We live in a polluted world. Toxic chemicals are added to our food, our household products, and body care products. There also are adverse health e ects from electronic devices such as cell phones and cordless phones. Each year, approximately 2,000 new chemicals are registered for use in everyday items including: food, personal care products, prescription drugs, household cleaners, and lawn care products.
Personal care products are laden with toxic chemicals. One out of five adults is potentially exposed every day to all the top seven common carcinogenic impurities in cosmetics and personal care products. Hydroquinone is the top most common impurity, potential contaminant in products used by 94 % of women and 69 % of men. Three chemicals are systematically absorbed, metabolized and excreted in urine following application on the skin in a cream preparation (Janiua et al. 2008).
Since World War II, over 85,000 synthetic chemicals have been registered with the US Environmental Protection Agency. ). The Toxic Substance Control Act of 1976 grandfathered 65,000 chemicals already in use with no further testing required. There is no single regulatory agent that oversees industrial chemicals to insure their safety. All chemicals are presumed safe until proven hazardous
Studies on the health e ects of toxins are typically based on short term observations. These studies assume that individuals have similar sensitivities,
metabolisms and elimination patterns. Usually these studies do not look at synergistic e ects of more than one toxin, do not account for epigenetic e ects and cannot address cumulative e ects.
Small amounts of bioaccumulative substances can lead to significant levels of toxins over time (Thorton et al. 2002) .
Individuals have varying sensitivities to toxins and varying abilities for the body to clear these toxins from the body.
Di erences in sensitivity can be due to increased exposure, nutrient deficiencies (such as Vitamin B6, magnesium, and selenium), a diet high in sugar, heavy metal exposure, stress, intestinal dysbiosis (“leaky gut”) and genetic variations in detoxification enzymes.
The process of removing toxins from the body involves converting the foreign chemicals to more water- soluble form so that it can be eliminated through the urine. This elimination process can be impaired by high toxic loads, impaired elimination (eg. constipation), nutrient imbalances, deficiency of detoxifying substances (antioxidants and cofactors) and a dysregulation of detoxifying enzymes. Di erences in intestinal microflora may significantly a ect xenobiotic (i.e., foreign) induced toxicity by either activating or inactivating these toxins via metabolism (Jeong et al. 2013).
TOXINS AND DISEASES
Environmental toxins have a principle role in causing cancer
(Lichtenstien et al. 2000) neurological defects and obesity.
Neurotoxic e ects
Industrial chemicals that injure developing brains and lead to disorders such as autism, ADHD, dyslexia and other cognitive impairments include: lead, methylmercury, polychlorinated biphenyls, arsenic, toluene, manganese, fluoride, (Grandjean, Landrigan 2014). A systematic review of toxicant-related studies in autism found that pesticides, phthalates, PCBs, solvents, toxic waste sites, air pollutants, and heavy metals were implicated in autism, with the strongest evidence found for air pollutants and pesticides (Rossignol et al. 2014). An increase in Parkinson disease has been associated with
pesticides (organophsphates, rotenone), herbicides (paraquat), organic solvents, and heavy metals (Manganese, copper, lead plus iron, and solvents (Goldman et al. 2010).
Obesity
Exposure to toxic chemicals may damage many of the natural weight control mechanisms (Baillie-Hamilton 2002) such as altering homeostatic set points, disrupting appetite controls, perturbing lipid homeostasis and stimulating adipogenic pathways (Grun 2010). Possible obesogens include
- Pesticidesandherbicides,
- phthalates(plasticizers),
- bisphenol A (BPA a plasticizer), chemicals indetergents,
- Perflourooctanoicacid(PFOA):nonstickwaterrepellants
- –Perfluorooctanoicacid(PFOA):nonstick;water-
repellants
- Polybrominateddiphenylethers(PBDEs):flame retardants
- Highfructosecornsyrup
- Ingredientsindetergents
SPECIFIC TOXINS
Persistent Organic Pollutants (POPs):
are substances that persist in the environment. They have high lipid solubility and accumulate in the fatty tissues for long periods of time. Hence, they can accumulate in fatty tissues through the food chain. As one moves up the food chain, the accumulation increases (Kelly et al. 2007). Fat stored POPs and impair detoxification (acting as CYP450 phase I enzyme inducers). At low levels they are associated with endocrine disruption, mitochondrial dysfunction, insulin resistance, neurotoxicity, immunotoxicity, liver toxicity, and genotoxicity. POPs include dioxin pesticides, and materials in flame retardants
Pesticides
Over one billion pounds of pesticides are produced annually in US. There are over 350 di erent pesticide
ingredients. Only a small fraction of pesticides reach the intended pests. The scientist who developed DDT won the 1948 Nobel Prize for Medicine, Dr. Paul Mueller of Switzerland. Although DDT was made illegal in the US in 1973, this writer was involved in shipping DDT to India in 1979 as part of the USAID development program. DDT is also shipped to Mexico for use on the produce they ship to the US. DDT is associated with an earlier age at menarche and increased risk of experiencing a shortened menstrual cycle (Ouyang et al. 2005).
