The document discusses the neurological and psychological symptoms of mercury poisoning from dental fillings based on numerous medical references. It details how chronic low-level exposure to mercury vapor from "silver" fillings can cause a wide range of nonspecific symptoms like fatigue, anxiety, mood issues, cognitive difficulties and more. Standard toxicology and medical references confirm that long-term mercury exposure can gradually induce neurological and psychiatric effects that are difficult to diagnose due to their variable nature.
This presentation is an overview of Mercury group of remedies in Homoeopathy. An attempt to explain this group according to different authors for convinience of scholars.
This document provides information on mercury poisoning, including its physical appearance, types, uses, sources of contamination, toxic dose, clinical features of acute and chronic poisoning, diagnosis, and treatment. It describes two types of mercury - mercuric and mercurous. Clinical features of acute poisoning include tremors, gastrointestinal issues, and renal failure from inhalation, ingestion, or injection. Chronic poisoning can cause neurological and psychiatric symptoms as well as kidney damage. Diagnosis involves tests of urine, blood, hair and imaging. Treatment consists of chelation therapy, supportive measures, and removal of any injected mercury.
This document discusses mercury poisoning from both acute and chronic exposure. It covers the various forms of mercury including elemental, inorganic, and organic mercury. Acute mercury poisoning can occur from ingestion, inhalation, or injection and causes symptoms affecting the gastrointestinal, renal, cardiovascular, and central nervous systems. Chronic mercury poisoning results from long term, low dose exposure and is characterized by tremors, neuropsychiatric effects, and gingival changes. Diagnosis involves measuring mercury levels in blood and hair. Chelating agents are used to treat mercury poisoning by enhancing renal excretion of the mercury-chelator complex.
It is heavy metal and bright silvery in appearance.It is liquid and is non poisonous if swallowed. However, it volatilizes at room temp and inhalation of vapors is toxic. It gets widely distributed throughout the body and causes toxic damage to brain, kidney, peripheral nervous system, mucous membranes etc
There are three forms of mercury poisoning: elemental, inorganic, and organic. Elemental mercury is found in thermometers and can volatilize easily. Inorganic mercury is found in traditional medicines and gold mining, while organic mercury is used in fungicides and pesticides. Mercury is highly absorbed through inhalation, ingestion, and dermal contact. Symptoms depend on the specific form and can include gastrointestinal, neurological, and renal effects. Diagnosis is made through blood and urine mercury levels. Chelation therapy with DMPS is the treatment of choice. Tetraethyllead poisoning occurs mainly through inhalation and causes ocular, dermal, and systemic effects ranging from mild to severe.
Mercury is a liquid metal that is highly toxic, especially in its vaporized form and when ingested as certain mercury compounds. The document discusses mercury's properties and various forms, how mercury poisoning affects the body and can cause damage to organs like the kidneys and brain, symptoms of both acute and chronic mercury toxicity, treatment options, and postmortem findings related to mercury poisoning.
The document discusses a case of 17 employees experiencing mercury poisoning from inhaling elemental mercury vapor released in a pharmaceutical factory laboratory. Their symptoms included sore throat, dizziness, and metallic taste. Treatment involved observation and symptomatic care; all patients recovered without complications. The document also provides background on the various forms of mercury, sources of exposure, toxic effects on organ systems, and challenges in diagnosing mercury poisoning due to nonspecific symptoms. Pregnant women are considered a high-risk group.
Mercury poisoning is caused by exposure to mercury or its compounds and can damage the brain, kidneys, and lungs. Symptoms include neurological and skin abnormalities. Mercury fillings can release vapor over time, exposing the patient. Removing fillings with drills creates particles that are inhaled and the mercury absorbed. Chelation therapy uses chelating agents like DMSA to bond to and remove heavy metals like mercury from the bloodstream to aid excretion and treat poisoning. However, chelation therapy also carries side effect risks like allergic reactions and organ damage in rare cases.
This presentation is an overview of Mercury group of remedies in Homoeopathy. An attempt to explain this group according to different authors for convinience of scholars.
This document provides information on mercury poisoning, including its physical appearance, types, uses, sources of contamination, toxic dose, clinical features of acute and chronic poisoning, diagnosis, and treatment. It describes two types of mercury - mercuric and mercurous. Clinical features of acute poisoning include tremors, gastrointestinal issues, and renal failure from inhalation, ingestion, or injection. Chronic poisoning can cause neurological and psychiatric symptoms as well as kidney damage. Diagnosis involves tests of urine, blood, hair and imaging. Treatment consists of chelation therapy, supportive measures, and removal of any injected mercury.
This document discusses mercury poisoning from both acute and chronic exposure. It covers the various forms of mercury including elemental, inorganic, and organic mercury. Acute mercury poisoning can occur from ingestion, inhalation, or injection and causes symptoms affecting the gastrointestinal, renal, cardiovascular, and central nervous systems. Chronic mercury poisoning results from long term, low dose exposure and is characterized by tremors, neuropsychiatric effects, and gingival changes. Diagnosis involves measuring mercury levels in blood and hair. Chelating agents are used to treat mercury poisoning by enhancing renal excretion of the mercury-chelator complex.
It is heavy metal and bright silvery in appearance.It is liquid and is non poisonous if swallowed. However, it volatilizes at room temp and inhalation of vapors is toxic. It gets widely distributed throughout the body and causes toxic damage to brain, kidney, peripheral nervous system, mucous membranes etc
There are three forms of mercury poisoning: elemental, inorganic, and organic. Elemental mercury is found in thermometers and can volatilize easily. Inorganic mercury is found in traditional medicines and gold mining, while organic mercury is used in fungicides and pesticides. Mercury is highly absorbed through inhalation, ingestion, and dermal contact. Symptoms depend on the specific form and can include gastrointestinal, neurological, and renal effects. Diagnosis is made through blood and urine mercury levels. Chelation therapy with DMPS is the treatment of choice. Tetraethyllead poisoning occurs mainly through inhalation and causes ocular, dermal, and systemic effects ranging from mild to severe.
Mercury is a liquid metal that is highly toxic, especially in its vaporized form and when ingested as certain mercury compounds. The document discusses mercury's properties and various forms, how mercury poisoning affects the body and can cause damage to organs like the kidneys and brain, symptoms of both acute and chronic mercury toxicity, treatment options, and postmortem findings related to mercury poisoning.
