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Most deodorants today contain aluminum, a known neurotoxin that can end up in your brain and cause oxidative damage and inflammation. Particularly when used in the underarm though, deodorants have a great potential to disrupt endocrine function by affecting the endocrine glands, altering the expression of certain hormones and impairing estrogen receptor methylation. Aluminum is one of the ingredients in main-brand deodorants responsible for endocrine disruption, and is now even considered a metalloestrogen; a heavy metal that has estrogenic effects on the body, much in the same way that BPA, Teflon, plastic cutlery & dishes, vaccines, non-native EMF, many allopathic medications (particularly birth control), pesticides (notably atrazine & glyphosate), and many other household, food, and cosmetic items in today’s toxic society do. I am convinced there is an agenda to demasculinize the alpha male and remove him from the family unit, and to irritate, taunt, and abuse the nurturing, protective, instinctive, and LOVING mother. This agenda is carried out so both of the parents neglect their children and feed them “quick poisons” (which make a quick dollar for big food corporations) while the state force-feeds them with disinformation from a young age, and indoctrinate them into never thinking for themselves. They end up with mindless, colorless, soulless, depressed, vulnerable, obedient, and easily-manipulative drones. Simply cattle to feed their system of debt slavery…income taxes are a scam! okay this is a post about deodorants but you guys are used to these tangents. Those who are still reading this I appreciate you. Anyways the kids are lured with cool commercials and peer influence into buying these main-brand poisonous personal care items and their parents are too busy to care.

Other ingredients that have known toxicity/carcinogenicity and are commonly used in deodorants are: triclosan, parabens, phtalates, propylene glycol, and many other petroleum-based artificial colors, scents, emulsifiers, and preservatives.

What deodorant should you use?

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  • The Health Effects of Aluminum Exposure


  • Breast Cancer and Deodorants/Antiperspirants: a Systematic Review.


  • Aluminium chlorohydrate and aluminium zirkonium tetrachlorohydrate glycine complex are the most frequently used active ingredients in commercial antitranspirants today.


  • The association between aluminum-containing products and Alzheimer’s disease.
  • For all antiperspirant/deodorant use, regardless of aluminum content, there was no association with AD (adjusted odds ratio (OR) = 1.2, 95% CI = 0.6-2.4). For aluminum-containing antiperspirants, the overall adjusted OR was 1.6 (95% CI = 1.04-2.4) with a trend toward a higher risk with increasing frequency of use (p for trend = 0.03), the adjusted OR in the highest tertile being 3.2.


  • Zirconium granuloma resulting from an aluminum zirconium complex: a previously unrecognized agent in the development of hypersensitivity granulomas.
  • We present the clinical and histologic findings of a case in which a patient developed an acute hypersensitivity reaction to an aluminum zirconium complex.


  • Cutaneous granulomas caused by an aluminum-zirconium complex: an ingredient of antiperspirants.


  • [Aluminum in deodorants].


  • Crystal deodorant dermatitis: irritant dermatitis to alum-containing deodorant.
  • Two patients developed an irritant dermatitis of the axillae shortly after using an over-the-counter “natural deodorant crystal” product containing alum.
  • We discuss this previously unreported, untoward reaction to alum, an ancient agent with newfound popularity as an alternative health product.


  • An earlier age of breast cancer diagnosis related to more frequent use of antiperspirants/deodorants and underarm shaving.
  • Reviewed literature insinuates absorption of aluminium salts facilitated by dermal barrier disruption. Case-controlled investigations are needed before alternative underarm hygiene habits are suggested.


  • Hyperaluminemia in a woman using an aluminum-containing antiperspirant for 4 years.


  • Aluminum in antiperspirants: more than just skin deep.


  • Aluminium, antiperspirants and breast cancer.
  • Results reported here demonstrate that aluminium in the form of aluminium chloride or aluminium chlorhydrate can interfere with the function of oestrogen receptors of MCF7 human breast cancer cells both in terms of ligand binding and in terms of oestrogen-regulated reporter gene expression. This adds aluminium to the increasing list of metals capable of interfering with oestrogen action and termed metalloestrogens.


  • Allergic contact dermatitis from aluminium in deodorants.



