The Toxins Ebook And Reference Guide

INTRODUCTION

I created this Environmental Toxins guide for my clients so that once they are able to get their lab data back to see which toxins are in their bodies, they will have a reference to look at that shows them the science and research done on those toxins, and what symptoms, condi ons, and diseases they are known to cause.

For example, we have seen clients with type 2 diabetes who didn't develop it because of their eating and lack of exercise, but rather from TOXINS in their body that are known to cause diabetes! Toxins like toxic mold, phthalates, and Triclosan for example, are known to all cause Type 2 Diabetes.

This is what I call a “living document” as I do update it when I have me or when our clients find new research material for me to add to the document. It has been a huge value to our clients so they have a starng point in understanding not only what these toxins are doing to their bodies to make them sick, but it also helps them learn where they are geng exposed.

I am excited to finally share this with everyone who is looking for help, and I hope you find this document useful in your journey for answers and solu ons.

If you are in possession of this Environmental Toxins ebook, I am guessing you have been looking for answers and solu ons to your health concerns.

While the rates of deaths from all chronic diseases, mental health disorders, and neurodegenera ve diseases keep reaching record numbers year a er year, I had to ask myself why, and what I determined was this:

Our current broken medical system is only looking at symptoms and how to make the symptoms go away. They are not looking for the root cause and addressing that instead.

Despite “medical advances” over the last 60 years, the United States ranks as the sickest modern na on in the world, which means other na ons aren’t doing that well either. From my perspec ve, the medical establishment has lost its roots as true healers and scien sts because of the corrup on from big pharma and the insurance industry. Because of this corrup on, physicians are at the mercy of what the pharmaceu cal industry and the health insurance industry tell them to do.

For example, even though Type 2 Diabetes is 100% reversible, you won’t hear most doctors tell their pa ents that. Instead, they give them medica on and then send them home with a handout from the American Diabetes Associa on that gives them advice that only exacerbates their condi on.

So what then can be done to really help people reverse their condi ons and experience true healing? I have been working in holis c medicine for over 20 years and have been able to witness science catching up to what some might call ancient prac ces, and what I’ve been able to witness and experience inspired me to create an educa onal pla orm that focuses on teaching not only doctors, but everyone, how science is now used to help find the root causes of disease, address them, and track progress along the way.

I’ve worked with people around the world to help them discover the root causes of their symptoms, condi ons, and diseases, and what I have learned has been literally life-saving for thousands.

A er tes ng thousands of people around the world for toxins that include heavy metals, toxic mold, and chemical toxins, I have discovered that 99% of ALL people who are chronically ill have at least 3 disease-causing toxins in their bodies.

What I have also discovered is how chemical toxins, heavy metals, and toxic mold can all adversely affect the body and mind in the same ways, from causing mental health disorders to autoimmune diseases, chronic fa gue, hormone and thyroid condi ons, gut disorders, and even cancers.

The two images below are taken from my Inflamma on Masterclass in Part 2 where I teach about the serious effects of various toxins. These two images from my masterclass h ps://inflamma onmasterclass.com/ depict just some of the symptoms, condi ons, and diseases that are the result of the toxins listed in this document.

Fortunately, tes ng has been developed so that people can see if they have been exposed to toxins that could be the root cause of their condi ons. The image below shows just an example of some of the chemical toxins, heavy metals, and toxic molds that can be tested for.

Tes ng can be easily done at home with a simple urine test that can detect the presence of toxic mold, heavy metals, and chemical toxins to show you what you might be exposed to that could be making and keeping you sick.

Take Mary’s case study for example:

Mary came to us with a host of symptoms that you can see in her symptom sheet below…

We had Mary fill out some specialized assessment forms that indicated she may have exposure to a host of different toxins, so Mary decided to get some tes ng done to see what the labs might reveal.

Like 99% of all people struggling with chronic illness and a host of symptoms, Mary’s tests came back showing many toxins. In the images below, I show the toxins found and the common condi ons and symptoms caused by the corresponding toxins found in her lab results.

No ce that these symptoms and condi ons are the SAME as the ones Mary was experiencing.

The next images show the progression of Mary’s detoxifica on and healing. You can see on the right side of the image below how Mary’s toxin levels started decreasing over me (between July 2021 and January 2022).

As you can see in the image above, from July 2021 to January 2022, her mold toxins started to decrease, some faster than others.

Then in the next image below you can see the follow-up test that was done, further showing reduced levels of toxic mold in her body. This most recent test was done on June 9th, 2022.

As you may have no ced, it can take some me for the body to detoxify. In fact, our studies show that it takes an average of 9 months to get toxins out of the body (heavy metals can take longer).

This next series of images shows Mary’s progress with her environmental toxins.

Like the test we ran for Mary for her toxic mold, this one for environmental toxins was also tested on the same dates: July 2021, then again in January 2022, and most recently June of 2022.

You can see from the image below that Mary made significant progress in elimina ng the environmental toxins from her body!

Finally, look at Mary’s symptom sheet below, and you will no ce her improvements in all the symptoms and condi ons correlated with the toxins leaving her body.

Mary found this Environmental Toxins ebook to be of great value so that she could look for the toxins she found in her labs, then find the informa on links associated with those par cular toxins, and read about the research and findings about how those toxins could be making her sick.

This document works best if you have done some labs to see what toxic exposures you have had. You can then look for those toxins in this reference guide and click on the links to read more about them.

*Note: Since 2020, many published research papers have been removed from the web or have now become hard to find. I men on this because I don’t check these links every day, and you may find that some links to the published research ar cles are no longer available.

I invite you to share any updated research ar cles you find with us so we can add them to this living document.

Thank you for learning how to take your health back into your own hands!

If you are interested in our approaches or maybe just want to get some labs done to see what root causes you may discover that are keeping you sick and unable to heal, I invite you to schedule an appointment with one of my coaches for a biological coaching visit at h ps://www.modernholis chealth.com/schedule/.

PARTI:ChemicalToxins

PARTIII:Mycotoxins

ENVIRONMENTALTOXICITY

Prepared by Dr. Elena Villanueva, DC

on February 23, 2022

Session date February 23, 2022

ChemicalToxins

While the health effects of our environmental changes are not fully understood, it is evident that many everyday chemicals are harmful to our health. Every day, we are unknowingly exposed to hundreds of toxic chemicals from sources all around us, such as pharmaceuticals, pesticides, packaged foods, household products, and environmental pollution. As we have become more exposed to chemical-laden products and toxic chemicals in food, air, and water, we have experienced, as a collective, an accelerated rate of chronic illnesses like cancer, heart disease, chronic fatigue syndrome, chemical sensitivity, autism spectrum disorders, AD(H)D, autoimmune disorders, Parkinson's disease, and Alzheimer's disease.

PHTHALATES

MEHHP is a metabolite of mono(2-Ethylhexyl) phthalate (MEHP), which belongs to the most common environmental toxin phthalates. Phthalates, often known as plasticizers, are a group of chemicals used to make plastics more flexible and harder to break.

Exposures: Phthalates are perhaps the most widespread group of toxic chemicals found in our environment. They are commonly found in aftershave lotions, aspirin, cosmetics, detergents, foods microwaved with plastic covers, oral pharmaceutical drugs, intravenous products prepared in plastic bags, hair sprays, insecticides, insect repellents, nail polish, nail polish remover, skincare products, adhesives, explosives, lacquer, janitorial products, perfumes, paper coatings, printing inks, safety glass, and varnishes.

Conditions: Phthalates have been implicated in reproductive damage, depressed leukocyte function, and cancer. Phthalates have also been found to impede blood coagulation, lower testosterone, and alter sexual development in children. Low levels of phthalates can feminize the male brain of the fetus, while high levels can hyper-masculinize the developing male brain. Phthalates have been classified as endocrine disruptors, which may cause reproductive damage. Phthalate exposure has also been associated with diabetes and insulin resistance, breast cancer, obesity, metabolic disorders, and immune disorders. Phthalate exposure and adverse child neurodevelopment, including the development of ADHD and autistic behaviors and lower cognitive and motor development, have also been reported.

Children and Environmental Toxins/Phthalate:

https://bmcendocrdisord.biomedcentral.com/articles/

Monoethyl Phthalate (MEP):

Type 2 diabetes risk: https://www.sciencedirect.com/science/article/abs/pii

Personal care products: https://www.nature.com/articles/jes2012105

Endocrine Disruptor: https://www.mdpi.com/2305-6304/7/2/21/htm

Mono-ethyl phthalate (MEtP):

male reproductive problems: https://www.ewg.org/sites/humantoxome/chemicals/chemical.php

Bisphenol A (BPA): Bisphenol A (BPA), a xenoestrogen, is one of the most widely used industrial compounds worldwide. One survey found that approximately 8 million tons of BPA are produced worldwide annually, and approximately 100 tons may be released into the atmosphere within one year. BPA has such a high yield because it can produce diverse polymer materials such as polycarbonate, epoxy resin, polysulfone resin, polyphenylene ether resin, and unsaturated polyester resin. When plastic products are heated or exposed to ultraviolet light, BPA is released from the polymers into the food and water; therefore, people often come into contact with BPA. Many studies have detected that BPA is widely present in food, the environment, and even human bodily fluids.

It is a starting material for the synthesis of plastics. BPA-based plastic is clear and tough and is made into plastic bottles, including water bottles, sports equipment, CDs, and DVDs. Epoxy resins containing BPA are used to line water pipes, coatings on the inside of many foods and beverage cans, and make thermal paper such as that used in sales receipts. The FDA has ended its authorization to use BPA in baby bottles and infant formula packaging, based on market abandonment, not safety. Research has linked exposure to fertility problems, male impotence, heart disease, and other conditions.

Conditions: BPA induces oxidative stress in the colon and liver, local inflammation, cellular apoptosis, and mitochondrial dysfunction in the colon and the liver. BPA is a xenoestrogen, exhibiting estrogen-mimicking, hormone-like properties that raise a concern about its suitability in some consumer products and food containers.

Among several environmental factors contributing to type 2 diabetes development, endocrine-disrupting chemicals (EDCs) have received special attention. These chemicals include a wide variety of pollutants, from components of plastic to pesticides, to modulate endocrine system function. EDCs can affect multiple cellular processes, including energy production and utilization, leading to alterations in energy homeostasis. Mitochondria are primarily implicated in cellular energy conversion, although they also participate in other processes, such as hormone secretion and apoptosis. Mitochondrial dysfunction due to reduced oxidative capacity, impaired lipid oxidation, and increased oxidative stress has been linked to insulin resistance and type 2 diabetes. Herein, we review the main mechanisms whereby metabolism-disrupting chemical (MDC), a subclass of EDCs that disturbs energy homeostasis, causes mitochondrial dysfunction, thus contributing to the establishment of insulin resistance and type 2 diabetes.