The document discusses a case of 17 employees experiencing mercury poisoning from inhaling elemental mercury vapor released in a pharmaceutical factory laboratory. Their symptoms included sore throat, dizziness, and metallic taste. Treatment involved observation and symptomatic care; all patients recovered without complications. The document also provides background on the various forms of mercury, sources of exposure, toxic effects on organ systems, and challenges in diagnosing mercury poisoning due to nonspecific symptoms. Pregnant women are considered a high-risk group.
Mercury poisoning is caused by exposure to mercury or its compounds and can damage the brain, kidneys, and lungs. Symptoms include neurological and skin abnormalities. Mercury fillings can release vapor over time, exposing the patient. Removing fillings with drills creates particles that are inhaled and the mercury absorbed. Chelation therapy uses chelating agents like DMSA to bond to and remove heavy metals like mercury from the bloodstream to aid excretion and treat poisoning. However, chelation therapy also carries side effect risks like allergic reactions and organ damage in rare cases.
The document discusses mercury, its sources and effects on human health. Mercury occurs naturally and is released into the environment through volcanic activity, coal burning and mining. It can accumulate in fish and shellfish consumed by humans. Exposure to mercury, even in small amounts, can harm the nervous, digestive and immune systems. Methylmercury exposure from eating contaminated fish poses the greatest health risk. Preventive measures include promoting cleaner energy to reduce coal burning and phasing out non-essential mercury-containing products.
This document discusses mercury toxicity. It begins by defining the three forms of mercury - elemental, organic, and inorganic. It then discusses the physical and chemical properties of mercury, sources of mercury exposure, epidemiology of mercury poisoning internationally and factors affecting toxicity. The document outlines signs and symptoms, toxicokinetics, mechanisms of toxicity including oxidative stress and epigenetic effects. It discusses methods of diagnosis and treatment for mercury intoxication which involves supportive care and chelation therapy.
Mercury is a liquid metal that can cause toxicity when exposure occurs through contaminated fish, dental fillings, thermometers or industrial discharges. Acute exposure to mercury vapor or ingestion of mercury salts can damage the lungs, kidneys and gastrointestinal tract. Chronic low-level exposure is associated with tremors, mood changes and tooth problems. High prenatal exposures are linked to developmental delays. Chelation therapies like succimer can help remove mercury from the body after exposure. Preventing fish consumption and workplace exposures can help reduce mercury toxicity risks.
This document summarizes information on arsenic and lead poisoning. It discusses the sources, physical properties, uses, and toxic effects of arsenic and lead. For both poisons, it describes the absorption, distribution, and mechanisms of toxicity. The clinical manifestations of acute and chronic poisoning are outlined for each element. Diagnosis involves measuring levels in blood and urine. Treatment of arsenic poisoning involves chelation therapy with BAL, penicillamine or DMSA. For severe lead poisoning, chelation with CaNa2EDTA or BAL is recommended along with supportive care. Mild to moderate lead poisoning is treated with oral chelation agents like D-penicillamine.
Lead toxicity can result from both acute and chronic exposure through various routes. Lead is slowly absorbed and distributed throughout the body, with the highest concentrations accumulating in bone and teeth. It can cause damage to multiple organ systems including the nervous, hematopoietic, cardiovascular, and renal systems. Symptoms range from abdominal pain and headaches with low levels of exposure to potentially fatal lead encephalopathy with very high exposure. Treatment involves removing the source of exposure, chelation therapy, and supportive care. Prevention focuses on maintaining low blood lead levels, especially in high-risk groups like children and pregnant women.
Arsenic poisoning can occur through ingestion, inhalation, or skin absorption of arsenic compounds. Acute arsenic poisoning causes gastrointestinal symptoms like vomiting and diarrhea, while chronic exposure can lead to skin lesions, peripheral vascular disease, and cancer. Diagnosis is made through laboratory tests of urine, blood, hair, nails, and tissue samples, which detect elevated arsenic levels. Treatment for acute poisoning involves gastric lavage, administration of chelating agents like BAL, and supportive care, while chronic cases require removing the source of exposure and long-term chelation therapy along with symptom management. Autopsy findings may show inflammation of the gastrointestinal tract and liver congestion in acute deaths.
This document discusses thallium, a soft, heavy metal that is toxic to humans. It provides details on:
1. Thallium's physical properties and common industrial and medical uses such as in rodenticides and depilatory creams.
2. How thallium is absorbed in the body, replaces potassium in enzymes, and damages cells, especially the nervous system.
3. Signs and symptoms of acute thallium poisoning including gastrointestinal issues, neuropathy, alopecia, and potentially death.
4. Diagnosis of thallium poisoning through monitoring levels in blood, urine, and hair. Treatment involves decontamination and chelation therapies to remove thallium from the
Lead is a toxic heavy metal that can cause lead poisoning through various sources like automobile exhaust, lead-based paints, contaminated food/water, and occupational exposures. Acute lead poisoning presents with abdominal colic, constipation, and in severe cases, encephalopathy and death. Chronic lead poisoning results in anemia, Burton lines on gums, wrist or foot drop, and potentially kidney and brain damage. Treatment involves chelation therapy with agents like BAL, EDTA, DMSA or penicillamine to remove lead from the body.
Mercury poisoning can occur from exposure to elemental, inorganic, and organic mercury. Elemental mercury exposure is usually from inhalation and causes respiratory and neurological symptoms. Inorganic mercury ingestion can cause gastrointestinal and kidney damage. Organic mercury exposure primarily from contaminated seafood causes delayed neurological effects like tremors and ataxia. Diagnosis is made through blood, urine, hair, and clinical exams. Chelation therapy with BAL or DMSA may be used for significant exposures. Public education is important to prevent mercury exposure and proper disposal.
This document discusses various types of non-metallic poisons, including their sources, mechanisms of action, symptoms, diagnosis, and treatment. It covers carbon monoxide, cyanide, methanol, ethylene glycol, acetaminophen, vitamins A, C, and D, niacin, chlorinated hydrocarbon insecticides, organophosphorus insecticides, and environmental pollutants. For each poison, it provides brief details about how it works and affects the body as well as approaches for addressing poisoning.