  • Exposure to triclosan augments the allergic response to ovalbumin in a mouse model of asthma.
  • Triclosan has had widespread use in the general population as an antibacterial and antifungal agent and is commonly found in consumer products such as soaps, deodorants, toothpastes, shaving creams, mouthwashes, and cleaning supplies.


  • Non-Ionic Surfactants Antagonize Toxicity of Potential Phenolic Endocrine-Disrupting Chemicals, Including Triclosan in Caenorhabditis elegans.
  • Triclosan (TCS) is a phenolic antimicrobial chemical used in consumer products and medical devices. Evidence from in vitro and in vivo animal studies has linked TCS to numerous health problems, including allergic, cardiovascular, and neurodegenerative disease.



  • Phtalates: new cardiovascular health disruptors?


– Personal care product use predicts urinary concentrations of some phthalate monoesters.


  • Estimated exposure to phthalates in cosmetics and risk assessment.
  • Total exposure levels from several sources may be greater and require further investigation.


  • Simultaneous determination of seven phthalates and four parabens in cosmetic products using HPLC-DAD and GC-MS methods.
  • Overall recoveries were 85-108% with RSD values of 4.2-8.8%. Only one of the 15 examined samples was free from phthalates and parabens. The remaining 14 samples were found to contain at least three or more of these phthalates and/or parabens. The predominant phthalates and parabens detected in the studied samples were methylparaben, propylparaben, diethyl phthalate, dibutyl phthalate, dicyclohexyl phthalate, and di-(2-ethylhexyl) phthalate.


  • Monitoring phthalate exposure in humans.
  • Public and scientific concern has increased in recent years about the potential health risks associated with exposure to phthalates. The main focus has moved away from the hepatotoxic effects to the endocrine disrupting potency of these chemicals.


  • Internal phthalate exposure over the last two decades–a retrospective human biomonitoring study.
  • Female subjects exhibited significantly higher daily intakes for the dibutyl phthalates (DnBP p=0.013; DiBP p=0.004)
  • Regarding daily DiNP exposure we found continuously increasing values, with the lowest median being 0.20 microg/kg bw/d for the subset of 1988 and the highest median for 2003 being twice as high.


  • Reproductive and developmental toxicity of phthalates.
  • Phthalates were postulated to produce endocrine-disrupting effects in rodents, where fetal exposure to these compounds was found to induce developmental and reproductive toxicity.
  • The adverse effects observed in rodent models raised concerns as to whether exposure to phthalates represents a potential health risk to humans. At present, di(2-ethylhexyl) phthalate (DEHP), di-n-butyl phthalate (DBP), and butyl benzyl phthalate (BBP) have been demonstrated to produce reproductive and developmental toxicity; thus, this review focuses on these chemicals.
  • At present, DEHP exposures in the general population appear to be close to the tolerable daily intake (TDI), suggesting that at least some individuals exceed the TDI. In addition, specific high-risk groups exist with internal levels that are several orders of magnitude above average.


  • Phthalate exposure among pregnant women in Jerusalem, Israel: results of a pilot study.
  • Nine metabolites were detected in at least 95% of the samples: mono(2-ethyl-5-carboxypentyl) phthalate, mono(2-ethyl-5-hydroxyhexyl) phthalate, mono(2-ethyl-5-oxohexyl) phthalate, mono(3-carboxypropyl) phthalate, mono(n-butyl) phthalate, monobenzyl phthalate (MBzP), monoethyl phthalate (MEP), mono(2-ethylhexyl) phthalate and monoisobutyl phthalate. Phthalate metabolite concentrations in these pregnant women were remarkably similar to those in the general United States female population. MBzP geometric mean concentrations were higher in women living in buildings existing 40 years or more (P=0.04). In women who used four or more personal care products (perfume, deodorant, lipstick, nail polish, or hand/face cream) in the 48 h prior to providing the urine sample, geometric mean MEP concentrations were more than 4 times higher than concentrations in women using only two or three of the aforementioned products (P=0.07).


  • Phthalates in cosmetic and personal care products: concentrations and possible dermal exposure.
  • For female adults, the maximal daily exposure of 78 μg/kg bw/d was determined for DEP. The maximal daily exposure was much lower for the other four phthalates (DEHP, 0.82 μg/kg bw/d; DnBP, 0.36 μg/kg bw/d; and DMP, 0.03 μg/kg bw/d). The exposure for DiBP was not calculated due to its very low levels (<10 μg/g) in products. Toddlers and infants in this case had a maximal daily exposure to DEP of 20 and 42 μg/kg bw/d, respectively.