The produce with the highest amount of pesticides are strawberries, bell peppers, spinach, cherries, peaches, cantaloupe, celery, apples, apricots, green beans, grapes and
Cucumbers. Strawberries are covered with plastic and repeatedly saturated with fumigants (methyl bromide) to kill weeds and soil microbes. In 2004 over 7 million pounds of methyl bromide were applied to fields.
Side e ects of methyl bromide include headaches, myalgia, blurred vision, nausea, dysequlibrium, lung damage, kidney damage, and CNS damage.
Atrozine is most widely used weed killer for corn, grains, citrus fruits and sugar cane. It lowers testosterone and increases aromatase increasing estrogen. It causes a decrease in fertility and neural damage for embryonic exposure (Environ Health Perspect online, Jan 24, 2006)
Organophosphates increase oxidative stress and inhibit acetylcholinesterase activity (Bayrami et al. 2012). Organophosphate pesticides have been associated with higher rates of ADHD (Chopra et al. 2014), anxiety, insomnia, depression, hyperglycemia (Malekirad et al 2013), and metabolic syndrome (Park S-K et al. 2010). Organophosphate pesticides exposure at levels common in the US may contribute to the prevalence of ADHD. The higher the exposure, the higher the odds of ADHD (Bouchard MF et al. 2010). Dioxin concentration associated with breast cancer incidence in women (Wamer et al. 2002). Perchorate adversely a ects thyroid function in women (Blount et al. 2006).
The United Nations Environment Programme decided that POP regulation needed to be addressed globally for the further. The US signed this treaty but as of 2014 had not yet ratified it. (Stockholm Convention on Persistent Organic Pollutants, pp 1-43).
Glyphosate
Glyphosate (used in Roundup) accumulates in the genetically modified plants we eat. It may chelate manganese and suppress the enzymes involved in detoxification. This may substantially explain the increase in autism, Alzheimer’s disease, Parkinson’s Disease, anxiety, osteoporosis, thyroid dysfunction and infertility which has increased since the introduction of glyphosate(Samsel, Sene , 2015).
Glyphosate disrupts gut bacteria and suppresses cYP450 by interfering with the detoxification of toxins. Glyphosate enhances the damaging e ects of other food borne chemical residues and environmental toxins. It interferes with the detoxification (CYP) enzymes and synergistically acts with the disruption of the biosynthesis of aromatic amino acids by gut bacteria. It impairs serum sulfate transport. (Samsel , Sene 2013). Glyphosate and other herbicides have been found to increase incidence of non-Hodgkin lymphoma (Hardell, Eriksson 1999).
Bisphenol A (BPA)
BPA has been used as plasticizer since 1957 despite lack of safety testing. It is used in plastic coatings, can linings (80 % of cans made in US), refrigerator shelving, dental sealants and composites, compact discs and DVDs, electrical insulators, baby bottles, and credit card receipts. It leaches over time becomes unstable. Urinary BPA concentration significantly associated with obesity (Trasande 2012). More than 90 % of people in the US have measurable BPA in their bodies. In 2010 Canada’s department of the environment declared BPA a “toxic substance”.
Phthalates
These plasticizers are commonly added to soap, shampoo and hair spray, water bottles, microwave containers, frozen food pouches, cling wrap, flexible plastic products, nail polish products, floor tiles,
enteric medication coatings, synthetic leathers, medical devices (IV and ET tubing), and children’s toys, pacifiers, and baby bottle nipples. Phthalates are readily released to environment, and can enter body through ingestion or inhalation. They have endocrine disrupting e ects linked to cancer, obesity, type II diabetes, allergies/ asthma, ADHD, birth defects. They have been linked to asthma in children (Bomehag et al. 2004).
Perfluoro-octanoic acid (PFOA)
PFC (perfluoro chemicals) used in nonstick cookware, water repellants and stain resistant fabrics. PFOA distributes to serum liver, and kidneys. It is not stored in adipose tissue and
not metabolized in body so the body repeatedly recirculates it through enterohepatic recirculation. It is an endocrine disruptor; has immunotoxic and hepatotoxic properties; increases lipid levels and the risk of strokes Animal studies linked to PFOA exposure to cancer of the liver, pancreas, prostate, and testicles. http://www.epa.gov/oppt/pfoa/pubs/pfoarisk.html Am J Gastroenterol. 2010 Jun;105(6):1354-63. Epub 2009 Dec 15. Toxicol Sci. 2007; 98(2):571-81
Toxicol Sci. 2006; 92(2):476–489
fluorototelomeres (PFOA precursors)
are found in microwaveable popcorn bags, fast food packaging, paper plates, candy wrappers, stain resistant fabrics, leather, dental floss, denture cleaners, shampoo, fire fighting foam, electrical insulation. These are very resistant to biodegradation and will persist long after they are banned. They are
found in the blood of 90 % of Americans and 96 % of the blood samples of children.
