Toxicological and Environmental Research

Charlton, NY, United States

Toxicological and Environmental Research

Charlton, NY, United States

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Zeliger H.I.,Toxicological and Environmental Research | Pan Y.,Environmental Health Center Dallas | Rea W.J.,Environmental Health Center Dallas
Interdisciplinary Toxicology | Year: 2012

The exhaled breath of more than four hundred patients who presented at the Environmental Health Center - Dallas with chemical sensitivity conditions were analyzed for the relative abundance of their breath chemical composition by gas chromatography and mass spectrometry for volatile and semi-volatile organic compounds. All presenting patients had no fewer than four and as many as eight co-morbid conditions. Surprisingly, almost all the exhaled breath analyses showed the presence of a preponderance of lipophilic aliphatic and aromatic hydrocarbons. The hydrophilic compounds present were almost entirely of natural origin, i.e. expected metabolites of foods. The lipophile, primarily C3 to C16 hydrocarbons and believed to have come from inhalation of polluted air, were, in all cases, present at concentrations far below those known to be toxic to humans, but caused sensitivity and signs of chemical overload. The co-morbid health effects observed are believed to be caused by the sequential absorption of lipophilic and hydrophilic chemicals; an initial absorption and retention of lipophile followed by a subsequent absorption of hydrophilic species facilitated by the retained lipophile to produce chemical mixtures that are toxic at very low levels. It is hypothesized that co-morbid conditions in chemically sensitive individuals can be predicted from analysis of their exhaled breath. Copyright © 2012 SETOX & IEPT, SASc.


Zeliger H.I.,Toxicological and Environmental Research
Reviews on Environmental Health | Year: 2013

The prevalence of type 2 diabetes (T2D) is increasing worldwide in pandemic-like numbers. It is considered, at least in part, to be an environmental illness. Recent research has shown that diabetes can be caused by exposure to persistent organic pollutants (POPs), exudates from common plastics, air pollution, primary and secondary tobacco smoke, and some pharmaceuticals. These chemicals vary widely in structure, chemical properties, and composition and are not currently believed to induce a similar effect. A unifying explanation for the induction of T2D by this diversified group of chemicals is proposed here. These toxicants have one thing in common. All are lipophilic species that permeate lipophilic body membranes, thereby promoting the absorption of toxic hydrophilic species that would otherwise not penetrate lipophilic membranes. It is further proposed that exposure to the lipophilic and hydrophilic species need not occur simultaneously but can occur sequentially, with the lipophile absorbed first and retained in body serum, followed by a subsequent exposure to the hydrophile. The lipophilic chemical can be one of the POPs (including dioxins, furans, polychlorinated biphenyls, polybrominated biphenyls, polybrominated diphenyl ethers, or organochlorine pesticides); a more rapidly metabolized or eliminated species including plastic exudates like phthalate esters and bisphenol A; air pollutants and tobacco smoke components including aliphatic, aromatic, or polynuclear aromatic hydrocarbons; or pharmaceuticals like some statins and second-generation antipsychotic drugs. This hypothesis suggests that the T2D pandemic as well as the rapid increase of other environmental disease prevalence is, at least in part, due to sequential exposure to levels of lipophilic and hydrophilic environmental pollutants that are much lower than those currently believed to be toxic. As a consequence of this hypothesis, the allowable levels of exposure to these pollutants should be dramatically lowered.


Zeliger H.I.,Toxicological and Environmental Research
Interdisciplinary Toxicology | Year: 2013

Many studies have associated environmental exposure to chemicals with neurological impairments (NIs) including neuropathies, cognitive, motor and sensory impairments; neurodevelopmental disorders (NDDs) including autism and attention deficit hyperactivity disorder (ADHD); neurodegenerative diseases (NDGs) including Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis (ALS). The environmental chemicals shown to induce all these diseases include persistent organic pollutants (POPs), the plastic exudates bisphenol A and phthalates, low molecular weight hydrocarbons (LMWHCs) and polynuclear aromatic hydrocarbons (PAHs). It is reported here that though these chemicals differ widely in their chemical properties, reactivities and known points of attack in humans, a common link does exist between them. All are lipophilic species found in serum and they promote the sequential absorption of otherwise non-absorbed toxic hydrophilic species causing these diseases. Copyright © 2013 SETOX & IEPT, SASc.