(chem toxin):

https://www.hindawi.com/journals/ije/2012/598180/ (metabolic disorder /obesity) https://pubmed.ncbi.nlm.nih.gov/32200274/ (same)

BPA

https://www.healthline.com/nutrition/what-are-obesogens

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678763/

In relation to kidney disease:

https://www.sciencedirect.com/science/article/abs/pii/S0013935118304420

In relation to kidney disease:

https://www.medicinenet.com/script/main/art.asp?articlekey=166773

In relation to kidney and heart disease:

https://www.sciencedaily.com/releases/2013/01/130109105714.htm

In relation to neurological illnesses, Parkinson's, Dementia, Child development, developmental, reproductive impairments, and changes in brain and behavior, endocrine (hormone disruptor): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4428475/

In relation to bone density:

BPA and bone loss:

https://pubmed.ncbi.nlm.nih.gov/29432759/

BPA ----> causes endocrine disruption > alters bone metabolism:

https://www.biomed.cas.cz/physiolres/pdf/67/67_S455.pdf

Bone health and BPA (and other chem toxins):

https://www.frontiersin.org/articles/10.3389/fendo.2017.00022/full

BPA blocks calcium and weakens bones:

A. Deutschmann, M. Hans, R. Meyer, H. Haberlein, D. Swandulla. “Bisphenol A Inhibits Voltage- activated Ca2 channels In Vitro: Mechanisms and Structural Requirements.” Molecular Pharmacology, 2012 Nov; DOI: 10.1124/mol.112.081372

https://saveourbones.com/alert-avoid-this-calcium-blocking-chemical-used-in- packaging/

2-Hydroxyisobutyric Acid (2HIB):

2-Hydroxyisobutyric Acid is formed endogenously as a product of branched-chain amino acid degradation and ketogenesis. 2HIB is a metabolite of methyl tertiary-butyl ether (MTBE) and ethyl tertiary-butyl ether (ETBE), blending gasoline components used as an oxygenate to raise the octane number and replace lead.

MTBE and ETBE are often introduced into water-supply aquifers by leaking underground storage tanks at gasoline stations or gasoline spilled onto the ground. Headaches, nausea, dizziness, irritation of the nose or throat, and feelings of being spaced out or confused. Long-term exposure to MTBE or ETBE may link to hepatic, kidney, central nervous system toxicity, and even cancer.

Conditions: Elevated levels indicate environmental exposure, and very high values have been reported in genetic disorders, headaches, nausea, dizziness, irritation of the nose or throat, and feelings of being spaced out or confused. Long-term exposure to MTBE or ETBE may link to hepatic, kidney, central nervous system toxicity (mental health disorders and neurodegenerative disease, and even cancer.

2-Hydroxyethyl Mercapturic (HEMA):

Parent: Ethylene oxide, Vinyl chloride, Halopropane

High HEMA may be due to exposure to ethylene oxide, which is used in many different industries, including agrochemicals detergents, pharmaceuticals, and personal care products. Ethylene oxide is also used as a sterilant on rubber, plastics, and electronics. Ethylene oxide may be challenging to detect since it is odorless at toxic levels. High HEMA may also be due to exposure to vinyl chloride, an intermediate in synthesizing several major commercial chemicals, including polyvinyl chloride, and used in the past as an aerosol propellant.

Chronic exposure to ethylene oxide has been determined to be mutagenic to humans. Multiple agencies have reported it as a carcinogen. Studies of people exposed to ethylene oxide show an increased incidence of breast cancer and leukemia. Exposure to vinyl chloride has been associated with an increased incidence of autism.

To reduce exposure to vinyl chloride, eliminate the use of plastic containers for cooking, reheating, eating, or drinking (especially warm or hot) food or beverages. Replace these containers with glass, paper, or stainless steel whenever possible. Elimination of vinyl chloride can also be accelerated by sauna treatment, the Hubbard detoxification protocol employing niacin supplementation, vitamin B-12 therapy, by glutathione (reduced) supplementation (oral, intravenous, transdermal, or precursors such as N-acetyl cysteine [NAC]).

Labs and a High HEMA reading: https://healthmatters.io/understand-blood-test-results/2hydroxyethyl-mercapturic-hema ToxGuide for Ethylene Oxide: https://www.atsdr.cdc.gov/toxguides/toxguide-137.pdf

Exposures to Ethylene Oxide in hospitals: https://aacrjournals.org/cebp/article/16/4/796/277142/Exposure-to-Ethylene-Oxide-inHospitals-Biological Cell toxicity, oxidative stress of HEMA: https://pubmed.ncbi.nlm.nih.gov/25968591/

Atrazine (chemical toxin): is a herbicide of the triazine class. It is used to prevent pre-emergent broadleaf weeds in crops such as maize (corn) and sugarcane and on turf such as golf courses and residential lawns. As a result, atrazine is the most commonly detected pesticide contaminant of ground, surface, and drinking water. Atrazine is also a potent endocrine disruptor that is active at low, ecologically relevant concentrations.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4825440/

(mitochondrial dysfunction and insulin resistance): https://pubmed.ncbi.nlm.nih.gov/19365547/ https://www.researchgate.net/publication/23441358_Effects_of_atrazine_on_hepatic_metabolism_a nd_endocrine_homeostasis_in_rainbow_trout_Oncorhynchus_mykiss thyroid/endocrine disruptor (which can influence bone density) https://www.sciencedirect.com/science/article/abs/pii/S0013935120303030 mitochondrial toxicity: hormone imbalances/osteoporosis: https://www.scientificamerican.com/article/atrazine-water-tiedhormonal-irregularities/ https://emagazine.com/midwest-tap-water-altering-hormones/ Endocrine disruptor: https://www.pnas.org/content/107/10/4612

Methylparaben (chem. toxin): is an anti-fungal agent often used in a variety of cosmetics and personal-care products. It is also used as a food preservative and has the E number E218.

Methylparaben is commonly used as a fungicide in Drosophila food media at 0.1%.

https://pubmed.ncbi.nlm.nih.gov/32019002/ (metabolic/endocrine disorders/obesity) https://www.nature.com/articles/srep25173 (metabolic/endocrine disorders/obesity)

https://www.biomed.cas.cz/physiolres/pdf/67/67_S465.pdf (metabolic disorders/obesity) https://www.ewg.org/skindeep/ingredients/703937-methylparaben/ https://www.safecosmetics.org/get-the-facts/chemicals-of-concern/parabens/

Ethylparaben (chem. toxin): Known human endocrine disruptor with strong evidence. Parabens is the name given to a group of p-hydroxybenzoic acid (PHBA) esters used in over 22,000 cosmetics as preservatives at concentrations up to 0.8% (mixtures of parabens) or up to 0.4% (single paraben).

The group includes Methylparaben, Ethylparaben, Propylparaben, Isopropylparaben, Butylparaben, Isobutylparaben, and Benzylparaben. Industry estimates of the daily use of cosmetic products that may contain parabens were 17.76 g for adults and 378 mg for infants. Parabens in cosmetic formulations applied to skin penetrate the stratum corneum in inverse relation to the ester chain length.

Health Issues associated with Ethylparaben: Endocrine Disruptor (hormones), Causes Obesity/weight gain, Skin Allergies/Rashes, Mimics synthetic estrogen

https://pubmed.ncbi.nlm.nih.gov/32019002/ https://www.nature.com/articles/srep25173 (same as the one above)

EWG Guide on Ethylparaben: https://www.ewg.org/skindeep/ingredients/702355ETHYLPARABEN/

Parabens in Skincare: https://www.safecosmetics.org/get-the-facts/chemicals-ofconcern/parabens/ Parabens and the effects on blood sugar/diabetes: https://journals.lww.com/environepidem/Fulltext/

Propylparaben: Paraben is found commonly in skincare and body products. Known endocrine disruptor. also has the same issues (is in the same family) as Ethylparaben. All parabens are in the same family.

Conditions: Endocrine Disruptor (hormones), Causes Obesity/weight gain, Blood Sugar dysregulation, Diabetes, Developmental damage, Infertility/ Reproductive Damage, Inflammation, Autoimmune disease, Cancer, Skin Allergies/Rashes, Mimics synthetic estrogen, DNA Damage, Male Infertility

EWG guide: https://www.ewg.org/skindeep/ingredients/705335-PROPYLPARABEN/

Sources: https://en.wikipedia.org/wiki/Propylparaben

Parabens in skincare products: https://www.safecosmetics.org/get-the-facts/chemicals-ofconcern/parabens/

2,4-D (chem. toxin) – was used in agent orange also:

http://npic.orst.edu/factsheets/archive/2%2C4-DTech.html

https://www.atsdr.cdc.gov/ToxProfiles/tp210.pdf

1.2 SUMMARY OF HEALTH EFFECTS Information regarding health effects in humans following exposure to 2,4-D comes from case reports of accidental or intentional ingestion of herbicide formulations containing 2,4-D, accidental inhalation, and/or skin contact with 2,4-D in products used by farmers and professional residential applicators and homeowners, and occupational exposure during manufacture. Effects reported following oral or dermal exposure to high amounts of 2,4-D include tachypnea, tachycardia, vomiting, leukocytosis, liver and kidney congestion in fatal cases, metabolic acidosis, and neurological effects characterized by sensory and motor abnormalities. In two reports of dermal exposure, signs, and symptoms of peripheral neuropathy persisted for a long time.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3483058/ (Review of 2,4- dichlorophenoxyacetic acid (2,4-D) biomonitoring and epidemiology)

http://www.inchem.org/documents/ehc/ehc/ehc29.htm (INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY)

4-Nonylphenol: NPEs are nonionic surfactants that are used in a wide variety of industrial applications and consumer products. Many of these, such as laundry detergents, are “down-the-drain” applications. Some others, such as dust-control agents and deicers, lead to direct release to the environment. NPEs, though less toxic and persistent than NP, are also highly toxic to aquatic organisms, and, in the environment, degrade into NP.

Metabolic Syndrome and Liver Stress: https://www.sciencedirect.com/science/article/pii/S2214750015300706

Endocrine disruption and Obesity: https://pubmed.ncbi.nlm.nih.gov/22739433/

Endocrine disruption and Gene toxicity: https://pubchem.ncbi.nlm.nih.gov/compound/4Nonylphenol#section%3DPharmacology-and-Biochemistry

Neurodegeneration induced by 4-Nonylphenol: https://scholarworks.utep.edu/open_etd/2827/

4-Nonylphenol Accelerates Alzheimer’s and Neuroinflammation: https://n.neurology.org/content/92/15_Supplement/P1.9-084

Risk management of NPE from the EPA: https://www.epa.gov/assessing-and-managing-chemicalsunder-tsca/risk-management-nonylphenol-and-nonylphenol-ethoxylates

DDA/DDT:

DDT was a commonly used pesticide for insect control in the United States until it was canceled in 1972 by the US EPA. DDT was used to control malaria and typhus.

DDT is a persistent organic pollutant that is readily adsorbed to soils and sediments, acting as sinks and long-term exposure sources. DDT is an endocrine disruptor and indicates a possible disruption in semen quality, menstruation, gestational length, and duration of lactation. Chronic exposure to DDT will build up in areas of the body with high lipid content and can affect reproductive capabilities and the embryo or fetus. It is considered likely to be a human carcinogen, especially for breast cancer. DDE is a metabolite of DDT and is excreted as DDA in urine.