  • Phthalates and their metabolites in breast milk–results from the Bavarian Monitoring of Breast Milk (BAMBI).
  • Infants nourished with formula, phthalate intake is of the same magnitude or slightly higher (DEHP) than for exclusively breast-fed infants.


  • Personal care product use and urinary levels of phthalate metabolites in Mexican women.
  • edians of urinary concentrations of some phthalate metabolites were significantly higher among users of the following personal care products compared to nonusers: body lotion (MEHHP, MECPP and sum of DEHP metabolites (ΣDEHP)), deodorant (MEHP and ΣDEHP), perfume (MiBP), anti-aging facial cream (MEP, MBP and MCPP) and bottled water (MCPP, MEHHP and MEOHP). Urinary concentrations of MEP showed a positive relationship with the number of personal care products used. Our results suggest that the use of some personal care products contributes to phthalate body burden that deserves attention due to its potential health impact.


  • Women’s exposure to phthalates in relation to use of personal care products.
  • Women’s use of PCPs, particularly of perfumes and fragranced products, was positively associated with urinary concentration of multiple phthalate metabolites.


  • Personal Care Product Use in Men and Urinary Concentrations of Select Phthalate Metabolites and Parabens: Results from the Environment And Reproductive Health (EARTH) Study.
  • We identified 10 PCPs of relevance and demonstrated that their use within 6 h of urine collection strongly predicted MEP and paraben urinary concentrations.


  • [Analysis of phthalates in aromatic and deodorant aerosol products and evaluation of exposure risk].
  • Results indicated that aromatic and deodorant aerosol products could be a significant source of phthalate exposure.


– Bisphenol A and phthalate levels in adolescents with polycystic ovary syndrome.

– Exposure to specific endocrine disruptors such as BPA could modify neuroendocrine, reproductive, and metabolic regulation favoring PCOS development in adolescents.


  • Phtalates: new cardiovascular health disruptors?
  • Humans are exposed to phtalates through different ways such as inhalation, ingestion and dermal contact.
  • A growing body of evidence investigated the association of phtalate exposure with cardiovascular risk factors, i.e., obesity, type 2 diabetes and hypertension. Phtalates are thought to contribute to obesity through their binding and activation of PPARγ receptor that in turn results in the upregulation of adipocyte production. Phtalates are also known to interfere with insulin signaling and to increase oxidative stress.


  • Prenatal exposure to phthalates and autism spectrum disorder in the MARBLES study.
  • When stratified by sex, among boys, MEP, monobenzyl phthalate, MCPP, MCNP, and sum of di(2-ethylhexyl) phthalate metabolites (ΣDEHP) were positively associated with Non-typical development risk.


  • Neurodevelopmental Disorders and Environmental Toxicants: Epigenetics as an Underlying Mechanism.
  • Experimental and epidemiological studies suggest that exposure to prenatal environmental toxicants is associated with neurodevelopmental disorders. In addition, there is also evidence that environmental toxicants can result in epigenetic alterations, notably DNA methylation.
  • In this review, we first focus on the relationship between neurodevelopmental disorders and environmental toxicants, in particular maternal smoking, plastic-derived chemicals (bisphenol A and phthalates), persistent organic pollutants, and heavy metals.


  • The association of environmental toxicants and autism spectrum disorders in children.
  • A number of environmental agents have been suggested as contributing factors to ASD pathogenesis, which includes heavy metals (Hg and Pb), persistent organic pollutants (DDT, PBDEs and PCBs) and emerging chemicals of concern (phthalates and BPA).
  • There are evidence supporting the etiological link between exposure to environmental toxicants and the development of ASD. Children exposed to these toxicants in the environment exhibit signature traits of ASD and have been reported with high body burdens of these chemicals and/or their metabolites, which may provide an explanation for the observed relation, yet comprehensive evidence in humans is limited, highlighting the need for further research.


