal (hypocatalasemia). Acatalesemia is a rare (frequency 0.2-0.4%) genetic defect occurring particularly in the Orient. Another group of individuals more sensitive to hydrogen peroxide exposure is persons with G6PD deficiency. It is estimated that about 400 million people throughout the world are deficient in G6PD. The frequency in G6PD deficiency in Europe is about 0.1%. Industry claimed that due to the low levels of hydrogen peroxide in saliva during use of tooth whitening products and conversion of exogenous hydrogen peroxide to water and oxygen, hydrogen peroxide would not be expected to persist long enough in the body to reach G6PD deficient erythrocytes and to provoke an oxidative response.

Studies on specific product types

Toothpastes and mouth-rinses

Exposure

According to SCCP (2007) the total amount of toothpaste ingested per day is 480 mg. Assuming 0.1% hydrogen peroxide, the amount of hydrogen peroxide ingested per day will be 0.008 mg/kg bw/d from toothpaste. The amount of mouth-rinses ingested is 3 g per day. Assuming 0.1% hydrogen peroxide, the amount of hydrogen peroxide ingested per day will be 0.05 mg/kg bw/d from mouth-rinses.

Mucous membrane irritation

Ulceration of gastric mucosa in rats was observed 1 hour after gavage with a dose corresponding to 5.4 mg/kg bw of hydrogen peroxide while no effects were found at 1.8 mg/kg bw of hydrogen peroxide. This is (1.8/0.008) 225 times higher than the dose expected using toothpaste containing 0.1% hydrogen peroxide. On the other hand it is only (1.8/0.05) 36 times higher than the dose expected using a mouth-rinse containing 0.1% hydrogen peroxide.

Clinical safety data

Several clinical studies with toothpaste containing up to 3% hydrogen peroxide have been carried out. All studies were conducted by the manufactures. The duration of the studies varied from 48 hours to 6 months. Only two studies with a total of 165 persons had a duration of 6 months. No product related adverse events were mentioned.
No treatment-related effects were reported in two 7 days studies with mouth-rinses containing 1.5% hydrogen peroxide. In a human study where a mouth-rinse containing 3% hydrogen peroxide were used 3 to 5 times per day, mucosal irritation was found in 2 individuals with prior tissue injury. The pre-existing lesions worsened after exposure to hydrogen peroxide. There is a need for independent long-term studies with both toothpaste and mouth-rinses.

Tooth whitening products

Exposure

It is difficult to assess the exposure, which may vary with the product and the level of active material (hydrogen peroxide) used.

In a study were salivary hydrogen peroxide was determined using a 6% hydrogen peroxide strip , assuming a salivary flow of 0.3 ml/min, the calculated exposure from 4 strips a day was 0.08 mg/kg bw/d. If mean + 2SD is used the exposure will be 0.17 mg/kg bw/d. It should be noted that the numbers may be minimum numbers since application of the strips most likely will stimulate salivary flow, which may be as high as 2.0 ml/min. Thus, the exposure may be underestimated.

The total amount of peroxide (mg) released during a 60 min bleaching period was determined from whole saliva collections with 4 different bleaching regimes (two tray-based [Whitestrips, Vivastyle] (tray-based) and two paint on products [Crest Night Effects, Colgate Simply White]). Amount of hydrogen peroxide released; Whitestrips: 1.39 + 0.62 mg, Vivastyle: 2.47 + 0.82 mg, Crest Night Effects: 0.23 + 0.13 mg, and Colgate Simply White: 2.67 + 0.88 mg. In terms of amount of peroxide per kg body weight the bleaching systems led to a single exposure of maximum 0.046 mg/kg bw of hydrogen peroxide (Colgate Simply White). Smoking did not affect the degrading of hydrogen peroxide from bleaching products.

The concentration of hydrogen peroxide in contact with the teeth will be close to the concentration in the bleaching product. The gingival concentration of hydrogen peroxide has been reported to be about 0.7% and 0.6% 5 minutes after application of a strip containing 10% and 6.5% hydrogen peroxide. The level was reduced to 0.1% and 0.2%, respectively after 30 min.