Endocrine effects: https://pubmed.ncbi.nlm.nih.gov/21792584/

Toxicological profile for DDT: https://www.atsdr.cdc.gov/toxprofiles/tp35.pdf

ToxGuide for DDT/DDD/DDE/DDA: https://www.atsdr.cdc.gov/toxguides/toxguide-35.pdf

Pharmacology/Toxicology for DDT: https://www.sciencedirect.com/topics/pharmacologytoxicology-and-pharmaceutical-science/ddt

Diethyldithiophosphate (DETP)

DEDTP is a metabolite of organophosphates which are one of the most common causes of poisoning worldwide and are frequently intentionally used as pesticides. Organophosphates function by inhibiting the action of cholinesterase enzymes in nerve cells. They can be absorbed through the lungs or skin or by eating contaminated food.

Even at low levels, organophosphates may be hazardous to the nervous system, especially in fetuses and young children. Repeated or prolonged exposure may induce impaired memory and concentration, disorientation, severe depression, irritability, confusion, headache, speech difficulties, delayed reaction times, nightmares, sleepwalking, drowsiness, or insomnia.

Organophosphates can also induce an influenza-like condition with headache, nausea, weakness, loss of appetite, and malaise. A direct correlation between the usage of organophosphates and diabetes has also been reported among agricultural populations.

DEDTP and neurotoxicity/seizures: (PDF) The neurotoxin diethyl dithiophosphate impairs ...www.researchgate.net › publication › 325739597_The_n...

Fourth National Report on Human Exposure to Environmental ...www.hsdl.org › view

Chemical toxins that cause seizures - PubMed - NIHpubmed.ncbi.nlm.nih.gov ›

Diphenyl Phosphate (DPP):

Diphenyl phosphate (DPHP) is an aryl phosphate ester (APE) used as an industrial catalyst and chemical additive and is the primary metabolite of flame retardant APEs, including triphenyl phosphate (TPHP). Minimal DPHP-specific toxicity studies have been published despite ubiquitous exposure within human populations following the metabolism of TPHP and other APEs. Similar to TPHP, DPHP impacts cardiac development, the potency of DPHP is significantly less than TPHP. DPHP disrupts pathways related to mitochondrial function and heme biosynthesis.

DPHP induced toxicity during embryonic development:

https://pubs.acs.org/doi/10.1021/acs.est.8b07238

Phosphorus flame retardants: https://www.ecocenter.org/our-work/healthy-stufflab/reports/toxic-inequities-2022-car-seat-report

Irritating to skin, toxic to aquatic organisms: https://datasheets.scbt.com/sc-225350.pdf

Ethylhexyl diphenyl phosphate (EHDPP) and reproductive organs: While DPHP is a metabolite of EHDPP, it is also a metabolite of TPHP and other OPEs and thus represents a combined biomarker of exposure to multiple parent OPEs:

https://www.healthvermont.gov/sites/default/files/documents/pdf/1241_94_7%20Ethylhe xyl%20diphenyl%20phosphate.pdf

Glyphosate: is an herbicide. It is applied to the leaves of plants to kill both broadleaf plants and grasses. The sodium salt form of glyphosate is used to regulate plant growth and ripen specific crops.

Glyphosate was first registered for use in the U.S. in 1974. Glyphosate is one of the most widely used herbicides in the United States. People apply it in agriculture and forestry, on lawns and gardens, and for weeds in industrial areas. Some products containing glyphosate control aquatic plants.

Glyphosate (chem toxin):

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5370400/ (complications with metabolic syndrome)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945755/ (complications with autoimmune disease)

https://www.researchgate.net/figure/Metabolic-pathways-for-glyphosate-in-the-humanbody_fig1_29953213 (complications with mitochondrial disorders)

https://www.beyondpesticides.org/assets/media/documents/lawn/activist/PorterLearningBehavior. pdf (neuro-endocrine-immune disorders)

https://www.mdpi.com/1099-4300/15/4/1416/htm (aggression and violence)

cancer: http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.582.7424&rep=rep1&type=pdf (Genotoxic effects of ethylene oxide, propylene oxide, and epichlorohydrin in humans: update review (1990–2001))

cancer: http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.582.7424&rep=rep1&type=pdf

cancer: https://www.bmj.com/content/365/bmj.l1613 (Probable carcinogenicity of glyphosate)

cancer: https://www.nrdc.org/experts/jennifer-sass/atsdr-report-confirms-glyphosate-cancer-risks (ATSDR Report Confirms Glyphosate Cancer Risks)

Glyphosate and Blood Sugar:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6134669

In relation to bone density:

https://saveourbones.com/4-hushed-up-ways-gmos-can-devastate-your-bones-and-your-health/ Glyphosate binds to minerals needed for health/bone health: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5823954

Info on glyphosate by an attorney website: https://www.baumhedlundlaw.com/toxic-tortlaw/monsanto-roundup-lawsuit/roundup-cancer-study/glyphosate-chelating-agent/

Glyphosate binds to minerals needed for bone density: https://detoxproject.org/glyphosate/glyphosate-chelating-agent/ Glyphosate depletes Manganese (Mn). Chondroitin sulfate synthesis depends on Mn, and these deficiencies lead to osteoporosis: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4392553/

Hydroxyethyl Mercapturic Acid: (a urinary metabolite found in urine as a result of a toxic load of VOCs— volatile organic compounds—toxic chemicals in your body)

https://www.cdc.gov/Nchs/Data/Nhanes/Nhanes_11_12/UVOC_G_MET_VOC_Metabolites.pdf

Dimethyldithiophosphate (DMDTP) (classified as an organophosphate) (chemical toxin)

https://www.ewg.org/sites/humantoxome/chemicals/chemical.php?chemid=10001 https://scholar.google.com/scholar?um=1&ie=UTF8&lr&q=related:anE2P6UXsLlI4M:scholar.google.com/ organophosphates and bone density: https://pubmed.ncbi.nlm.nih.gov/10577647/ https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(99)04466-9/fulltext https://www.bmj.com/content/350/bmj.h2088/rr-36 https://cot.food.gov.uk/sites/default/files/cot/opchap.pdf

Diethyl phosphate (DEP) (chem toxin): Organophosphate pesticides were previously marketed for home use and are now used on produce. Known neurotoxins that are particularly toxic to developing fetuses, infants, and children:

DEP and Gut dysfunction: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6572208/

DEP/thyroid dysfunction/--->bone loss: https://www.sciencedirect.com/science/article/pii/S016041201933020X

Diethyldithiophosphate (DEDTP): Classified as an organophosphate pesticide. Organophosphate pesticides are used in commercial agriculture to control pests on fruit and vegetable crops. They are also used in home gardens, for flea control on pets, and in some no-pest strips. In the past, organophosphates were widely used inside homes to control other pests like termites and ants, but these uses have been discontinued.

Organophosphate: https://biomonitoring.ca.gov/chemicals/diethyldithiophosphate-dedtp

Toxin breakdown and risks of DEDTP: https://datasheets.scbt.com/sc-250605.pdf

Dimethylphosphate (DMP): Used in insect repellant, plastic, and rocket propellant. DMP is linked to liver toxicity, and its breakdown product is linked to male reproductive system problems in people. Dimethyl phthalate has been found in 6 of the 9 people tested in EWG/Commonweal studies.

Loss of oxygen-carrying function of red blood cells: https://www.researchgate.net/publication/343755672

DMP attenuates oxidative stress and inhibits cellular signaling:

https://www.tandfonline.com/doi/full/10.1080/0886022X.2016.1256319

Consumer safety report: https://www.cpsc.gov/s3fs-public/ToxicityReviewOfDMP.pdf

EWG report: https://www.ewg.org/sites/humantoxome/chemicals/chemical.php? chemid=70001

2-Hydroxyethyl

Acid (HEMA):

HEMA is a metabolite of ethylene oxide and/or vinyl chloride. Ethylene oxide is widely used to produce agrochemicals, detergents, pharmaceuticals, personal care products, and cosmetics. Ethylene oxide is also the raw material to make sterilant in rubber, plastics, and electronics. Vinyl chloride is an intermediate used to synthesize several major commercial chemicals, including polyvinyl chloride and an aerosol propellant. Exposure may come from the use of plastic containers for cooking, reheating, eating, or drinking (especially warm or hot) food or beverages.

Ethylene oxide may be challenging to detect since it is odorless at toxic levels. High HEMA may also be due to exposure to vinyl chloride, an intermediate in synthesizing several major commercial chemicals, including polyvinyl chloride, and used in the past as an aerosol propellant.

Ethylene oxide is toxic by inhalation and may cause acute poisoning, accompanied by various symptoms, including headache, nausea, and vomiting. It is a proven carcinogen and may be mutagenic to humans upon chronic exposure. Studies of humans exposed to ethylene oxide show an increased incidence of breast cancer and leukemia. High concentrations of vinyl chloride may cause central nervous system depression, nausea, headache, dizziness, liver damage and liver cancer, degenerative bone changes, thrombocytopenia, enlargement of the spleen, autism, and even death.

Chronic exposure to ethylene oxide has been determined to be mutagenic to humans. Multiple agencies have reported it as a carcinogen. Studies of people exposed to ethylene oxide show an increased incidence of breast cancer and leukemia. Exposure to vinyl chloride has been associated with an increased incidence of autism.

To reduce exposure to vinyl chloride, eliminate the use of plastic containers for cooking, reheating, eating, or drinking (especially warm or hot) food or beverages. Replace these containers with glass, paper, or stainless steel whenever possible. Elimination of vinyl chloride can also be accelerated by sauna treatment, the Hubbard detoxification protocol employing niacin supplementation, vitamin B12 therapy, by glutathione (reduced) supplementation (oral, intravenous, transdermal, or precursors such as N-acetyl cysteine [NAC]).

Mitochondrial damage, cytotoxicity, and Cell death:

https://healthmatters.io/understand-blood-test-results/2-hydroxyethyl-mercapturic-hema

https://pubchem.ncbi.nlm.nih.gov/compound/2-Hydroxyethyl-methacrylate

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4145906/

https://www.greatplainslaboratory.com/gpl-tox/

Mercapturic

Methylhippuric Acid (2MHA) / 3MHA/ and 4MHA:

These are metabolites of xylenes, solvents found in paints, lacquers, cleaning agents, pesticides, and gasoline. Exposure to xylenes generates methyl hippuric acid isomers. High exposures to xylene create an increase in oxidative stress, causing symptoms such as nausea, vomiting, dizziness, central nervous system depression, a significant increase in the prevalence of respiratory diseases, neurocognitive impairment, cancer, and death.

https://www.sciencedirect.com/science/article/pii/S2590182621000011

In regard to thyroid: https://www.sciencedirect.com/science/article/pii/S037842741630090X

Xylenes and the effects on several systemic engines including thyroid, liver, and central nervous system: https://onlinelibrary.wiley.com/doi/pdf/10.1002/3527600418.mb133020e0015

In regard to endocrine toxicity (thyroid and reproductive hormones): https://www.researchgate.net/publication/26818676_Endocrinal_toxicity_of_industrial_solve nts_-_A_mini_review

Phenoxybenzoic Acid (3 PBA) – widely used in insecticides. Exposure during pregnancy doubles the likelihood of autism. Pyrethrins may affect neurological development, disrupt hormones, induce cancer, and suppress the immune system.