  • The role of phthalate esters in autism development: A systematic review.
  • Among the three case control studies, two of them showed a significant relation between exposure to phthalate and ASD and the last case control study had negative results. Indeed, this case control studies showed a compromised phthalate metabolite glucuronidation pathway, as a probable explanation of mechanism of the relation between phthalate exposure and ASD.
  • This review reveals evidence showing a connection between exposure to phthalates and ASD. 


  • Phthalate concentrations in house dust in relation to autism spectrum disorder and developmental delay in the CHildhood Autism Risks from Genetics and the Environment (CHARGE) study.
  • Among TD children, VABS communication, daily living, and adaptive composite standard scores were lower, in association with increased diethyl phthalate (DEP) concentrations in dust. Participants with higher dibutyl phthalate (DBP) concentrations in house dust also trended toward reduced performance on these subscales. Among ASD and DD boys, higher indoor dust concentrations of DEP and DBP were associated with greater hyperactivity-impulsivity and inattention.
  • The associations observed for DEP and DBP with impairments in several adaptive functions and greater hyperactivity, along with evidence for increased risk of DD raise concerns that these chemicals may affect neurodevelopment in children.


  • Bisphenol A Exposure in Children With Autism Spectrum Disorders.
  • The metabolomics analyses showed the number of absolute partial correlations >|0.30| between metabolite concentrations and total BPA was ∼3 times greater with the ASD group than the controls (P < 0.001), and the number of absolute partial correlations > |0.30| for % bound BPA was ∼15 times higher with ASD (P < 0.001). The results suggest there is an association between BPA and ASD.


  • Di-(2-ethylhexyl) phthalate and autism spectrum disorders.
  • The fully oxidized form 5-oxo-MEHP showed 91.1% specificity in identifying patients with ASDs. Our findings demonstrate for the first time an association between phthalates exposure and ASDs, thus suggesting a previously unrecognized role for these ubiquitous environmental contaminants in the pathogenesis of autism.


  • Does perinatal exposure to endocrine disruptors induce autism spectrum and attention deficit hyperactivity disorders? Review.
  • Perinatal exposure to EDCs appears to be associated with the occurrence of ASD as well as ADHD. Disruption of thyroid hormone function and gamma-aminobutyric acid (GABA)ergic mechanisms may offer an explanation for the observed relations; though, conclusive evidence in humans is limited.


  • Associations between indoor environmental factors and parental-reported autistic spectrum disorders in children 6-8 years of age.
  • Results from the second phase of the DBH-study (DBH-II) indicate PVC flooring to be one important source of airborne phthalates indoors, and that asthma and allergy prevalence are associated with phthalate concentrations in settled dust in the children’s bedroom. Because these associations are among the few linking ASD with environmental variables, they warrant further and more extensive exploration.

SLS, SDS, ALS, & Other Surfactants


– Comparing Surfactant Penetration into Human Skin and Resulting Skin Dryness Using In Vivo and Ex Vivo Methods.

– “individual surfactant (sodium laureth (1) ether sulfate and cocamidopropyl betaine) extracted from the skin, were found to correlate well with 14C-SDS penetration into the skin ex vivo for anion-based surfactant systems.”


– Growth and antioxidant response in Ceratophyllum demersum L. under sodium dodecyl sulfate (SDS), phenol and joint stress.

– Our results showed that the toxicity of SDS and phenol may be antagonistic in C. demersum in its natural environment, and their mixture did not produce more severe effects on the growth of C. demersum than each toxin individually. Furthermore, the chlorophyll content can be considered an indicator of the combined toxicity of SDS and phenol.


  • The protective role of Spirulina platensis to alleviate the Sodium dodecyl sulfate toxic effects in the catfish Clarias gariepinus (Burchell, 1822).
  • Thus, the present study suggests that SP could protect the catfish against SDS-induced injury by scavenging ROS, sustaining the antioxidant status and diminishing DNA oxidative damage.


  • Irritating effects of sodium lauryl sulfate on human primary keratinocytes at subtoxic levels of exposure.
  • Keratinocyte morphophysiological changes and inflammatory responses were significant at ≥25 μM SLS. The keratinocytes became less stiff due to changes in the distribution of F-actin filaments and α-tubulin; these changes were significant even at lower doses of SLS (≤10 μM). The morphophysiological changes of keratinocytes were clearly seen at a relatively high dose of SLS, while the mechanical properties of keratinocytes responded linearly to SLS at lower doses. Therefore, changes in mechanical properties can be used as new endpoints for in vitro toxicity testing with keratinocytes.