Arsenic toxicity in animals can occur through ingestion, inhalation, or dermal exposure. The document discusses the sources, clinical signs, post-mortem findings, diagnosis, and treatment of arsenic poisoning in various animal species. It provides lethal dose information for different animals and details the mechanisms of toxicity, which involve inhibition of enzymatic reactions through binding to sulfhydryl groups. Distribution is widespread in the body with high concentrations in the liver, kidneys, and other organs.
Arsenic is a toxic metallic element that can cause poisoning through various routes of exposure. It acts by binding to sulfhydryl groups in enzymes and proteins, interfering with oxidative phosphorylation and other metabolic pathways. Acute arsenic poisoning presents with gastrointestinal symptoms, hemolysis, renal failure, and shock. Chronic arsenic poisoning can result in skin lesions, cancers, and neurological effects. Diagnosis involves blood, urine, hair, and imaging tests to detect arsenic levels. Treatment focuses on supportive care and chelation therapy to remove arsenic from the body.
Mercury is a liquid metal that can be toxic in high amounts. It occurs naturally and is used in things like dental fillings and thermometers. Chronic mercury poisoning can cause psychological, digestive, neurological, and other health problems. Diagnosis involves testing urine levels. Treatment focuses on removing mercury exposure sources and chelation therapy. While mercury fillings are generally considered safe, some report health issues from dental amalgam and prefer removal and detoxification. More research continues on any potential effects, especially for young children.
A presentation on Arsenic Poisoning, from a brief history, compounds, uses, circumstances of poisoning, types with clinical symptoms, diagnosis, treatment and postmortem findings. Subject from Forensic Medicine and Toxicology.
#arsenicpoisoning #arsenic
Lead poisoning is caused by ingesting or inhaling lead from sources like contaminated paint, dust, soil, or water. It can be prevented by drinking purified water and avoiding lead-based materials. Symptoms include vision problems, lack of motor skills, weight loss, abdominal pain, and fatigue. Lead poisoning occurs worldwide.
Arsenic poisoning results from ingesting arsenic, which may be present in items like laundry products, tobacco smoke, bone meal, kelp, beer, salt, seafood, or untreated water. Drinking purified water can help prevent it. Symptoms are stomach aches, nausea, vomiting, diarrhea, skin damage, and vision issues. Arsenic poisoning is mainly found in developing countries with limited
Mercury is a heavy metal that occurs naturally and can be toxic to humans. It exists in elemental, inorganic, and organic forms, with organic mercury posing the greatest risk. Sources of mercury exposure include mining, fossil fuel combustion, industrial manufacturing, and consumption of contaminated fish. Mercury poisoning can cause neurological, kidney, and developmental issues. Symptoms range from rashes and irritability to tremors, impaired vision and hearing, and Minamata disease.
This document discusses lead poisoning, its sources, uses, health effects, diagnosis, and treatment. It provides information on:
1. Common sources of lead exposure including paint, petrol, household dust, batteries, ceramics, etc.
2. Compounds containing lead like lead acetate, lead tetraoxide, and their uses.
3. How lead is absorbed in the body, stored in bones and tissues, and its toxic effects on organs like the brain and kidneys.
4. Symptoms of lead poisoning in children and adults.
5. Tests to diagnose lead poisoning through blood, urine, and bone tests.
6. Chelation therapies used to treat lead poisoning by removing
The Coalition of Mercury-Safe Dentistry aims to end the use of dental mercury amalgam fillings and educate dental professionals and patients about their removal. The coalition seeks to assist those in the dental field and patients in understanding the health risks of mercury from dental fillings. Several organizations agree that the risks of illness from mercury in dental fillings pose unreasonable dangers to patient and dental staff health.
This document discusses developmental neurotoxicity and the vulnerability of the developing brain. It covers several key points:
- The brain is particularly vulnerable to injury during development due to an immature blood-brain barrier, increased chemical absorption, and critical windows of development.
- Common neurotoxicants include heavy metals like lead and mercury, which can cause issues like reduced IQ and impaired learning from early life exposures.
- Lead toxicity is associated with effects on calcium channels and glutamate signaling, while mercury primarily affects the brain and nervous system after accumulating in fish.
- Other topics covered include the blood-brain barrier, causes of neurotoxicity, types of neuropathology like neuropathies and axonopath
The document discusses mercury, its sources and effects on human health. Mercury occurs naturally and is released into the environment through volcanic activity, coal burning and mining. It can accumulate in fish and shellfish consumed by humans. Exposure to mercury, even in small amounts, can harm the nervous, digestive and immune systems. Methylmercury exposure from eating contaminated fish poses the greatest health risk. Preventive measures include promoting cleaner energy to reduce coal burning and phasing out non-essential mercury-containing products.
This document discusses mercury toxicity. It begins by defining the three forms of mercury - elemental, organic, and inorganic. It then discusses the physical and chemical properties of mercury, sources of mercury exposure, epidemiology of mercury poisoning internationally and factors affecting toxicity. The document outlines signs and symptoms, toxicokinetics, mechanisms of toxicity including oxidative stress and epigenetic effects. It discusses methods of diagnosis and treatment for mercury intoxication which involves supportive care and chelation therapy.
Mercury is a liquid metal that can cause toxicity when exposure occurs through contaminated fish, dental fillings, thermometers or industrial discharges. Acute exposure to mercury vapor or ingestion of mercury salts can damage the lungs, kidneys and gastrointestinal tract. Chronic low-level exposure is associated with tremors, mood changes and tooth problems. High prenatal exposures are linked to developmental delays. Chelation therapies like succimer can help remove mercury from the body after exposure. Preventing fish consumption and workplace exposures can help reduce mercury toxicity risks.
This document summarizes information on arsenic and lead poisoning. It discusses the sources, physical properties, uses, and toxic effects of arsenic and lead. For both poisons, it describes the absorption, distribution, and mechanisms of toxicity. The clinical manifestations of acute and chronic poisoning are outlined for each element. Diagnosis involves measuring levels in blood and urine. Treatment of arsenic poisoning involves chelation therapy with BAL, penicillamine or DMSA. For severe lead poisoning, chelation with CaNa2EDTA or BAL is recommended along with supportive care. Mild to moderate lead poisoning is treated with oral chelation agents like D-penicillamine.
Lead toxicity can result from both acute and chronic exposure through various routes. Lead is slowly absorbed and distributed throughout the body, with the highest concentrations accumulating in bone and teeth. It can cause damage to multiple organ systems including the nervous, hematopoietic, cardiovascular, and renal systems. Symptoms range from abdominal pain and headaches with low levels of exposure to potentially fatal lead encephalopathy with very high exposure. Treatment involves removing the source of exposure, chelation therapy, and supportive care. Prevention focuses on maintaining low blood lead levels, especially in high-risk groups like children and pregnant women.