Concentration and pulmonary function in children:

https://www.sciencedirect.com/science/article/abs/pii/S0269749120368676

3PBA and neuro and immunotoxicity: https://pubmed.ncbi.nlm.nih.gov/29040392/

Breast Cancer: https://pubmed.ncbi.nlm.nih.gov/19853000/

Overview: https://sitem.herts.ac.uk/aeru/ppdb/en/Reports/692.htm

Toxicity, spleen and lymph node damage, headache, nausea, suppression of immune system: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3646417/

Male endocrine function: https://pubmed.ncbi.nlm.nih.gov/18479728/

Heart and seizure concerns:

https://www.sciencedirect.com/science/article/pii/S0147651321008010

Concern for older adults: https://www.nature.com/articles/s41370-020-00276-3

Prenatal exposure and neurodevelopment:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5577985/

Pesticides and autism: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4181911/

Perchlorate

This chemical is used to produce rocket fuel, missiles, fireworks, flares, explosives, fertilizers, and bleach. Studies show that perchlorate is often found in water supplies. Many food sources are also contaminated with percolate. Percolate can disrupt the thyroid’s ability to produce hormones. The EPA has also labeled perchlorate a likely human carcinogen. Patients that are high in perchlorate can use a reverse osmosis water treatment system.

Perchlorate and Thyroid: https://www.atsdr.cdc.gov/toxfaqs/tfacts162.pdf

Health Effects of Perchlorate: (including thyroid, eye, skin, and respiratory tract irritation, coughing, nausea, vomiting and diarrhea, sore throat, coughing, labored breathing, deep burns, loss of vision, abdominal pain.) https://www.epa.gov/sites/production/files/201403/documents/ffrrofactsheet_contaminant_perchlorate_january2014_final.pdf

MEOHP is a metabolite of mono(2-Ethylhexyl) phthalate (MEHP), which belongs to the most common environmental toxin phthalates. Phthalates, often known as plasticizers, are a group of chemicals used to make plastics more flexible and harder to break. They are widely used in cosmetics, adhesives, detergents, lubricating oils, automotive plastics, and plastic clothes.

People are exposed to phthalates by eating or drinking contaminated foods and breathing in air containing phthalate vapors or dust. Inhaling phthalates can irritate the nose and throat, causing coughing, wheezing, headache, dizziness, and nausea.

Phthalates have been classified as endocrine disruptors, which may cause reproductive damage, depressed leukocyte function, and even cancer. Phthalate exposure has also been associated with diabetes and insulin resistance, breast cancer, obesity, metabolic disorders, and immune disorders. Phthalate exposure and adverse child neurodevelopment, including the development of ADHD and autistic behaviors and lower cognitive and motor development, have also been reported.

Mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP)/MEHP

MEOHP and Cancer:

https://www.sciencedirect.com/science/article/pii/S0013935119306991

Phthalates and Reproductive, Endocrine toxicity and cancer:

https://royalsocietypublishing.org/doi/10.1098/rstb.2008.0268

Phthalates and breast cancer:

https://www.tandfonline.com/doi/abs/10.3109/13697137.2013.865720

Phthalates breast cancer, developmental issues, decreased fertility, obesity, and asthma.

https://www.bcpp.org/resource/phthalates/

Phthalates and breast cancer:

https://www.sciencedirect.com/science/article/abs/pii/S0278691518303855

Monoethyl Phthalate (MEP) (MEtP):

Neurological, altered endocrine function and reproductive and developmental effects

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2873014/ Alzheimer's disease, endocrine disruptors, neuropathology, Parkinson's disease:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4428475/

ButylParaben: Antimicrobial in beauty care products

Neurotoxicity, neurodevelopmental disturbances, and behavioral changes:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4428475/

Histamine release and cell-mediated immunity:

https://pubchem.ncbi.nlm.nih.gov/compound/Butylparaben

Antimicrobial ingredient in beauty products: https://www.drugs.com/inactive/butylparaben12.html

N-Acetyl (2-Cyanoethyl) Cysteine (NACE):

NACE is a metabolite of acrylonitrile used in the production of acrylic fibers, resins, and rubber. Acrylonitrile is metabolized by the cytochrome P450s and then conjugated to glutathione. Supplementation with glutathione should assist in the detoxification of acrylonitrile.

Parent: Acrylamide Acrylamide can polymerize to form polyacrylamide. These chemicals are used in many industrial processes such as plastics, food packaging, cosmetics, dyes, and the treatment of drinking water. Food and cigarette smoke are also two major sources of exposure. Acrylamide has been found in foods like potato chips and French fries. This is because asparagine, an important amino acid for central nervous system function, can produce acrylamide when cooked at high temperatures in the presence of sugars. Foods that are rich in asparagine include asparagus, potatoes, legumes, nuts, seeds, beef, eggs, and fish and are potential sources of exposure to acrylamide. High levels of acrylamide can elevate a patient’s risk of cancer. In addition, acrylamide is known to cause neurological damage.

N-Acetyl (2, Hydroxypropl) Cysteine (NAHP): (this is an Acrolein Metabolite)

Parent: Propylene oxide. This chemical is used in the production of plastics and is used as a fumigant. Propylene oxide is used to make polyester resins for the textile and construction industries. It is also used in the preparation of lubricants, surfactants, and oil demulsifiers. It has also been used as a food additive, an herbicide, a microbicide, an insecticide, a fungicide, and a miticide.

Propylene oxide is a probable human carcinogen. Common symptoms of toxicity are in the central nervous system. Propylene oxide is a mild CNS depressant and can lead to symptoms including fatigue, lack of concentration, drowsiness, etc.

Propylene oxide and cancer:

Carcinogenic Effects of Exposure to Propylene Oxide: https://www.cdc.gov/niosh/docs/89-111/default.html

N-acetyl-S-(2-carbamoylethyl)-cysteine (NAE):

Hazard Summary:

https://www.epa.gov/sites/production/files/2016-09/documents/propylene-oxide.pdf

genetic toxic effects:

http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.582.7424&rep=rep1&type=pdf

Insulin Resistance and Metabolic disorders: urinary acrolein metabolites were associated with diabetes and insulin resistance: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5700808/ Common exposures from NAHP (where it comes from):

https://healthmatters.io/understand-blood-test-results/n-acetyl2-hydroxypropylcysteine-nahp

Parent: Styrene/Ethylbenzene. Styrene is used to manufacture plastics in building materials and is found in car exhaust fumes. Polystyrene and its copolymers are widely used as food packaging materials. The ability of styrene monomers to leach from polystyrene packaging to food has been reported. Occupational exposure due to the inhalation of large amounts of styrene adversely impacts the central nervous system, causes concentration problems, muscle weakness, fatigue, and nausea, and irritates the mucous membranes of the eyes, nose, and throat.

https://www.sciencedirect.com/science/article/abs/pii/S0147651397915268

https://www.atsdr.cdc.gov/toxprofiles/tp110.pdf

https://ntp.niehs.nih.gov/ntp/roc/content/profiles//styrene.pdf

https://oehha.ca.gov/media/downloads/air/report/ethylbenzenesrp082707.pdf

https://www.epa.gov/sites/default/files/2016-09/documents/ethylbenzene.pdf

N-acetyl phenyl cysteine (NAP): Parent: Benzene.

Benzene is an organic solvent that is widespread in the environment. Benzene is a by-product of all industrial processes and combustion, including motor vehicle exhaust and cigarette smoke, and is released by outgassing from synthetic materials. Benzene is a highly toxic chemical that is mutagenic and carcinogenic. High exposures to benzene cause nausea, vomiting, dizziness, lack of coordination, central nervous system depression, and death. It can also cause hematological abnormalities.

https://www.who.int/publications/i/item/WHO-CED-PHE-EPE-19.4.2 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3363002/ https://emergency.cdc.gov/agent/benzene/basics/facts.asp https://www.cancer.gov/about-cancer/causes-prevention/risk/substances/benzene https://www.cancer.org/cancer/cancer-causes/benzene.html

Phenylglyoxylic Acid (PGO):

Triclosan:

Toxic Chemical Information from the EWG: https://www.ewg.org/areas-focus/toxicchemicals/triclosan

Products containing Triclosan: https://www.beyondpesticides.org/resources/antibacterials/triclosan/products-containingtriclosan

The FDA banned Triclosan in Sept. 2016, but it is still found in consumer products:

https://scienceofparkinsons.com/2017/09/08/quats-going-on/

Affects endocrine, immune, central nervous system (brain), reproductive, and developmental systems:

https://www.sciencedirect.com/science/article/abs/pii/S0045653518318290

Triclosan is a neurotoxin: https://link.springer.com/article/10.1007/s12035-018-1083-z

Disrupts heart and skeletal muscle Ca2+ signaling, damages liver function, alters gut microbiota, causes colonic inflammation, and promotes apoptosis in cultured neocortical neurons and neural stem cells. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6275195/ Triclosan, in a minute amount, cannot only affect the genes and enzymes involved in neurotransmission, but it can also damage the neurons. This could affect the motor function of an organism. https://telanganatoday.com/beware-triclosan-in-soap-and-toothpaste-you-usedaily-could-be-dangerous Microbial diversity, Autoimmunity & Alzheimer's:

https://academic.oup.com/emph/article/2013/1/173/1861845

Tiglylglycine (TG): is associated with both mitochondrial and/or genetic disorders. Toxic chemical exposure may be one of the most common causes of mitochondrial dysfunction. In mitochondrial disorders of the respiratory chain, TG values are usually more moderately increased than in the genetic disorders. In the medical literature, a normal value is less than 3.8 mmol/mol creatinine in children. It is an intermediate product of the catabolism of isoleucine and ketone bodies.

Mitochondrial and Genetic disorders: https://healthmatters.io/understand-blood-testresults/tiglylglycine

N-Acetyl (3,4-dihydroxybutyl) cysteine (NADB):

A chemical made from the processing of petroleum. It is often a colorless gas with a mild gasoline-like odor. Mostly this chemical is used in the production of synthetic rubber.

This metabolite is evidence of exposure to synthetic rubber such as tires. The primary route of exposure is inhalation. Some exposure may occur through ingestion of contaminated food or water or through dermal contact. Newer playgrounds and athletic fields are now made with ground-up tires, which may lead to increased exposure for children. 1,3 butadiene is a known carcinogen and has been linked to an increased risk of cardiovascular disease.

https://healthmatters.io/understand-blood-test-results/n-acetyl34-dihydroxybutylcysteinenadb

https://pubmed.ncbi.nlm.nih.gov/15093281/

3-hydroxypropylmercapturic acid (3-HPMA):

Parent: Acrolein3-HPMA is the main urinary metabolite of acrolein. Acrolein is an environmental pollutant, commonly used as an herbicide and in many different chemical industries. Acrolein is also present in the burning of cigarettes, gasoline, and oil. Certain bacteria produce acrolein, such as Clostridium. Acrolein metabolites are associated with diabetes and insulin resistance.