  • Ammonium lauryl sulfate-induced apoptotic cell death may be due to mitochondrial dysfunction triggered by caveolin-1.
  • Therefore, we conclude that ALS-induced apoptosis may be due to mitochondrial dysfunction triggered by the inhibition of caveolin-1, and that chronic pulmonary exposure to ALS may cause adverse health effects such as cancer and fibrosis by impairing the host’s pulmonary immune system.


  • Degradation of SDBS in water solutions using plasma in gas-liquid interface discharge: Performance, byproduct formation and toxicity evaluation.
  • The toxicity evaluation showed that plasma treatment could reduce the acute toxicity effectively initially, and also indicated that the formed intermediates of formate, oxalate, malonate and sulfate had no negative effects. However, further treatment caused an increase in toxicity, which was mainly correlated with the excessive residual H2O2 formed during the plasma process.


  • Re: in vivo evaluation of fluoride and sodium lauryl sulphate in toothpaste on buccal epithelial cells toxicity.


  • [Biopharmaceutical study of the association of colloidal N-butyl bromide of scopolamine and sodium lauryl sulfate. I].


  • The influence of lauryl sulphate on the sensitization of guineapigs to chrome and nickle.


  • [Studies on the growth of mycobacterium tuberculosis. IX. The effects of sodium lauryl sulfate upon the variation of Mycobacterium tuberculosis and saprophytic acid-fast bacilli. 3. The changes in immunity and toxicity of BCG and Mycobacterium tuberculosis var. hominis F. induced by the repeated subculture on Oka-Katakura’s media containing sodium lauryl sulfate].


  • Toxicologic studies on sodium lauryl glyceryl ether sulfonate and sodium lauryl trioxyethylene sulfate.


  • The chronic toxicity of sodium alkylbenzene-sulfonate by food and water administration to rats.


  • Toxicity os sodium lauryl sulphate, sodium lauryl ethoxysulphate and corresponding surfactants derived from synthetic alcohols.


  • SLS evokes a precipitous transient depressor response in dogs. However, SLS has marked acute effect on lungs, kidneys, and especially liver. The hepatotoxicity of SLS seems to preclude its intravenous use in man.



  • Adverse reactions of externally applied drugs and inert substances.
  • Lanolin, cetyl alcohol and myristyl alcohol, sorbitol, isopropyl-myristate as well as polyethylene glycols (PEG) penetrate the skin like active substances.
  • Other substances, such as tar, for example, are applied locally although they may have a carcinogenic potential when misused, or when contraindications for its use are disregarded.
  • Some have been connected with skin allergies. In addition, some preservatives have mutagenic properties. Many vehicles cause dehydration of the horny layer and thus result in chronic surface damage. This is true for hygroscopic substances such as PEG as well as for liquid paraffins, lipid solvents (alcohol, acetone), solvents such as propylene glycol and for some O/W emulsifiers


  • Deficit in the epidermal barrier induces toxicity and translocation of PEG modified graphene oxide in nematodes.
  • AAK-2 functioned synergistically with BLI-1 or IFB-1 in the regulation of GO-PEG toxicity. Our data provide the molecular basis for the role of epidermal barrier against the toxicity and translocation of nanomaterials in organisms.


  • A simple method for decreasing the toxicity of polyethylene glycol in mammalian cell hybridization.
  • This technique should be particularly useful in studies on mammalian cell hybridization using cell lines that are particularly sensitive to the toxic effect of PEG.


  • Efficacy and toxicity of the solvent polyethylene glycol 400 in monkey model.
  • Monkeys (N = 11) rendered epileptic by aluminum-hydroxide were administered PEG 400 by constant rate (1 ml/hr) intravenous infusion for 3–4 weeks, preceded and followed by several weeks of baseline. (its funny that the scientists in this study gave epilepsy to monkeys by aluminum hydroxide injection. Aluminum hydroxide is the most widely used vaccine adjuvant and is also present in sunscreens and even some deodorants. -vv)
  • At a concentration of 60%, PEG 400 significantly reduced seizure frequency, but also exhibited severe side effects. These findings suggest that experimental testing of anticonvulsants may be compromised when this or similar solvents are used chronically.