Arsenic poisoning can occur through ingestion, inhalation, or skin absorption of arsenic compounds. Acute arsenic poisoning causes gastrointestinal symptoms like vomiting and diarrhea, while chronic exposure can lead to skin lesions, peripheral vascular disease, and cancer. Diagnosis is made through laboratory tests of urine, blood, hair, nails, and tissue samples, which detect elevated arsenic levels. Treatment for acute poisoning involves gastric lavage, administration of chelating agents like BAL, and supportive care, while chronic cases require removing the source of exposure and long-term chelation therapy along with symptom management. Autopsy findings may show inflammation of the gastrointestinal tract and liver congestion in acute deaths.
This document discusses thallium, a soft, heavy metal that is toxic to humans. It provides details on:
1. Thallium's physical properties and common industrial and medical uses such as in rodenticides and depilatory creams.
2. How thallium is absorbed in the body, replaces potassium in enzymes, and damages cells, especially the nervous system.
3. Signs and symptoms of acute thallium poisoning including gastrointestinal issues, neuropathy, alopecia, and potentially death.
4. Diagnosis of thallium poisoning through monitoring levels in blood, urine, and hair. Treatment involves decontamination and chelation therapies to remove thallium from the
Lead is a toxic heavy metal that can cause lead poisoning through various sources like automobile exhaust, lead-based paints, contaminated food/water, and occupational exposures. Acute lead poisoning presents with abdominal colic, constipation, and in severe cases, encephalopathy and death. Chronic lead poisoning results in anemia, Burton lines on gums, wrist or foot drop, and potentially kidney and brain damage. Treatment involves chelation therapy with agents like BAL, EDTA, DMSA or penicillamine to remove lead from the body.
Mercury poisoning can occur from exposure to elemental, inorganic, and organic mercury. Elemental mercury exposure is usually from inhalation and causes respiratory and neurological symptoms. Inorganic mercury ingestion can cause gastrointestinal and kidney damage. Organic mercury exposure primarily from contaminated seafood causes delayed neurological effects like tremors and ataxia. Diagnosis is made through blood, urine, hair, and clinical exams. Chelation therapy with BAL or DMSA may be used for significant exposures. Public education is important to prevent mercury exposure and proper disposal.
This document discusses various types of non-metallic poisons, including their sources, mechanisms of action, symptoms, diagnosis, and treatment. It covers carbon monoxide, cyanide, methanol, ethylene glycol, acetaminophen, vitamins A, C, and D, niacin, chlorinated hydrocarbon insecticides, organophosphorus insecticides, and environmental pollutants. For each poison, it provides brief details about how it works and affects the body as well as approaches for addressing poisoning.
Arsenic toxicity in animals can occur through ingestion, inhalation, or dermal exposure. The document discusses the sources, clinical signs, post-mortem findings, diagnosis, and treatment of arsenic poisoning in various animal species. It provides lethal dose information for different animals and details the mechanisms of toxicity, which involve inhibition of enzymatic reactions through binding to sulfhydryl groups. Distribution is widespread in the body with high concentrations in the liver, kidneys, and other organs.
Arsenic is a toxic metallic element that can cause poisoning through various routes of exposure. It acts by binding to sulfhydryl groups in enzymes and proteins, interfering with oxidative phosphorylation and other metabolic pathways. Acute arsenic poisoning presents with gastrointestinal symptoms, hemolysis, renal failure, and shock. Chronic arsenic poisoning can result in skin lesions, cancers, and neurological effects. Diagnosis involves blood, urine, hair, and imaging tests to detect arsenic levels. Treatment focuses on supportive care and chelation therapy to remove arsenic from the body.
Mercury is a liquid metal that can be toxic in high amounts. It occurs naturally and is used in things like dental fillings and thermometers. Chronic mercury poisoning can cause psychological, digestive, neurological, and other health problems. Diagnosis involves testing urine levels. Treatment focuses on removing mercury exposure sources and chelation therapy. While mercury fillings are generally considered safe, some report health issues from dental amalgam and prefer removal and detoxification. More research continues on any potential effects, especially for young children.
A presentation on Arsenic Poisoning, from a brief history, compounds, uses, circumstances of poisoning, types with clinical symptoms, diagnosis, treatment and postmortem findings. Subject from Forensic Medicine and Toxicology.
#arsenicpoisoning #arsenic
Lead poisoning is caused by ingesting or inhaling lead from sources like contaminated paint, dust, soil, or water. It can be prevented by drinking purified water and avoiding lead-based materials. Symptoms include vision problems, lack of motor skills, weight loss, abdominal pain, and fatigue. Lead poisoning occurs worldwide.
Arsenic poisoning results from ingesting arsenic, which may be present in items like laundry products, tobacco smoke, bone meal, kelp, beer, salt, seafood, or untreated water. Drinking purified water can help prevent it. Symptoms are stomach aches, nausea, vomiting, diarrhea, skin damage, and vision issues. Arsenic poisoning is mainly found in developing countries with limited
Mercury is a heavy metal that occurs naturally and can be toxic to humans. It exists in elemental, inorganic, and organic forms, with organic mercury posing the greatest risk. Sources of mercury exposure include mining, fossil fuel combustion, industrial manufacturing, and consumption of contaminated fish. Mercury poisoning can cause neurological, kidney, and developmental issues. Symptoms range from rashes and irritability to tremors, impaired vision and hearing, and Minamata disease.
This document discusses lead poisoning, its sources, uses, health effects, diagnosis, and treatment. It provides information on:
1. Common sources of lead exposure including paint, petrol, household dust, batteries, ceramics, etc.
2. Compounds containing lead like lead acetate, lead tetraoxide, and their uses.
3. How lead is absorbed in the body, stored in bones and tissues, and its toxic effects on organs like the brain and kidneys.
4. Symptoms of lead poisoning in children and adults.
5. Tests to diagnose lead poisoning through blood, urine, and bone tests.
6. Chelation therapies used to treat lead poisoning by removing
The Coalition of Mercury-Safe Dentistry aims to end the use of dental mercury amalgam fillings and educate dental professionals and patients about their removal. The coalition seeks to assist those in the dental field and patients in understanding the health risks of mercury from dental fillings. Several organizations agree that the risks of illness from mercury in dental fillings pose unreasonable dangers to patient and dental staff health.