HEAVY METALS

Heavy metals and their toxic effects: https://rarediseases.org/rare-diseases/heavy-metal-poisoning/

Arsenic:

Central Nervous System: The brain is a soft target for arsenic toxicity as it freely crosses the bloodbrain barrier. Arsenic exposure is associated with a wide range of neurological complications in humans, such as impaired memory, poor concentration, Parkinson's disease, Guillain-Barre-like neuropathy, verbal comprehension, encephalopathy, and peripheral neuropathy.

Arsenic-induced oxidative stress in the brain causes oxidative DNA damage and subsequent brain cell death and induces the degeneration of dopaminergic neurons resulting in Parkinson-like symptoms.

Type 2 Diabetes: Chronic exposure to arsenic causes decreased expression of PPAR-γ, which may reduce the sensitivity of insulin responsible for the induction of type II diabetes by arsenic.

Cardiovascular Dysfunction: Long-term exposure to inorganic arsenic may cause various cardiovascular disorders such as atherosclerosis, hypertension, ischemic heart diseases, and ventricular arrhythmias.

Mechanisms pertaining to arsenic toxicity: https://europepmc.org/article/PMC/3183630

Arsenic Induces Accumulation of α- Synuclein: Implications for Synucleinopathies and Neurodegeneration: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5036614/ The Effects of Arsenic Exposure on Neurological and Cognitive Dysfunction in Human and Rodent Studies: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4026128/ Synergistic Neurotoxic Effects of Arsenic and Dopamine in Human Dopaminergic Neuroblastoma SH-SY5Y Cells: https://academic.oup.com/toxsci/article/102/2/254/1670790?login=true

Nickel:

Nickel and Chronic Fatigue Syndrome:

https://www.researchgate.net/publication/232047380_Nickel_Allergy_is_Found_in_a_Majorit y_of_Women_with_Chronic_Fatigue_Syndrome_and_Muscle_Painand_may_be_Triggered_by_Cigarette_Smoke_and_Dietary_Nickel_Intake

Nickel toxicity and metabolic disorders:

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0202683

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6112671/

Nickel and seizures: First Epileptic Seizure Induced by Occupational Nickel

Nickel and seizures: Toxicity to heavy metals and relationship to seizure thresholds

Heavy Metal Poisoning: NORD (National Organization for ...rarediseases.org › Rare Diseases)

Barium:

Barium is an alkaline metal. Its salts are used in various industries, including mining, ceramics, plastics, adhesives, and as a green coloring in fireworks. It is also used as a rodenticide. In the 18th and 19th centuries, it was used medicinally as a tonic and treatment of a wide variety of conditions, including asthma, tuberculosis, and heart failure. With its rise in popularity as a therapeutic agent came its first report of toxicity in overdose in 1794.

Barium poisoning is uncommon but potentially life-threatening. It can result in an increase in hypokalaemia which is a deficiency of potassium. When severe, hypokalemia leads to weakness which may progress to respiratory paralysis and cardiac arrhythmia. A low potassium level can make muscles feel weak, cramp, twitch, or even become paralyzed, and it can also cause stress to the kidneys, and abnormal heart rhythms may develop. Chronic issues with hypokalemia can also lead to a loss in bone density (osteoporosis).

Barium and epilepsy: Effects of barium on stimulus-induced rises of [K+]o in human

Barium and seizures: Common and Rare Side Effects for barium-methycellulose

Barium and its effects when it enters the bloodstream from perforations in the Gastrointestinal tract (leaky gut): https://www.atsdr.cdc.gov/toxprofiles/tp24-c2.pdf

The reported health effects include cardiovascular and kidney diseases, metabolic, neurological, and mental disorders: https://link.springer.com/article/10.1007/s10653-014-9622-7

Cesium:

Cesium Causes severe Hypokalemia, Hypomagnesia, and Heart Arrest:

https://pubmed.ncbi.nlm.nih.gov/19655100/

Cesium and Hypokalemia/Hypomagnesia:

https://www.researchgate.net/publication/26717303_Clinical_Effects_of_Cesium_Intake

Hypokalemia and Osteoporosis: https://pubmed.ncbi.nlm.nih.gov/19655100/

Hypokalemia and Calcification of arteries:

Dietary potassium regulates vascular calcification and arterial

Hypomagnesia and Osteoporosis: Magnesium deficiency: possible role in osteoporosis

Hypomagnesia and Osteoporosis: Magnesium and Osteoporosis: Current State of Knowledge

Hypomagnesia, Diabetes, and Osteoporosis:

Low Magnesium Exacerbates Osteoporosis in Chronic Kidney ...

Mercury:

Mercury poisoning refers to toxicity from mercury consumption. Mercury is a type of toxic metal that comes in different forms within the environment. The most common cause of mercury poisoning is from consuming too much methylmercury or organic mercury, which is linked to eating seafood. Small amounts of mercury are present in everyday foods and products, which may not affect your health. Too much mercury, however, can be poisonous.

Mercury itself is naturally occurring, but the amounts in the environment have been on the rise from industrialization. The metal can make its way into soil and water, and eventually to animals like fish. Consuming foods with mercury is the most common cause of this type of poisoning. Children and unborn babies are the most vulnerable to the effects of mercury poisoning. You can help prevent toxicity by limiting your exposure to this potentially dangerous metal.

Symptoms of mercury poisoning:

Mercury is most notable for its neurological effects. In general, the U.S. Food and Drug Administration trusted source says that too much mercury can cause:

anxiety depression

irritability

memory problems numbness

pathologic shyness

tremors

More often, mercury poisoning builds up over time. However, a sudden onset of any of these symptoms could be a sign of acute toxicity. Call your doctor right away if you suspect mercury poisoning.

Mercury poisoning symptoms in adults with advanced poisoning might experience:

hearing and speech difficulties

lack of coordination muscle weakness

nerve loss in hands and face trouble walking

vision changes

WHO information site and fact sheet

https://www.who.int/news-room/fact-sheets/detail/mercury-and-health https://www.epa.gov/mercury

Thallium:

Effect of Thallium on the human body: https://www.atsdr.cdc.gov/toxprofiles/tp54.pdf https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1788683/pdf/brmedj02223-0013b.pdf https://calpoison.org/news/thallium-poisoning

Where Thallium comes from: https://dermnetnz.org/topics/thallium-poisoning/ Thallium, hair loss, and abdominal pain: https://www.hindawi.com/journals/criem/2018/1313096/ Thallium and skin conditions:

https://jamanetwork.com/journals/jamadermatology/fullarticle/410601

Health effects of Thallium: https://www.lenntech.com/periodic/elements/tl.htm

Signs and symptoms of chronic poisoning include: tiredness, headaches, depression, hallucinations, psychosis, dementia, poor appetite, leg pains, hair loss, and disturbances of vision.

Sudden hair loss followed by diffuse alopecia is one of the characteristic dermatological signs of thallium poisoning. Hair loss due to atrophy of the hair follicles primarily affects the scalp, temporal parts of the eyebrows, eyelashes, and limbs. Axillary regions are less affected. Hair discoloration may also occur.

Other dermatological features include:

Skin rash, redness, and scaling of the palms and soles, acneform, or pustular eruptions of the face. Transverse white lines on the nails (Mee’s lines) appear in the nail plate about one month after the poisoning.

Other findings may include crusted eczematous lesions, hypohidrosis (reduced sweating), anhidrosis (absence of sweating), palmar erythema, painful glossitis (sore tongue) with redness of the tip of the tongue, and stomatitis.

Hair roots may have dark brown or black pigmentation. With chronic exposure, these darker regions appear in bands, demonstrating multiple thallium exposures.

Other widespread Effects and Symptoms of Thallium Toxicity:

Severe abdominal pain/cramping

All over body pain

Weakness in upper/lower extremities

Confusion

Thallium Is corrosive to GI mucosa

Thallium deposition occurs primarily in tissues with high potassium concentrations such as neuronal, myocardial, hepatic, renal, and dermal tissues

Thallium replaces potassium in numerous potassium-dependent enzyme systems, usually with superior affinity over potassium

Thallium damages the 60s subunit of ribosomes, resulting in impaired protein synthesis.

The combined effect of these acute cellular dysfunctions is the failure of aerobic respiration and poor cellular energy production, resulting in chronic fatigue and excess sleeping.

Can lead to sensory neuropathy due to acute myelin fragmentation and axonal degeneration (neural damage/neuropathy, brain, etc)

Central nervous system findings are mediated by multi-focal edematous changes and chromatolysis, particularly in the frontal lobe, motor cortex, basal ganglia, and pyramidal cells.

Thallium damages kidney tissue

Nystagmus, confusion, anxiety, tremor, ataxia, optic neuritis, altered mental status, s

Alopecia (hair loss), a hallmark of thallium poisoning, occurs 7-12 days after other symptoms begin.

Hair loss commonly involves the scalp, and often involves body hair, temporal parts of the eyebrows, eyelashes, and limbs. Axillary regions are less affected. Hair discoloration may also occur, and is generally not permanent and is cleared from the blood relatively quickly.

Beryllium:

The commercial use of beryllium requires the use of appropriate dust control equipment and industrial controls at all times because of the toxicity of inhaled beryllium-containing dust that can cause a chronic life-threatening allergic disease in some people called berylliosis. Beryllium is a component of several dental alloys.

Toxicological profile for Beryllium:

https://www.atsdr.cdc.gov/toxprofiles/Beryllium_addendum.pdf

Beryllium and Lung Cancer: https://pubmed.ncbi.nlm.nih.gov/19384680/

Occupational exposure to beryllium and cancer risk: https://pubmed.ncbi.nlm.nih.gov/22276590/

OSHA on health effects of exposure to beryllium via inhalation or skin contact: https://www.osha.gov/beryllium/health-effects

OSHA and Beryllium: https://www.osha.gov/beryllium

Non-small cell lung cancer and Beryllium: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4931124/

Gadolinium:

Gadolinium-based contrast agents for MR cancer imaging:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552562/

The role of Gadolinium for imaging of cancer lesions: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6927639/

Long term use of Gadolinium on the central nervous system: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5756358/

Gadolinium Toxicity Lawsuits: https://www.levinlaw.com/gadolinium-toxicity-lawsuits

Gadolinium-based MRI contrast agents and induced mitochondrial toxicity and cell death in human neurons: https://journals.lww.com/investigativeradiology/Fulltext/2019/08000/Gadolinium_Based_MR I_Contrast_Agents_Induce.1.aspx

Palladium:

Primarily used in industry in electrical contacts as a catalyst, used to purify hydrogen gas, and in dentistry as an alloy in gold crowns and bridges along with some surgical instruments or jewelry. Palladium is cytotoxic and kills or damages cells. Damages cell mitochondria and inhibits enzyme activity function. More readily absorbed via the lungs than via the gastrointestinal tract.