The maximum concentration of hydrogen peroxide in the saliva after teeth bleaching has been reported to be 0.1% corresponding to about 5 µg/cm2. The saliva concentration seems to be similar with a 200 mg strip containing 6.5% hydrogen peroxide and a 100 mg strip containing 14% hydrogen peroxide.

For gel strips it has been reported users occasionally may swallow the strip, resulting in an exposure of about 12 mg hydrogen peroxide (0.2 mg/kg bw). When trays are used, overfilling of the tray and excessive biting on the tray are factors that may cause additional release of the bleaching agent.

From the exposure studies the systemic absorption of hydrogen peroxide is estimated to be in the range from 0.03 mg/kg bw/d to 0.2 mg/kg bw/d. Consequently, an exposure from tooth whitening products with 6% hydrogen peroxide of 0.2 mg/kg bw/d may be used in safety calculation.

Mucous membrane irritation

Ulceration of gastric mucosa in rats was observed 1 hour after gavage with a dose corresponding to 5.4 mg/kg bw of hydrogen peroxide while no effects were found at 1.8 mg/kg bw of hydrogen peroxide. This is only (1.8/0.2) 9 times higher than the dose expected using tooth whitening products containing 6.0% hydrogen peroxide. In cases where gel strips were swallowed accidentially, gastric symptoms have been reported.

Carcinogenicity

A tumour frequency of 5% was found in Sencar mice after skin painting with the initiator DMBA followed by skin painting with hydrogen peroxide at a concentration corresponding to 470 µg/cm2day 2 times a week for 25 weeks. Since the maximum concentration of hydrogen peroxide in the saliva after teeth bleaching has been reported to be about 5 µg/cm2, the amount by cm2 in users of tooth whitening products that also are exposed to carcinogenic polycyclic hydrocarbons from smoking is only about (470/5) 94 times than the amount giving 5% tumour in mice.

Clinical safety data

The cosmetic industry and their organisations have pointed out that over 100 published and unpublished clinical studies, comprising approximately 4000 subjects in total, are available. In addition, there exists a 7.5-year follow-up study on a small group of tooth whitening products users. It should be noted that only 9 of the 15 persons in the long-term study agreed to clinical examination. Six studies, all with less than 100 people, had up to 6 months follow-up. The majority of the studies seemed to have lasted less than 1.5 month and involve less than 150 persons. Only one 28-day study has been reported with adolescence (12 – 18 years old). For a case-reference study to detect a doubling of the risk for an adverse effect that occurs at a level of 1:1000 in the reference group, the study group must have at least 1000 people. The majority of the studies were judged to be at high risk of bias and were either sponsored or conducted by the manufacturers. Thus, there is a need of independent and well conducted clinical studies during the use of tooth whitening products as well as long-term clinical data and epidemiological studies that assess the possible adverse effects of tooth whitening products within the oral cavity.

In a large survey of dentists, 91% of 8,143 dentists stated that they had used vital tooth bleaching. Side effects reported by the respondents included the following: 62.2% noted tooth hypersensitivity, 45.9% reported soft-tissue irritation, 2.1% noted systemic effects, and 18.8% reported no side effects.

Tooth sensitivity is a common side-effect of external tooth bleaching. Data from various studies of tooth bleaching revealed that up to 65% of the patients reported increased tooth sensitivity. Tooth sensitivity normally persists for up to 4 days after the cessation of bleaching treatment, but a longer duration of up to 39 days has been reported. In clinical trials with bleaching with hydrogen or carbamide peroxide in custom-made trays, 25 to 40% of the patients reported gingival irritation during treatment.