Electromagnetic Fields (EMF)
EMF can cause calcium leakage in the cells by disrupting voltage-gated calcium ion channels and may interfere with vesicle transport of molecules into the cells. Cell phones can alter micro RNA expression the brain (Dasdag S et al. 2015 .
Further calcium loss makes holes in membranes allowing leakage of damaged DNA which may lead to cancer and infertility
EMF exposure may have e ects on the nervous system, cardiovascular system (Liu X et al. 2013). It can cause damage to the blood brain barrier leading to cognitive impairment (Tang et al. 2015). It a ects the fetus’ brain when the mother uses a cell phone during pregnancy (Aldad TS et al. 2012) .
Cell phone and cordless phone use can increase the risk of brain cancer (Hardell, Carlberg 2013; Ostrom QT et al 2015).
Studies report cellphone use can result in genotoxicity, single- and double-strand DNA damage, chromatin condensation, loss of DNA repair capacity in human stem cells, reduction in free- radical scavengers (particularly melatonin), abnormal gene transcription, neurotoxicity, carcinogenicity, damage to sperm morphology and function, e ects on behaviour, and e ects on brain development in the fetus Cellphone exposure has been linked to altered fetal brain development and ADHD-like behaviour in the o spring of pregnant mice.
Heavy metals
Volatile derivatives from metals such as mercury, arsenic, bismuth (Meyer et al. 2008) and non absorbed heavy metals (Breton et al. 2013).disrupt the gut microflora. Metal toxicity cause direct and indirect damage to mitochondria, depletion of glutathione causing free radical generation and increased mitochondrial damage (Pieczenik, Neustadt 2007).
Lead toxicity
Lead toxicity was recorded as early as 6500 BC. The Roman Empire used lead in their plumbing (aqueducts, cooking utensils, wine urns, grape juice vessels, makeup, and sweetening agents. Lead is currently found in batteries, car radiators, ceramic cookware with lead glazes, paint, tin cans, and cosmetics including lipstick. In one study blood levels were 20 % higher for women reporting use of ayurvedic and or traditional Chinese medicine herbs
Ninety five percent of the lead body burden is in the skeleton
Bone lead considered a biomarker of cumulative exposure. Ninety to ninety five percent of the body burden of lead is in the bone which accumulates over the life time. Lead accumulates in regions undergoing the most active calcification during the time of exposure (Aufderheide, Wittmers, 1992).
Lead levels in post menopausal women have been correlated with lower bone density. When bone loss occurs with,osteoporosis lead is also released from bone. Bone mineral density was significantly inversely
related with blood lead level in menopausal women (Lee, Kim 2012).
Lead can disrupt hemoglobin synthesis, damage the blood brain barrier lead to structural changes in the brain, damage mitochondrial membrane structure and damage cardiac conduction pathways. At low levels, bond lead was associated with all-cause and cardiovascular mortality (Weisskopt et al. 2009).
Low levels of lead have adverse e ects (Needelman 2004).
Developing nervous system adversely a ected at levels of less than 10 ug/dL (ATSDR) and is associated with greater impulsivity, irritability attention di culties (Miodovnik, Landrigan 2009), loss of intelligence, disruptive behavior, motor deficits, cognitive dysfunction, memory loss and depression. Lead levels less than 10 ug/dL are inversely associated with children’s IQ scores at 3 & 5 years of age (Canfield 2003). These findings suggest that more U.S. children may be adversely a ected by environmental lead than previously estimatedand there may be no threshold for children and developmental e ects
A lead based paint ban was passed by the League of Nations in 1922. The US declined to adopt this measure.
Mercury
Methylmercury inhibits the electron transport activity and impairs mitochondrial function (Mori et al. 2011; Tonazzi A, Indiveri 2002). The Apo-E4 gene (which is associated with a higher risk of Alzheimer’s disease), is
associated with reduced mercury detoxifying capacity. The Apo E 2 variant greatest mercury detoxifying capacity (Godrey et al. 2003).
Arsenic
Arsenic is associated with an increased risk of diabetes mellitus , hypertension, ischemic heart disease, and cerebral infarction (Wang C-H et al. 2002).
Wang C-H et al. Biological gradient between long- term arsenic exposure and carotid atherosclerosis. Circulation. 2002 205:1804-1809.
PRECAUTIONARY PRINCIPLEWhen an activity raises the possibility of harm to human
health or the environment, precautionary measures should be taken even if some cause and e ect relationships are not fully established scientifically. The proponent of a proposed chemical should bear the burden of proof of the chemical’s safety rather than testing the chemical on the public before the adverse e ects of the proposed chemical are known.
In this context the proponent of an toxin, rather than the public, should bear the burden of proof.”
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