Using palladium to fight cancer: https://www.news.uct.ac.za/article/-2018-10-05-usingpalladium-to- fight-cancer

Overview of toxicity of Palladium: https://www.biologicalmedicineinstitute.com/palladium

Cytotoxic and apoptotic effects of the combination of palladium and curcumin on non-small lung cancer cell lines: https://pubmed.ncbi.nlm.nih.gov/28187956/

Chemical properties of palladium and health effects: https://www.lenntech.com/periodic/elements/pd.htm

Levels of platinum, palladium, and lead in California water: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1475032/ Platinum/Palladium group elements in seawater off of California coast: https://cdnsciencepub.com/doi/pdf/10.1139/v83-136

Water treatment and implementing Palladium Catalysts:

https://pubs.acs.org/doi/10.1021/acsestengg.0c00227

Palladium-catalyzed reductions of water contaminants: https://cfpub.epa.gov/ncer_abstracts/INDEX.cfm/fuseaction/display.publications/abstract_id /540

In vitro evaluation of the potential toxic effects of palladium nanoparticles on fibroblasts and lung epithelial cells: https://pubmed.ncbi.nlm.nih.gov/28473196/ Palladium and its inorganic compounds: https://onlinelibrary.wiley.com/doi/10.1002/3527600418.mb744005e0022

Platinum:

Used in catalytic converters, laboratory equipment, electrical contacts and electrodes, platinum resistance thermometers, dentistry equipment, and jewelry. Being a heavy metal, it leads to health problems upon exposure to its salts, but due to its corrosion resistance, metallic platinum has not been linked to adverse health effects.

Platinum neurotoxicity pharmacogenetics:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2651829/

Platinum biomonitoring summary:

https://www.cdc.gov/biomonitoring/Platinum_BiomonitoringSummary.html

WHO report on Platinum: http://www.inchem.org/documents/ehc/ehc/ehc125.htm

Platinum-based chemotherapy in advanced non-small-cell lung cancer:

https://pubmed.ncbi.nlm.nih.gov/27010977/

Platinum drugs in the treatment of non-small lung cancer:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2376170/ Platinum-based versus non-platinum based chemotherapy: https://ascopubs.org/doi/10.1200/JCO.2005.03.045

Aluminum:

Aluminum is the second most abundant metallic element in the Earth's crust after silicon, yet it is a comparatively new industrial metal that has been produced in commercial quantities for just over 100 years. Some of the many uses for aluminum are in transportation (automobiles, airplanes, trucks, railcars, marine vessels, etc.), packaging (cans, foil, etc.), construction (windows, doors, siding, etc), consumer durables (appliances, cooking utensils, etc.), electrical transmission lines, machinery, and many other applications. Small amounts of aluminum can be found dissolved in water. Aluminum is also found in consumer products such as antacids, astringents, buffered aspirin, food additives, and antiperspirants.

Aluminum statistics: https://www.usgs.gov/centers/nmic/aluminum-statistics-and-information

PubChem article: https://pubchem.ncbi.nlm.nih.gov/compound/Aluminum

Aluminum toxicity and effects on the body: https://www.winchesterhospital.org/healthlibrary/article?id=164929

Oxidative stress, pro-inflammatory, peptide denaturation...: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7071840/

Aluminum overload, dementia: https://www.sciencedirect.com/topics/medicine-anddentistry/aluminum-overload

Toxicological profile of Aluminum, aluminum in food: https://www.atsdr.cdc.gov/toxprofiles/tp22.pdf

Aluminum toxicity in soybean: https://content.ces.ncsu.edu/aluminum-toxicity-in-soybean

Aluminum toxicity in chronic kidney disease: https://www.uptodate.com/contents/aluminumtoxicity-in-chronic-kidney-disease

Serum concentrations of heavy metals in women with endometrial polyps: https://pubmed.ncbi.nlm.nih.gov/31478412/

Tungsten:

Tungsten is a refractory metal that is used in a wide range of applications. It was initially perceived that tungsten was immobile in the environment, supporting tungsten as an alternative for lead and uranium in munition and military applications. Recent studies report movement and detection of tungsten in soil and potable water sources, increasing the risk of human exposure. Tungsten is a common contaminant at mining sites, industrial sites that use the metal, and at DoD sites involved in the manufacture, storage, and use of tungsten-based ammunition. It is also found in detectable amounts in municipal solid waste and landfill leachate because of its use in common household products such as filaments in incandescent light bulbs

Tox Profile: https://www.atsdr.cdc.gov/toxprofiles/tp186-c3.pdf

EPA Overview: https://www.epa.gov/sites/production/files/201403/documents/ffrrofactsheet_contaminant_tungsten_january2014_final.pdf

Uranium:

Uranium is a heavy metal that has been used as an abundant source of concentrated energy for over 60 years. Uranium occurs in most rocks in concentrations of 2 to 4 parts per million and is as common in the Earth's crust as tin, tungsten, and molybdenum. Uranium occurs in seawater and can be recovered from the oceans.

On August 6, 1945, a 10-foot-long (3 meters) bomb fell from the sky over the Japanese city of Hiroshima. Less than a minute later, everything within a mile of the bomb's detonation was obliterated. A massive firestorm rapidly destroyed miles more, killing tens of thousands of people. This was the first-ever use of an atomic bomb in warfare, and it used one famous element to wreak its havoc: uranium. This radioactive metal is unique in that one of its isotopes, uranium-235, is the only naturally occurring isotope capable of sustaining a nuclear fission reaction. (An isotope is a version of the element with a differing number of neutrons in its nucleus.)

https://www.livescience.com/39773-facts-about-uranium.html

Kidney Disease and Uranium: https://web.evs.anl.gov/uranium/guide/ucompound/health/index.cfm#:~:text=Chemical%20T oxicity&text=The%20main%20chemical%20effect%20associated,which%20then%20enters%2 0the%20bloodstream.

Health effects: https://www.ncbi.nlm.nih.gov/books/NBK158798/

MYCOTOXINS

Prepared by: Dr. Elena Villanueva, DC on February 23, 2022

Session date: February 23, 2022

Virtually every neurological disease has been associated with mycotoxin exposure, including autism, Alzheimer’s disease, amyotrophic lateral sclerosis, multiple sclerosis, and Parkinson’s disease. There is a strong association between mycotoxin exposure and cancers, especially liver and kidney cancers. Diseases and symptoms linked to mycotoxin exposure include fever, pneumonialike symptoms, heart disease, rheumatic disease, asthma, sinusitis, nose bleeding, cancer, memory loss, vision loss, chronic fatigue, skin rashes, depression, ADHD, anxiety, and liver damage. A study of patients with chronic fatigue found that all the patients had high levels of mycotoxins in the urine.

Mold and your health, hives correlation:

http://www.idph.state.il.us/envhealth/factsheets/mold.htm

Mold toxicity and non-respiratory effects on the body:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4982651/

Neurotoxicity of Trichothecenes and other mycotoxins:

https://pubmed.ncbi.nlm.nih.gov/32805342/

ASPERGILLUS:

Aspergillus is the most prevalent mold group in the environment, and there are hundreds of different species. It has caused billions of dollars in damage to crops and livestock. Common Aspergillus mycotoxins tested in the MycoTOX Profile include aflatoxin, ochratoxin, sterigmatocystin, gliotoxin, and citrinin. The main target of these toxins is the liver. These toxins have been found in all major cereal crops, including peanuts, corn, cotton, millet, rice, sorghum, sunflower seeds, wheat, and a variety of spices. They are also found in eggs, milk, and meat from animals fed contaminated grains. Diseases caused by Aspergillus are called aspergillosis. The most common route of infection is through the respiratory system. Aspergillus can cause severe asthma when the mold colonizes the lung, forming a granulomatous disease.

Ochratoxin A is the most common mycotoxin produced by both Aspergillus and Penicillium species. It causes acute depletion of striatal brain dopamine and its metabolites, accompanying evidence of neuronal cell apoptosis in the substantia nigra, striatum, and hippocampus. Depletion of dopamine in these brain areas is commonly associated with Parkinson’s disease, which is frequently treated with L-DOPA to replace dopamine in the brain depleted areas.

Ochratoxin A (OTA) is a nephrotoxic, immunotoxic, and carcinogenic mycotoxin. Molds produce this chemical in the Aspergillus and Penicillium families. Exposure is primarily through contaminated foods such as cereals, grape juices, dairy, spices, wine, dried vine fruit, and coffee. Exposure to OTA can also come from inhalation exposure in water-damaged buildings. OTA can lead to kidney disease and adverse neurological effects. Studies have shown that OTA can cause significant oxidative damage to multiple brain regions and the kidneys. Dopamine levels in the brain of mice have been shown to be decreased after exposure to OTA. Effects of OTA on Blood glucose levels: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5408218/

Ochratoxin An (OTA) is a poison created by various Aspergillus and Penicillium species — it is a standout amongst the most-inexhaustible nourishment tainting mycotoxins. It is likewise a successive contaminant of water-harmed houses and warming channels. The presentation can likewise originate from inward breath in water-harmed structures.

GLIOTOXIN:

Gliotoxin (GTX) is produced by the mold genus Aspergillus and perhaps Candida species. Aspergillus spreads in the environment by releasing conidia capable of infiltrating the small alveolar airways of individuals. To evade the body’s defenses, Aspergillus releases gliotoxin to inhibit the immune system. One of the targets of gliotoxin is PtdIns (3,4,5) P3. This results in the downregulation of phagocytic immune defense, leading to the exacerbation of polymicrobial infections. Gliotoxin impairs the activation of T-cells and induces apoptosis in monocytes and monocyte-derived dendritic cells. These impairments can lead to multiple neurological syndromes.

AFLATOXIN M1 (AFM1):

Aflatoxin M1 (AFM1) is the main metabolite of aflatoxin B1, a mycotoxin produced by different species of the genus Aspergillus. Aflatoxins are some of the most carcinogenic substances in the environment. Aflatoxin susceptibility is dependent on multiple different factors such as age, sex, and diet. Aflatoxin can be found in beans, corn, rice, tree nuts, wheat, milk, eggs, and meat. In cases of lung aspergilloma, aflatoxin has been found in human tissue specimens.

Aflatoxin can cause liver damage, cancer, mental impairment, abdominal pain, hemorrhaging, coma, and death. Aflatoxin has been shown to inhibit leukocyte proliferation.

Clinical signs of aflatoxicosis are non-pruritic macular rash, headache, gastrointestinal dysfunction (often extreme), lower extremity edema, anemia, and jaundice. The toxicity of aflatoxin is increased in the presence of ochratoxin and zearalenone.

AFLATOXINS:

A group of growth strains that influence plant items, aflatoxins, have been connected to liver disease, hepatitis, cirrhosis, and other medical problems. Introduction happens when devouring polluted plant items, eating meat or dairy from creatures that have eaten defiled feed, or breathing in residue while working with sullied items.