The safety of three months use of strips was evaluated. The product was designed as a one-week use and the present conditions represent a twelve times overuse. Forty subjects were divided into two groups and were assigned to either 6% hydrogen peroxide strips or 9.5% hydrogen peroxide strips. Subjects used their product on the maxillary teeth for 30 minutes twice a day for 3 months. For the 6% hydrogen peroxide strips, 6% of subjects had oral soft tissue adverse effects and 44% reported tooth sensitivity. For the 9.5% hydrogen peroxide strips, 6% of subjects had oral soft tissue adverse effects and 59% reported tooth sensitivity. One severe tooth sensitivity adverse effect was reported with the 9.5% hydrogen peroxide strips. All of the adverse effects resolved when product use was discontinued.

Special investigations

Enamel and Dentine Surface Morphology and Chemistry. Scanning electron microscopy (SEM) has been used for qualitatively analysing the surface morphology of enamel and dentine specimens following bleaching. In addition profilometry has been used to measure the surface roughness. The majority of these in vitro studies indicate that hydrogen peroxide and carbamide peroxide containing products have no significant deleterious effects on enamel and dentine surface morphology and that the contrasting studies that do show an effect, in general, have some limitations in the in vitro methodologies used. It should be noted, however, that two clinical cases of serious adverse effects on enamel associated with whitening agents, both of which involved the use of “over-the-counter” products have been reported.

Enamel and Dentine Surface Microhardness. Surface microhardness (SMH) measurement has been a frequently used technique for evaluating the effects of peroxide and bleaching products on enamel and dentine. There are numerous published in vitro reports in the literature detailing the detrimental effects or lack of effects of peroxide-containing tooth whitening products on enamel microhardness, enamel resistance to abrasion, dentin microhardness, dentin roughening, and restoration microhardness. The results are dependent on the methodology used and the materials or products tested. An effect is often observed with artificial saliva containing no organic components or if no fluoride treatments to aid remineralisation is used. Moreover, it has been found that bovine enamel has a three-fold faster rate of lesion progression compared to human enamel. The majority of the more recent studies indicate that hydrogen peroxide and carbamide peroxide containing products have no significant deleterious effects on human enamel and dentine SMH.

Subsurface Enamel and Dentine. Since hydrogen peroxide will diffuse through enamel towards the enamel-dentine junction, some studies have investigated the effects of bleach agents on subsurface enamel and dentine. This is typically accomplished by bleaching whole teeth or fragments and then cutting and polishing the specimens to reveal the internal subsurface enamel and dentine areas, followed by microhardness measurements. An alternative approach to investigating the effects of bleaching on subsurface enamel, dentine and the enamel-dentine junction is to use confocal laser scanning microscopy which enables their ultrastructure to be investigated. The majority of relevant in vitro studies indicate that hydrogen peroxide and carbamide peroxide containing products have no significant deleterious effects on subsurface enamel and dentine microhardness or ultrastructure. It should be noted, however, that the effects of bleaching agents on the mechanical properties of enamel have not been extensively studied. Although it is difficult to clinically associate enamel cracking or fractures with previous bleaching treatments, there is increasing evidence that enamel structural changes may occur due to exposure to such substances.

Effects of Acid Challenges and Abrasion on Bleached Enamel/Dentine. Some studies have reported that pre-bleaching human enamel and dentine with hydrogen peroxide or carbamide peroxide had no subsequent deleterious effect on enamel and dentine loss caused by citric acid erosive challenges or brushing with toothpaste. Other studies indicated that acidic agents or long duration of bleaching may lead to an increased susceptibility to enamel loss by tooth brushing abrasion.

Effects on Restorative Materials. Porcelain or other ceramic restoratives as well as dental gold appear generally unaffected by bleaching procedures. Composite restorations, on the whole would seem to be more reactive to bleach effects, but these still may include only minor etching or softening depending upon treatment conditions. In studies of strip bleaching gels, glass ionomers were largely unaffected. Zinc phosphate cement has been observed to be completely solubilized by a carbamide peroxide bleaching gel. Dental amalgams show signs of oxidative reactivity with bleaching gels with minor localized spotting and colour changes observed on amalgam surfaces. in vitro studies, under exaggerated conditions of use, have demonstrated release of very small amounts of mercury from amalgams, which are at levels well within the limits for mercury exposure in the guidelines of WHO.