This document discusses developmental neurotoxicity and the vulnerability of the developing brain. It covers several key points:
- The brain is particularly vulnerable to injury during development due to an immature blood-brain barrier, increased chemical absorption, and critical windows of development.
- Common neurotoxicants include heavy metals like lead and mercury, which can cause issues like reduced IQ and impaired learning from early life exposures.
- Lead toxicity is associated with effects on calcium channels and glutamate signaling, while mercury primarily affects the brain and nervous system after accumulating in fish.
- Other topics covered include the blood-brain barrier, causes of neurotoxicity, types of neuropathology like neuropathies and axonopath
How did the idea that a mercury-based preservative (thimerosal) causes autism come to be?
This timeline is the historical account of an unbelievable, but true, story.
It’s the story of parents who knew something was wrong and never gave up. The story of brave scientists who told the scientific truth. And a story of unsung heroes - the child victims whose lives were devastated and forever changed by vaccines.
To the heroes who have sacrificed so much: this timeline is to honor you with the hope that our nation will have a true understanding of your suffering.
This document discusses heavy metals and their effects on human health. It provides background on heavy metals and lists some of the most hazardous ones, including arsenic, lead, mercury, and cadmium. It discusses factors that affect metal toxicity like dose, duration of exposure, and route of exposure. It then goes into more detail on the sources, absorption, distribution, mechanisms of toxicity, symptoms, diagnosis, and regulations for specific metals like lead, mercury, arsenic, cadmium, and others. The document provides a comprehensive overview of several heavy metals and their impacts on the human body.
This document provides an introduction to the field of toxicology. It discusses the history of toxicology, including famous historical poisonings. It describes toxicology as the study of the harmful effects of chemicals on living organisms. The document outlines some key concepts in toxicology including dose-response relationships, types of poisoning, factors affecting toxicity, classification of poisons, routes of administration, diagnosis of poisoning, and medico-legal aspects of toxicology. It provides an overview of the general considerations and approaches in the study of toxicology.
Neurotoxicity, commonly caused by cytotoxic cancer therapy, can damage the central or peripheral nervous system. Ifosfamide chemotherapy can cause central neurotoxicity like encephalopathy or myelopathy. It is metabolized into neurotoxic compounds that damage mitochondria. Methylene blue may help restore mitochondrial function and prevent or treat ifosfamide neurotoxicity. Chemotherapy-induced peripheral neuropathy is a common side effect of neurotoxic drugs like platinum analogs, taxanes, and vinca alkaloids. It involves damage to dorsal root ganglia and axons, disrupting transport and causing length-dependent nerve damage. Symptoms include numbness, tingling and pain in hands and feet. Risk factors include
The document provides a list of over 100 potential symptoms that may be linked to chronic illnesses. It notes that laboratory diagnostics currently have limitations in detecting pathogens in sufferers. The list of symptoms is intended to help sufferers document their condition and progress in relation to therapies by tracking which symptoms they experience. The symptoms cover a wide range of issues including fatigue, pain, cognitive problems, and sensory disturbances.
1. Asthma is a chronic inflammatory disorder of the bronchi characterized by episodic and reversible bronchospasm caused by an exaggerated response to various stimuli like allergens.
2. It affects 10% of children and 5-7% of adults worldwide. The pathogenesis involves inflammation, airflow limitation, and airway hyperresponsiveness triggered by allergens, viruses, pollutants, and other factors.
3. New understanding of the role of leukotrienes, mast cells, eosinophils and cytokines in asthma pathology has led to more targeted drug therapies that inhibit these inflammatory pathways.
This document discusses toxicology and toxidromes. It defines toxicology as the study of poisons and their effects. It describes different areas of toxicology like forensic, environmental and occupational toxicology. It also discusses factors that affect toxic responses and the medicolegal aspects of poisoning cases. Finally, it defines toxidromes as syndromes caused by specific poisons and names some common toxidromes like anticholinergic, sympathormimetic, cholinergic, opioid and benzodiazepine toxidromes, describing the symptoms and causes of each.
This document discusses various uncommon or "zebra" diseases and conditions that may be tested on medical board exams. It covers zebras in several categories including cardiovascular, toxicology, infectious disease, neurology/neurosurgery, OB-GYN, and others. The objectives are for attendees to be able to recognize these zebras on board exams and rule them in or out more quickly and confidently. Various examples of zebras are provided within each specialty category along with their key features and treatments.
1) Asthma is a chronic lung disease characterized by inflammation of the airways and periods of wheezing, chest tightness, and shortness of breath.
2) Risk factors for asthma include family history, allergies, viral infections, obesity, and exposure to environmental factors like cigarette smoke and air pollution.
3) Symptoms of an asthma attack include coughing, wheezing, chest tightness, and shortness of breath. Long term complications if asthma is uncontrolled include reduced lung function, sleep disturbances, limitations to physical activity, and potentially life-threatening asthma attacks.
The document discusses asthma, defining it as a condition where the airways narrow and swell causing breathing difficulties. It outlines the common symptoms of asthma like wheezing, coughing, and shortness of breath. Additionally, it covers the causes, types, pathophysiology, diagnosis, and treatment of asthma.
This document provides an overview of asthma, including its definition, types, pathophysiology, clinical manifestations, diagnostic evaluations, and management. Asthma is a chronic inflammatory disease of the airways characterized by wheezing, breathlessness, chest tightness, and cough. It is caused by a combination of genetic and environmental factors and can be triggered by allergens, infections, pollutants, and other irritants. Diagnosis involves assessing symptoms, performing pulmonary function tests, and ruling out other conditions. Treatment focuses on reducing inflammation and controlling symptoms.
1. Disorders of olfaction can be conductive, resulting from nasal obstruction, or sensorineural, due to damage to the olfactory neuroepithelium.
2. Common causes of sensorineural disorders include upper respiratory infections, head trauma, tumors near the olfactory region, congenital defects, toxins, age-related changes, and neurodegenerative diseases.
3. Specific conditions that can cause olfactory disorders are post-viral olfactory dysfunction, Kallmann syndrome, septo-optic dysplasia, holoprosencephaly, exposure to metals or other toxins, Alzheimer's disease, Parkinson's disease, and epilepsy presenting with olfactory auras.