Effects on blood sugar levels: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6024316/

Aflatoxin B1– Of the four aflatoxins that are known to cause malignant growth in people and creatures, aflatoxin B1 is the most dangerous and is characterized by the World Wellbeing Association as a class 1 cancer-causing agent. Even though it assaults the liver, this mycotoxin can likewise influence the kidneys, lungs, and different organs.

hepatic carcinogenesis: https://www.intechopen.com/chapters/68699

Cancer inducing: https://pubmed.ncbi.nlm.nih.gov/30468841/

Aflatoxin B2: Like aflatoxin B1, aflatoxin B2 is created by the growths of Aspergillus flavus and A. parasiticus. It is also a poison and cancer-causing agent that defiles sustenance items, principally influences the liver and kidneys, and enters the body through the lungs, mucous films (nose and mouth), or even the skin, yet is less powerful than aflatoxin B1.

Aflatoxin G1: Conceived from a dirt-borne growth like different aflatoxins, G1 additionally defiles a broad scope of sustenance items including peanuts, cottonseed supper, oilseeds, vegetable oils, corn, and different grains in human nourishment and creature feed. Aflatoxin pollution is most regular in sticky conditions, particularly in tropical and subtropical districts.

Aflatoxin G2: The least poisonous aflatoxin, G2 is as yet perilous to people and creatures. Although less deadly than a portion of different aflatoxins, G2 can likewise cause liver issues (counting malignant growth, constant hepatitis, and jaundice) and seems to assume a job in Reye’s disorder. Like all aflatoxins, it can likewise unfavorably influence the invulnerable framework.

Aflatoxin M1: on blood glucose levels: https://link.springer.com/article/10.1007/s11356-021-14871-w

PENICILLIUM:

There are over 200 species of the genus Penicillium that have been discovered. Penicillium chrysogenum is the most common of these species. It is often found in indoor environments and is responsible for many allergic reactions. Penicillium is also a known contaminant in many different food items. Many different citrus fruits can become contaminated with Penicillium, but it can also contaminate seeds and grains. One reason that Penicillium is such a common infestation is because of its ability to thrive in low humidity. In the home, Penicillium can be found in wallpaper, carpet, furniture, and fiberglass insulation. The most common mycotoxin produced by Penicillium includes mycophenolic acid and ochratoxin.

Neurotoxicity of Trichothecenes and other mycotoxins:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3179161/

MYCOPHENOLIC ACID:

Mycophenolic Acid (MPA) is produced by the Penicillium fungus. MPA is an immunosuppressant that inhibits the proliferation of B and T lymphocytes. MPA exposure can increase the risk of opportunistic infections such as Clostridia and Candida. MPA is associated with miscarriage and congenital malformations when the woman is exposed in pregnancy.

Citrinin: Citrinin is a mycotoxin produced by several species of the genera Aspergillus, Penicillium, and Monascus and it occurs mainly in stored grain. Citrinin is generally formed after harvest and occurs mainly in stored grains, it also occurs in other plant products.

https://www.sciencedirect.com/topics/immunology-and-microbiology/citrinin https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5412229/ https://www.longdom.org/open-access/the-occurrence-properties-and-significance-ofcitrinin-mycotoxin-2157-7471-1000321.pdf

Stachybotrys Chartarum (also known as black mold):

Like nearly all kinds of toxic mold, S. chartarum is dangerous primarily because it produces mycotoxins—in this case, a class known as Trichothecenes. Specific mycotoxins produced by black mold include Satratoxin G, Satratoxin H, Isosatratoxin F, Roridin A, Roridin E, Roridin H, Roridin L- 2, Verrucarin A, and Verrucarin J. Collectively, Trichothecenes are some of the most dangerous moldrelated pathogens known to medical science.

Stachybotrys is a greenish-black mold. This mold can grow on materials with high cellulose and low nitrogen content, such as gypsum board, paper, fiberboard, and ceiling tiles. Stachybotrys is known for its production of highly toxic macrocyclic trichothecene mycotoxins. Two of the more common mycotoxins produced by Stachybotrys are roridin E and verrucarin. In addition to these mycotoxins, the fungus produces nine phenylspirodrimanes and cyclosporine, which are potent immunosuppressors. These immunosuppressors, along with the mycotoxin trichothecenes, may be responsible for the high toxicity of Stachybotrys.

Health Effects: S. chartarum can cause various adverse health effects in humans (and pets). Shortterm exposure to black mold often leads to respiratory distress (e.g., coughing, sneezing, and wheezing), irritation of the eyes and mucus membranes, and skin rashes. People with seasonal allergies, mold allergies, asthma, certain pulmonary diseases (including COPD and cystic fibrosis), and compromised immune systems may also experience chronic fatigue, persistent headaches, and nausea and vomiting.

Long-term exposure to black mold has been linked to the following conditions in previously healthy individuals: cognitive difficulties (like confusion or “brain fog”), anxiety and depression, and stomach and muscle cramps.

Macrocyclic trichothecenes are known to be highly cytotoxic and are potent inhibitors of protein synthesis. This can affect almost all cells in the body. The health effects of trichothecenes are known, as cancer patients were administered a trichothecene called anguidine in a 1978 and 1979 clinical study in the hope that its inhibition of protein synthesis would selectively kill the faster multiplying cancer cells. The study was terminated due to the severe symptoms/side effects of anguidine, which included: nausea, vomiting, diarrhea, burning erythema, ataxia, chills, fever, hypotension, hair loss, and confusion. These side effects were very similar to the symptoms described by individuals living or working inside Stachybotrys infested homes and buildings.

TRICHOTHECENES:

Trichothecenes are produced by several genera of fungi, including Fusarium, Stachybotrys, Myrothecium, Trichothecium, Trichoderma, and others.

Fusarium is a major agricultural plant pathogen in temperate growing regions where it causes Fusarium head blight in wheat, barley, triticale, and other grains. Fusarium molds are the most economically important source of trichothecene mycotoxins. - Feed for agricultural animals used for human consumption. Huge economical impact when the feed for animals is contaminated. Strict regulations and testing in Europe, less in the U.S.

In North America, the trichothecenes produced by Fusarium are the major contaminants in cereal crops. Mold-infected grains have been associated with ill health in livestock and man for over 100 years. In European Russia and Eastern Siberia, “scabby grains” and “moldy hay” have long been recognized as toxic.

Chronic Symptoms and conditions include:

Epithelial irritation or dermonecrosis, gastrointestinal irritation, immunosuppression (Joffe, 1974), leukopenia with granulocytopenia, and a relative lymphocytosis, anemia, central and autonomic nervous system dysfunction, thrombocytopenia and decreased fibrinogen, and petechial hemorrhages on the skin of the trunk, lateral surfaces of the arms, the thighs, face, and head, secondary to the anemia.

Acute Symptoms usually last 3-9 days and include:

Burning sensation of the mouth, tongue, esophagus, and stomach and inflammation of the gastrointestinal mucosa accompanied by vomiting, diarrhea, salivation, dizziness, and tachycardia

General Information on Health Effects of Trichothecenes: https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/stachybotrys Neurotoxicity of Trichothecenes and other mycotoxins: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3179161/

RORIDIN E:

Roridin E is a macrocyclic trichothecene produced by the mold genera Fusarium, Myrothecium, Trichoderma, Trichothecium, Cephalosporium, Verticimonosporium, and Stachybotrys (i.e., black mold). Trichothecenes are frequently found in buildings with water damage but can also be found in contaminated grain. This is a very toxic compound, which inhibits protein biosynthesis by preventing peptidyl transferase activity.

Trichothecenes are considered highly toxic and have been used as biological warfare agents. Even low levels of exposure to macrocyclic trichothecenes can cause severe neurological damage, immunosuppression, endocrine disruption, cardiovascular problems, and gastrointestinal distress.

VERRUCARIN A:

Verrucarin A is a macrocyclic trichothecene mycotoxin produced from Stachybotrys, Fusarium, and Myrothecium molds. Trichothecenes are frequently found in buildings with water damage but can also be found in contaminated grain. This is a very toxic compound, which inhibits protein biosynthesis by preventing peptidyl transferase activity. Trichothecenes are considered extremely toxic and have been used as biological warfare agents. Even low levels of exposure to macrocyclic trichothecenes can cause severe neurological damage, immunosuppression, endocrine disruption, cardiovascular problems, and gastrointestinal distress.

A standout amongst the most dangerous trichothecenes, Verrucarin A is likewise delivered by parasites and shape. Like Roridin E, Verrucarin An is found in molds in soggy situations as well as in molds that normally happen on an assortment of yields proposed for human and creature utilization.

Satratoxin G (mycotoxin-mold):

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1513335/ (breathing issues)

https://pubmed.ncbi.nlm.nih.gov/16835065/ (Satratoxin G from the black mold Stachybotrys chartarum evokes olfactory sensory neuron loss and inflammation in the murine nose and brain)

https://www.mdpi.com/1422-0067/12/8/5213/htm (Mechanisms of Mycotoxin-Induced Neurotoxicity through Oxidative Stress Associated Pathways)

Satratoxin G: The majority of the trichothecenes are very harmful; tests have discovered that Satratoxin G is the riskiest to individuals and creatures. The dark shape Stachybotrys chartarum produces a few kinds of trichothecenes; however, it creates Satratoxin G and H in more prominent sums than different poisons.

Satratoxin H: Not all strains of the dark form (Stachybotrys chartarum) produce mycotoxins, yet the ones that do commonly create more than one kind, including Satratoxin H. The shape is found on some agrarian materials and in clammy or water-harmed situations. Proof recommends that the form is a significant issue in North America.

Apoptosis in PC12 cells from Satratoxin: PC12 cells are a type of catecholamine cells that synthesize, store and release norepinephrine and dopamine.

https://pubmed.ncbi.nlm.nih.gov/15659314/ (Involvement of reactive oxygen species and stress-activated MAPKs in satratoxin H-induced apoptosis) Satratoxin H is known to induce apoptosis as well as genotoxicity in PC12 cells.

https://pubmed.ncbi.nlm.nih.gov/22863859

Respiratory, immunologic, and neurologic symptoms that are sometimes etiologically linked to aberrant indoor growth of the toxic black mold, Stachybotrys chartarum: https://academic.oup.com/toxsci/article/104/1/4/1717327 https://www.clinicaltherapeutics.com/article/S0149-2918(18)30229-7/pdf

Neurotoxicity of Satratoxin: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2808125/ https://www.jimmunol.org/content/182/10/6418 (inflammatory/immune response)

Isosatratoxin F: Another trichothecene mycotoxin created by Stachybotrys chartarum, Isosatratoxin F is one of the supporters of “wiped out structure disorder,” where medical problems of structure tenants are legitimately attached to time spent in form contaminated structures. A 1984 World Wellbeing Association Panel report recommended that up to 30 percent of new and redesigned structures are potential reasons for medical issues because of poor air quality.