Uptake of Bleaches and Transport to Dental Pulp. Hydrogen peroxide is readily transported through tooth enamel into dentin and pulp. Despite this uptake, the development of pulpal damage associated with vital tooth bleaching is low. It is pointed out that peroxide concentration from 14% hydrogen peroxide gel was far below levels required for the initiation of significant enzyme inhibition. Vital tooth bleaching produces histological evidence of minor inflammation of superficial layers of pulp adjacent to the pulp-dentin junction. The minor inflammatory response of the pulp to the introduction of bleaching seems to be concurrent with the pain response expressed by consumers having increased hypersensitivity.

Bleaching agents can also enter the pulp via leakage from tooth restorations, particularly at the cemento-enamel junction and following thermal stress (Crim, 1992). Histological evaluation of the pulp after vital bleaching with 10 % carbamide peroxide revealed mild inflammatory changes in 4 out of 12 teeth both after 4 days and 14 days treatment, and no changes after 14 days treatment followed by “recovery” phase of 14 days (González-Ochoa 2002).

Catalase activity in the dental pulp is very low and there is virtually no glutathione peroxide activity (Bowles and Burns, 1992). Application of a 3% hydrogen peroxide solution to the dentin of rat incisors caused emphysema and capillary stasis, and slowed down the blood circulation in the underlying pulp. Direct application of hydrogen peroxide to the pulp itself caused permanent damage to the capillary net (Gaengler, 1976). This study describes, however, extreme conditions which would not be expected to be present when hydrogen peroxide is used by humans in oral hygiene products.

Summary

The EU regulation states that the hydrogen peroxide content of oral hygiene products should not exceed 0.1%. In the case of toothpastes and mouth-rinses the exposure times are short and a risk assessment has been made on the basis of MOS. Tooth whitening products are available in many forms, e.g. trays with gel, gel strips, paste-on gel. Moreover, although the majority of the products contain hydrogen peroxide or carbamide peroxide, other chemicals such as sodium percarbonate, sodium perborate, and potassium peroxymonosulphate may be used. The later chemicals are briefly discussed in Appendix, and should be regulated similarly as hydrogen peroxide on the basis of hydrogen peroxide or reactive oxygen products released. Sodium perborate fulfils the criteria of a classification of toxic to reproduction category 2 (R61). Additionally, there is a current proposal that sodium perborate should be so classified (http://ecb.jrc.it/classification-labelling/search-classlab/  (Search Working Database)).

In the case of tooth whitening products the exposure time will be considerable. The safety of tooth whitening products is based both on calculations of MOS as well as consideration of possible acute and long-term effects.

All trials with tooth whitening products were short term and the majorities of the studies were judged to be at high risk of bias and were either sponsored or conducted by the manufacturers. The majority of the studies are in vitro studies. Moreover, no in vivo studies including multipliable use of tooth whitening products are available. Therefore, in order to carry out a robust risk assessment there is a need for long-term and independent clinical data and long-term epidemiological studies in order to evaluate possible adverse effects within the oral cavity associated with use of tooth whitening products. These studies should include participants representing diverse populations and be performed as described in the SCCP document “A guidance document on epidemiological and clinical studies on tooth whitening products” (SCCP/0974/06).

Source & ©: SCCP,  Opinion on Hydrogen peroxide, in its free form or when released, in oral hygiene products (2007), 3.3 Toxicological evaluation, 3.3.13. Safety evaluation & 3.3.14. Discussion p.62-68


FacebookTwitterEmail
Themes covered
Publications A-Z
Leaflets

Get involved!

This summary is free and ad-free, as is all of our content. You can help us remain free and independant as well as to develop new ways to communicate science by becoming a Patron!

PatreonBECOME A PATRON!