Zeliger H.I.,Toxicological and Environmental Research
Interdisciplinary Toxicology | Year: 2013

Environmental chemical exposure has been linked to numerous diseases in humans. These diseases include cancers; neurological and neurodegenerative diseases; metabolic disorders including type 2 diabetes, metabolic syndrome and obesity; reproductive and developmental disorders; and endocrine disorders. Many studies have associated the link between exposures to environmental chemicals and cardiovascular disease (CVD). These chemicals include persistent organic pollutants (POPs); the plastic exudates bisphenol A and phthalates; low molecular weight hydrocarbons (LMWHCs); and poly nuclear aromatic hydrocarbons (PAHs). Here it is reported that though the chemicals reported on differ widely in chemical properties and known points of attack in humans, a common link exists between them. All are lipophilic species that are found in serum. Environmentally induced CVD is related to total lipophilic chemical load in the blood. Lipophiles serve to promote the absorption of otherwise not absorbed toxic hydrophilic species that promote CVD. Copyright © 2013 SETOX & IEPT, SASc.


PubMed | Toxicological and Environmental Research
Type: Journal Article | Journal: Interdisciplinary toxicology | Year: 2013

Environmental chemical exposure has been linked to numerous diseases in humans. These diseases include cancers; neurological and neurodegenerative diseases; metabolic disorders including type 2 diabetes, metabolic syndrome and obesity; reproductive and developmental disorders; and endocrine disorders. Many studies have associated the link between exposures to environmental chemicals and cardiovascular disease (CVD). These chemicals include persistent organic pollutants (POPs); the plastic exudates bisphenol A and phthalates; low molecular weight hydrocarbons (LMWHCs); and poly nuclear aromatic hydrocarbons (PAHs). Here it is reported that though the chemicals reported on differ widely in chemical properties and known points of attack in humans, a common link exists between them. All are lipophilic species that are found in serum. Environmentally induced CVD is related to total lipophilic chemical load in the blood. Lipophiles serve to promote the absorption of otherwise not absorbed toxic hydrophilic species that promote CVD.


PubMed | Toxicological and Environmental Research
Type: Journal Article | Journal: Reviews on environmental health | Year: 2013

The prevalence of type 2 diabetes (T2D) is increasing worldwide in pandemic-like numbers. It is considered, at least in part, to be an environmental illness. Recent research has shown that diabetes can be caused by exposure to persistent organic pollutants (POPs), exudates from common plastics, air pollution, primary and secondary tobacco smoke, and some pharmaceuticals. These chemicals vary widely in structure, chemical properties, and composition and are not currently believed to induce a similar effect. A unifying explanation for the induction of T2D by this diversified group of chemicals is proposed here. These toxicants have one thing in common. All are lipophilic species that permeate lipophilic body membranes, thereby promoting the absorption of toxic hydrophilic species that would otherwise not penetrate lipophilic membranes. It is further proposed that exposure to the lipophilic and hydrophilic species need not occur simultaneously but can occur sequentially, with the lipophile absorbed first and retained in body serum, followed by a subsequent exposure to the hydrophile. The lipophilic chemical can be one of the POPs (including dioxins, furans, polychlorinated biphenyls, polybrominated biphenyls, polybrominated diphenyl ethers, or organochlorine pesticides); a more rapidly metabolized or eliminated species including plastic exudates like phthalate esters and bisphenol A; air pollutants and tobacco smoke components including aliphatic, aromatic, or polynuclear aromatic hydrocarbons; or pharmaceuticals like some statins and second-generation antipsychotic drugs. This hypothesis suggests that the T2D pandemic as well as the rapid increase of other environmental disease prevalence is, at least in part, due to sequential exposure to levels of lipophilic and hydrophilic environmental pollutants that are much lower than those currently believed to be toxic. As a consequence of this hypothesis, the allowable levels of exposure to these pollutants should be dramatically lowered.

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