Roridin A: Like other macrocyclic trichothecenes, Roridin An is created by the shape and related to various intense and unending respiratory tract medical issues. Tests have demonstrated that presentation to Roridin A can cause nasal irritation, an abundance of bodily fluid emission, and harm to the olfactory framework.

Roridin E: In the same way as other mycotoxins, Roridin E can cause the above respiratory and olfactory issues and disturb the blend of DNA, RNA, and protein which can affect each cell in the body. Roridin E develops in soggy indoor conditions. However, a dirt parasite can likewise be delivered that defiles groceries and is passed down the natural pecking order to creatures and afterward to people.

Roridin H: Influencing human and creature wellbeing in many indistinguishable ways from other trichothecene mycotoxins, Roridin H is delivered by form, particularly Stachybotrys chartarum, which develops well on many structure materials subject to soggy conditions, including wood- fiber, versifiers, roof tiles, water-harmed gypsum board, and cooling channels.

Roridin L-2: This mycotoxin is likewise created by molds, including dark shape. Strikingly, ecological tests cannot generally recognize Stachybotrys since its spores are enormous and substantial and not effectively scattered into the air. Sadly, mycotoxin atoms, including the exceptionally dangerous Rorodin l2, are light and effectively airborne and breathed in by inhabitants of a contaminated structure.

Verrucarin J: One more mycotoxin created by Stachybotrys chartarum, Verrucarin particles are little enough to be airborne and effectively breathed in. Examinations have verified that inward breath is the riskiest type of presentation. Nevertheless, trichothecene mycotoxins can undoubtedly cross cell films, which means they can likewise be ingested through the mouth and even the skin.

FUSARIUM:

Fusarium’s major mycotoxins are zearalenone (ZEN) and fumonisin. Fusarium fungi grow best in temperate climate conditions. They require lower temperatures for growth than Aspergillus. Fusarium grows worldwide on many different types of grains, including corn and wheat. Exposure to mycotoxins from Fusarium can lead to both acute and chronic effects. These symptoms can include abdominal distress, malaise, diarrhea, emesis, and death. ZEN possesses estrogenic effects and has been implicated in reproductive disorders.

Neurotoxicity of Trichothecenes and other mycotoxins: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3179161/

Diacetoxyscirpenol (DAS): In the fusarium family: also called anguidine, is a mycotoxin from the group of type A trichothecenes. It is a secondary metabolite product of fungi of the genus Fusarium and may cause toxicosis in farm animals. Highly irritating to the skin and mucous membranes in all species. Skin irritation was experienced by laboratory workers accidentally exposed to trichothecene producing fungal cultures or crude extracts of T-2 toxin.

lymphoid necrosis, hematotoxicity, and gastrointestinal toxicity:

https://www.sciencedirect.com/topics/medicine-and-dentistry/diacetoxyscirpenol

https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5367 (Risk to human and animal health related to the presence of 4,15-diacetoxyscirpenol in food and feed)

Blood disorders: https://pubmed.ncbi.nlm.nih.gov/9608725/

Blood and reproductive disorders: https://www.sciencedirect.com/topics/pharmacologytoxicology-and-pharmaceutical-science/diacetoxyscirpenol

Liver toxicity, Genotoxicity, and other adverse effects of DAS:

https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5367

Biological compound breakdown: https://www.sciencedirect.com/topics/agricultural-andbiological-sciences/diacetoxyscirpenol

Fumonisins B1 (mycotoxin-mold): oxidative stress leading to mitochondrial toxicity has been identified as one of the mechanisms by which fumonisins can lead to adverse effects such as hepatotoxicity, nephrotoxicity, cardiotoxicity, and cancer.

Liver tumors, neural tube defects, and cardiovascular problems:

https://link.springer.com/article/10.1007/s00204-015-1645-z

Mitochondrial Toxicity: https://pubmed.ncbi.nlm.nih.gov/32667064/

FB1 is neurotoxic, hepatotoxic, and nephrotoxic:

https://journals.sagepub.com/doi/abs/10.1177/0960327108099525

Impairs gut and immune function: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3942744 (intestinal health)

Gut health and osteoporosis: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7069453/

Gut health, vit D/K, and osteoporosis:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6119671/

Gut health and osteoporosis: https://nbihealth.com/is-your-gut-causing-osteoporosis/ https://cdn-ext.agnet.tamu.edu/wp-content/uploads/2019/03/EDL-087-fumonisin-facts.pdf

Fumonisins B2: oxidative stress leading to mitochondrial toxicity has been identified as one of the mechanisms by which fumonisins can lead to adverse effects such as hepatotoxicity, nephrotoxicity, cardiotoxicity, and cancer.

F B2 and Nephrotoxicity: https://www.sciencedirect.com/topics/pharmacology-toxicologyand- pharmaceutical-science/fumonisin-b2

Neurotoxic Effects of Fumonisins:

https://www.sciencedirect.com/science/article/pii/S1566070214001167

Fumonisins B1 & Fumonisins B2 Equal in Toxicity:

https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/fumonisin-b2

Enniatin B:

Review of Mycotoxin Enniatin B:

https://www.frontiersin.org/articles/10.3389/fpubh.2017.00304/full

https://www.mdpi.com/2072-6651/12/6/415/htm

Fumonisin B3: Commonly found in corn-based products

https://pubmed.ncbi.nlm.nih.gov/11297276/

Infects many cereals and other foods: https://lktlabs.com/product/fumonisin-b3/

FB3 has been detected in corn and corn-based foods and livestock feeds: https://www.caymanchem.com/product/20434/fumonisin-b3

https://cdn-ext.agnet.tamu.edu/wp-content/uploads/2019/03/EDL-087-fumonisin-facts.pdf

https://pubmed.ncbi.nlm.nih.gov/14630058/

High Risk for Esophageal Cancer via food introduction:

https://pubmed.ncbi.nlm.nih.gov/15254715/

Mycotoxins in our Foods: https://fppn.biomedcentral.com/articles/

Nivalenol (NIV):

STERIGMATOCYSTIN (STG):

Sterigmatocystin (STG) is a mycotoxin that is closely related to aflatoxin. STG is produced from several types of mold, such as Aspergillus, Penicillium, and Bipolaris. It is carcinogenic, particularly in the cells of the GI tract and liver. STG has been found in the dust from damp carpets. It is also a contaminant of many foods, including grains, corn, bread, cheese, spices, coffee beans, soybeans, pistachio nuts, and animal feed. In cases of lung aspergilloma, STG has been found in human tissue specimens.

The toxicity of STG affects the liver, kidneys, and immune system. Tumors have been found in the lungs of rodents that were exposed to STG. Oxidative stress becomes measurably elevated during STG exposure, which causes a depletion of antioxidants such as glutathione, particularly in the liver.

ZEARALENONE (ZEA)

Zearalenone (ZEA) is a mycotoxin produced by species of the mold genera Fusarium and Gibberella. It has been shown to be hepatotoxic, hematotoxic, immunotoxic, and genotoxic. ZEA is commonly found in several US, European, Asian, and African foods, including wheat, barley, rice, and maize.

ZEA has estrogenic activity, and exposure to ZEA can lead to reproductive changes. ZEA’s estrogenic activity is higher than that of other non-steroidal isoflavones (compounds that have estrogen-like effects) such as soy and clover. ZEA exposure can result in thymus atrophy and altered spleen lymphocyte production and impaired lymphocyte immune response, which leads to patients being susceptible to disease.

ENNIATIN B:

Enniatin B1 is a fungal metabolite categorized as a cyclohexa-depsipeptides toxin produced by the molds of the Fusarium species. These species are common cereal contaminants. Grains in many different countries have recently been contaminated with high levels of enniatin. The toxic effects of enniatin are caused by the inhibition of the acyl-CoA cholesterol acyltransferase, depolarization of mitochondria, and inhibition of osteoclastic bone resorption. Enniatin has antibiotic properties, and chronic exposure may lead to weight loss, fatigue, and liver disease.

DIHYDROCITRINONE:

Dihydrocitrinone is a metabolite of Citrinin (CTN), a mycotoxin produced by mold species of the genera Aspergillus, Penicillium, and Monascus. CTN exposure can lead to nephropathy because of its ability to increase the permeability of mitochondrial membranes in the kidneys. The three most common exposure routes are ingestion, inhalation, and skin contact. CTN has been shown to be carcinogenic in rat studies. Multiple studies have linked CTN exposure to a suppression of the immune response.

Think Kidney Stress: is a metabolite of Citrinin (CTN), which is a mycotoxin that is created by the shape species Aspergillus, Penicillium, and Monascus. CTN presentation can prompt nephropathy on account of its capacity to build the penetrability of mitochondrial films in the kidneys. The three most basic presentation courses are ingestion, inward breath, and skin contact. CTN has been demonstrated to be cancer-causing in rodent contemplates.

https://www.sciencedirect.com/topics/immunology-and-microbiology/citrinin

When kidneys do not function optimally, extra parathyroid hormone is typically released in the blood to move calcium from inside the bones into the blood. Chronic kidney stress of this type over a long period can result in mineral and bone disorders because the kidneys do not properly balance the mineral levels in the body.

Mycotoxins and the microbiome: https://www.researchgate.net/publication/320223010_Impact_of_mycotoxins_on_the_intesti ne_are_ mucus_and_microbiota_new_targets

CHAETOGLOBOSIN A:

Chaetoglobosin A (CHA) is produced by the mold Chaetomium globosum (CG). CG is commonly found in homes that have experienced water damage. Up to 49% of water-damaged buildings have been found to have CG. CHA is highly toxic, even at minimal doses. CHA disrupts cellular division and movement.

Most exposure to CG is through the mycotoxins because the spores tend not to aerosolize. Exposure to CHA has been linked to neuronal damage, peritonitis, and cutaneous lesions.

Patulin (mycotoxin-mold):

https://www.mdpi.com/1422-0067/21/21/8187/htm (discussed many mold types and their issues including Patulin – notice where it discusses hepatotoxicity (liver) – which can cause the liver to make more fat to protect itself from this toxin)

Sources and Health Considerations:

https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/patulin

Adverse Health Effects with Patulin and other Mycotoxins:

https://www.who.int/news- room/fact-sheets/detail/mycotoxins

Mycotoxins and their effect on GI health and Immune health:

https://www.frontiersin.org/articles/10.3389/fcimb.2018.00060/full

OTHER:

Gliotoxin:

The most well-known reason for shape maladies in people is Aspergillus fumigatus, which produces gliotoxin, a mycotoxin that smothers the invulnerable framework. Found in numerous homes and structures, A. fumigatus ordinarily contaminates people with traded off insusceptible frameworks but can be fatal: Obtrusive Aspergillosis (IA) is the main source of death in immunocompromised individuals.

Citrinin is a mycotoxin that is often found in food. It is a secondary metabolite produced by fungi that contaminate long-stored food and it causes different toxic effects, like nephrotoxic, hepatotoxic, and cytotoxic effects. Citrinin is mainly found in stored grains, but sometimes also in fruits and other plant products.

Definition: https://en.wikipedia.org/wiki/Citrinin

Citrinin and Food: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5086634/