This document discusses diseases caused by smoking. It begins by explaining how smoking damages DNA and increases risks of cancer, heart disease, and strokes. It then lists 11 ways smoking impacts the body, such as causing lung cancer, respiratory diseases, digestive issues, skin aging, and gum disease. The document provides statistics on passive smoking risks and details treatments using nicotine replacements. It stresses the importance of preventing smoking to avoid chronic illnesses and waste of human potential.
This document discusses diseases caused by smoking. It begins by explaining how smoking damages DNA and increases the risks of cancer, heart disease, and strokes. It then lists several changes in the body caused by smoking, including effects on the lungs, respiratory system, brain, skin, and other organs. Examples of lung diseases from smoking include lung cancer and COPD. The document also provides preventative measures like avoiding secondhand smoke. It describes treatments to quit smoking like nicotine patches and gum. Statistics show that around 30 deaths per day are caused by secondhand smoke. The conclusion emphasizes stamping out smoking is important to reduce disease.
This document discusses states of normal and impaired consciousness, including coma. It describes coma as an extreme state of unresponsiveness where an individual exhibits no voluntary movement or behavior. The document outlines an approach for clinically evaluating a comatose patient, including examining vital signs, skin features, breath odor, and performing a neurological examination to help identify potential underlying causes of coma. It also introduces the Glasgow Coma Scale for assessing the level or depth of impaired consciousness or coma.
Chap 1 General principles involved in the management of poisoningChanukya Vanam . Dr
1. General principles involved in the management of poisoning
2. Antidotes and the clinical applications.
3. Supportive care in clinical Toxicology.
4. Gut Decontamination.
5. Elimination Enhancement.
6. Toxicokinetics.
The document discusses abnormalities of smell and olfactory disorders. It describes the main components of the olfactory system and pathways. Several types of smell disorders are defined, including anosmia, hyposmia, dysosmia, and phantosmia. Causes of smell disturbances include upper respiratory infections, head trauma, nasal/sinus disease, tumours, and neurodegenerative diseases. Clinical evaluation involves a history, smell tests, and physical exam including the nose and sinuses. Treatment depends on whether the impairment is conductive or sensorineural.
This document discusses dyspnea (shortness of breath) and asthma. It begins by defining dyspnea and describing its pathophysiology, which involves a mismatch between afferent signals from lung receptors and efferent motor signals. It then discusses the various causes and categories of dyspnea, including cardiac, pulmonary, cardiac/pulmonary, and non-cardiac/non-pulmonary. The document provides details on differentiating dyspnea through history, physical exam, and investigations. It also discusses types of dyspnea and provides a diagnostic algorithm. Later sections focus on asthma, covering etiology, risk factors, physical exam findings, investigations such as spirometry, and classifications of asthma exacerbations.
Role of antidepressants in allergic rhinitisNada Naeem
This document discusses the connection between allergic rhinitis (AR) and depression. It notes that adolescents with AR are more likely to experience anxiety, depression, and impaired sleep. The mechanisms behind this connection may involve cytokines, sleep disruption, and the emotional toll of chronic symptoms. Treatment options presented include antihistamines, corticosteroids, immunotherapy, and the antidepressant desipramine, which has antihistamine properties and may help treat AR symptoms and depression. More research is still needed to understand the role of antidepressants among other AR treatment options in improving quality of life.
The document discusses allergies, defining them as immune responses to normally harmless substances. It describes common allergen types like pollen, dust, foods and identifies symptoms like sneezing, watery eyes. Allergens are classified by their route of exposure - inhaled, injected, ingested, contacted. Diagnosis involves skin prick or patch tests. Treatment includes avoidance, medications like antihistamines, decongestants, steroids and immunotherapy injections.
The puffer fish contains a powerful toxin called tetrodotoxin that is 10,000 times more lethal than cyanide. It works by blocking sodium channels in nerves, preventing the transmission of electrical signals and causing paralysis. Symptoms of pufferfish poisoning include numbness, weakness, difficulty breathing, and paralysis that can lead to death within 4-6 hours if untreated. While there is no antidote, supportive care focused on the symptoms can allow survivors to fully recover if they make it past the first 24 hours. The toxin is so potent that properly preparing pufferfish is tightly regulated to avoid fatal poisonings from this delicacy in Japan.
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Overview of Mercury Toxicity - Medical Books
1. My Dentist Hurt My Feelings (for Several Decades) a small treatise on the nasty psychological side effects from the mercury vapor emitted from “silver” dental fillings by Stevenson Munro a Fifth Business Production
2. Nineteen fillings by the age of 16. All my life I’ve struggled with being tired, anxious, moody, spacey, forgetful, reclusive and uncoordinated.
3. German Chemist Alfred Stock’s First-Hand Account of Mercury Vapor Poisoning. P. Stortebecker, MD, PhD, Mercury Poisoning from Dental Amalgam – A Hazard to the Human Brain , Bio-Probe, Orlando, FL, 1986 First Stage : Predominantly psychic symptoms. Fatigue. Diminished working capacity. Irritability. Slight swelling of mucous membranes in upper nasal region. Second Stage : Extreme Fatigue. Lack of concentration. Impaired memory for names, numbers, etc. Irritability and moodiness. Sensation of a “sheer stupidity.” Nasal obstruction and dryness, a “stuffed nose”. Nasal discharge, viscous, sticky, sometimes bloody. Ringing in the ears. Hearing impairment. Headache, often frontal. Stomatitis, bleeding gums on tooth-brushing. Irregular heart activity. Sometimes diarrhea. Frequent urination. Slight tremor. Third Stage : Troublesome headache. Dizziness. Vertigo. Tremor. Mental incapacity. Despondency and depression. Back pain. Painful and difficult urination. Colitis with diarrhea. Nasal catarrh, with bloody nasal crusts. Loss of smell. Stomatitis, bleeding gums. Paradentosis, loose teeth. Increased salivation. Pharyngitis and laryngitis, etc. Stock’s worst complaints were his EXTREME FATIGUE and lack of working capacity. I personally experienced all of Alfred Stock's reported symptoms.
4. Metallic mercury has been known since ancient times, as has its capacity for producing illness. The metal is appreciably volatile, so that toxicity results from inhalation exposure of the vapor. Often, the earliest signs of neurotoxicity are personality changes. At first subtle differences in mood and behavior may be noted only by family members or close friends or associates of the affected individual. As exposure continues, behavior may become increasingly neurotic or even psychotic. Pathological shyness or reclusiveness is a characteristic sign, sometimes alternating with exaggerated irritability. Mild sensory loss may appear early, with tingling in toes, fingers, or around the lips. A mild tremor develops, which becomes more severe as exposure continues. Twitching eyelids may appear first, followed by a tremor of the hands. Fine motor control becomes difficult; as evidenced by noticeable changes in handwriting or drawing. Many of these signs and symptoms appeared in hatters using volatile mercury salts for treating felt. Hence the "mad hatter" of Alice in Wonderland may have basis in fact. Reeves, A.L.; Toxicology: Principles and Practice , Vol. 1, 1981, p. 127 Modern toxicology book confirms Stock’s symptom profile for mercury vapor poisoning
5. Standard medical reference confirms toxicity Cecil Textbook of Medicine, 21 st ed., Vol. 1, p. 72 Elemental mercury is a liquid at environmental temperatures but vaporizes with agitation as well as gently heating. Bulk mercury is used in dental amalgams. . . Elemental mercury is readily absorbed from the alveoli; subsequently it can enter the brain. With mild exposure, the manifestations are likely to be subtle and diagnosis is difficult. Insomnia, nervousness, mild tremor, impaired judgment and coordination, decreased mental efficiency, emotional lability, headache, fatigue, loss of sexual drive, and depression are early manifestations and are often mistakenly ascribed to psychogenic causes. Abdominal cramps, dermatitis, and diarrhea may also occur, and the victim may complain of a metallic taste. As the poisoning becomes more severe, persistent involuntary tremors of the extremities are noted. Thereafter, other signs of mercury poisoning may appear, including amblyopia, polyneuropathy, erythroderma, acrodynia, joint pains, swollen gums with a blue line around the teeth, sialorrhea, and paresthesias. The major manifestation of chronic mercury vapor exposure may be kidney damage, including the nephrotic syndrome. Because of the body’s metabolism of mercury, blood and urine levels may be unreliable and clear evidence of poisoning may be documented only after administering drugs that augment mercury excretion in the urine. In most cases, improvement occurs after removal from exposure or treatment with appropriate chelating agents.
6. Not a fluke: another standard medical reference says the same thing . . . Harrison’s Principles of Internal Medicine, 15 th ed., Vol. 2, p. 2593 CLINICAL TOXICOLOGY Inhalation of metallic mercury vapor is the form of mercury exposure that has been best studied in terms of toxicity. High levels of exposure are most likely in an occupational setting in which mercury vapors are generated by heat-induced volatilization of metallic mercury. Cough, dyspnea, and tightness or burning pain in the chest are common symptoms that may be accompanied by diffuse infiltrates or a pneumonitis-like appearance on chest x-ray. Respiratory distress, pulmonary edema, lobar pneumonia, fibrosis, and desquamation of the bronchiolar epithelium can occur in relatively severe cases and have sometimes lead to death. Acute inhalation of mercury vapor can also cause neurologic toxicity manifested by tremors (beginning in the hands), emotional lability, headaches, and polyneuropathy. Chronic exposure to metallic mercury produces a characteristic intention tremor and mercurial erethism , a constellation of findings including excitability, memory loss, insomnia, timidity, and sometimes delirium that was described in workers with occupational exposure in the felt-hat industry – hence the expression “mad as a hatter.” Dentists with occupational exposure to mercury score below normal on neurobehavioral tests of motor speed, visual scanning, verbal and visual memory, and visuomotor coordination. Low-level exposure from dental amalgams may also be associated with adverse immunological reactions with certain major human leukocyte antigen genotypes; further research is needed in this area.
10. Casarett and Doull’s Toxicology: The Basic Science of Poisons , 6 th ed., pp. 834-837
11. Gerstner and Huff, “The Clinical Toxicology of Mercury”in the Journal of Toxicology and Environmental Health 2:491-526, 1977
12. Verity & Sarafian (2000) Mercury and Mercury Compounds. In: Experimental and Clinical Neurotoxicology 2 nd ed. Spencer PS et al., ed. , Oxford University Press, New York / Oxford pp. 763-770, 2000
13. Kark RAP (1994) Clinical and neurochemical aspects of inorganic mercury intoxication. In: Investigations of the Nervous System. Vol. 64. DeWolfe FA ed. Handbook of Clinical Neurology. Vinken PJ, Bruyn GU eds. Elsevier/North Holland, Amsterdam pp. 367- 411
14. “ There have been epidemics of mercury poisoning among wildlife and human populations in many countries. With very few exceptions and for numerous reasons, such outbreaks were misdiagnosed for months or even years . Reasons for these tragic delays included the insidious onset of the affliction, vagueness of early clinical signs, and the medical profession's unfamiliarity with the disease.” Hardman JG, Limbird LE, Eds., GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS , 10th ed., McGraw Hill (2001) So why didn’t any of my doctors ever tell me?
15. Hg0 poisoning is hard to detect, because the symptoms are so variable Continued exposure to moderately high concentrations of mercury vapor in air - which do not trigger the acute pulmonary syndrome - induces classical mercurialism, a chronic intoxication that displays clinical sequelae mainly arising from the central nervous system. Because of its ability to penetrate the blood-brain barrier, elemental mercury slowly accumulates in the most important human organ. Yet, the induced disease does not appear as a typical entity but as a wide spectrum of clinical pictures, ranging from almost imperceptible disturbance to complete incapacitation. Depending on mercury concentration, on length of exposure, and probably on individual sensitivity, manifestations of intoxication emerge insidiously; they gradually progress to various degrees of severity; and they create protean clinical pictures with broad spectrums of signs and symptoms. Gerstner and Huff, “The Clinical Toxicology of Mercury” Journal of Toxicology and Environmental Health 2:491-526, 1977
16. Affect. Mercurialism also manifests itself in an alteration of the emotional state. With an insidious onset, the mood generally swings toward the depressive side. Exposed persons experience feelings of fatigue and listlessness; they lose interest in their surroundings and in their own life; they withdraw more and more from social contacts; they become increasingly irritable and sensitive, reacting strongly to relatively innocent remarks uttered by family or friends; and they have a tendency for sweating and blushing. In this blushing - or reddening - the classical term "erethism“ finds its origin. In very severe cases, the depression may reach suicidal proportions. Or the clinical picture may simulate manic-depressive psychosis with hallucinations and delusions. Mentality . Insidious in onset and difficult to recognize, a deterioration of intelligence gradually emerges during chronic exposure to elemental mercury. Previously bright persons become dull and slow in thinking. They suffer from a progressive decline affecting memory as well as the faculties for logical reasoning and concentration on particular problems. Hg0 poisoning induces a wide range of psychiatric disturbances Gerstner and Huff, “The Clinical Toxicology of Mercury” Journal of Toxicology and Environmental Health 2:491-526, 1977
17. Experts Agree: It’s an Intriguing Neurotoxin. Nothing else even comes close! “ Inhaled mercury vapor produces a range of fascinating and bizarre changes in human behavior from the grotesque to the extremely subtle. Modern psychological tests reveal subtle mood changes and less obvious personality changes. Erethism is a wide spectrum of psychological and personality disturbances. One end of the spectrum involves delirium, hallucinations, excessive shyness, and fits of rage. . . [while] irritability, insomnia, and lassitude may be the lower end of the erethism spectrum. . . No other metal can affect the central nervous system in this way. In fact, it is doubtful that any chemical, even hallucinogenic drugs, can compare with mercury vapor. It is a tantalizing problem to the neuroscientist. What a pity so little effort has been devoted to elucidating the physiological and biochemical mechanisms!” Clarkson, T.W. “Human Toxicology of Mercury” The Journal of Trace Elements in Experimental Medicine 11:303-317 (1998)
18. What is a safe level of vapor? The U.S. Environmental Protection Agency sets a non-occupational “reference air concentration”. In 1996, the RfC was: 0.300 ug Hg0/m3 The U.S. Agency for Toxic Substances and Disease Registry (ATSDR) publishes a “Minimal Risk Level” for non-occupational exposure. In 1999, the MRL for mercury vapor was set at: 0.200 ug Hg0/m3
19. So What’s in Our Mouths? Lichtenberg, H, “Mercury vapor in the oral cavity in relation to the number of amalgam fillings and chronic mercury poisoning” Journal of Orthomolecular Medicine 11:2 1996 pp. 87-94 Range: 3 ug – 195 ug
20. Oops Where’s the FDA? Dental amalgam has never been subjected to safety testing. It’s been “grandfathered in” as safe by the FDA. Where’s the Maine DEP and Department of Health? I have a little story . . . What other pre-Civil War medical devices would you like to be subjected to? The last Quacks: from “quacksilber”, quicksilver, the German word for mercury . . .
21. Like old folks in search of affordable prescription drugs, I went to Canada to search for accurate health information
22. So - I received 16 to 18 fillings too many before I could vote or die in war for my country
23.
24. A SAFE AMOUNT OF POISON ISN’T THE SAME AS A SAFE AMOUNT OF POISON WITH AN ANTIDOTE: 12 out of the 26 study participants were employed in chloralkali plants – thus, they were guaranteed a large margin of protection from mercury vapor exposure. Chlorine gas combines with mercury in the air and precipitates it to the ground. It also combines with mercury in the body, protecting the brain and heart from mercury vapor’s toxic effects. Dental amalgam bearers DON’T have this luxury. The vapor from their fillings goes straight into the blood stream and mercury collects at high levels in their brain.
25. SAFETY LEVELS SHOULD PROTECT THE MOST VULNERABLE: The 26 study participants were “self-selected” employees of mercury-using industries. That is, if they felt rotten in the presence of mercury vapor, then they could quit. Only the “mercury hardy” would stay employed, conceivably, to show up for the study. Amalgam wearers can’t take their fillings out when they feel bad -- they’re stuck with them for life. Even Canada's “safe exposures” are too much. The assumptions used (from Fawer et al., 1983) to determine “safe” levels of mercury vapor exposure are seriously flawed
26. In support of “you-feel-like-shit-before-you-shake” hypothesis: Exhibit A “ Personality changes are the most common findings in chronic mercurial poisoning. In mild cases these may occur with no other signs or symptoms apparent. The psychopathologic effects have been described as erethism, irritability, irascibility, critical excitability, fearfulness, restlessness, insomnia, inability to concentrate, melancholy, depression, shyness, timidity, moroseness, fatigue, weakness, and drowsiness. The person may appear indecisive and have memory deficit. Headache and digestive disturbances often are present.” Zenz C, Occupational Medicine, Chicago, Ill, 1975
27.
28. Like Fawer et al ., this study had a significant self-selection bias. More than 80% of the workers studied had worked in the mercury cell rooms for 2-14 years, while 85% of workers leaving the mercury cell rooms in the previous 10 years had done so voluntarily.
29. What of the chlorine gas “antidote”? The effect of chlorine on mercury vapor intoxication. Autoradiographic study Viola PL & Cassano GB Med Lavoro 59 1968 437-44 Sixteen Swiss Albino Mice -- 8 exposed to Hg0, and 8 exposed to Hg0 AND chlorine gas.
30. “ After about six weeks of exposure to mercury vapors the rats revealed hyper-excitement, sometimes followed by ataxia and tremor. The rats exposed to mercury and chlorine vapors showed mild dyspnea, cough and diarrhea in the second week. After eight weeks, ten out of forty rats of the first group died while four out of forty of the second group died.” 80 Wistar Rats Exposed: 40 to Hg0, and 40 to Hg0 + chlorine vapors The effect of chlorine on mercury vapor intoxication. Autoradiographic study Viola PL & Cassano GB Med Lavoro 59 1968 437-44 80 Wistar Rats Exposed: 40 to Hg0, and 40 to Hg0 + chlorine vapors
31. The Disturbing Conclusion “ The severe neurological symptoms presented by the rats exposed to mercury vapors only and the mild gastrointestinal disorders observed in the animals exposed to mercury and chlorine vapors indicated quite different intoxication pictures. The different type of poisoning . . . seems to be clearly explained by the higher mercury levels found in the brain, which were ten times higher than those observed in the nervous tissue of rats exposed to mercury and chlorine vapors. From the data reported in this paper we may conclude that chlorine vapors added to an atmosphere containing mercury vapors not only reduce mercury absorption [by 40%], but also determine a different distribution pattern of the metal in the body. The reason for this appears to be the transformation of mercury vapors into mercurous chloride. In fact, mercurous chloride passes the blood brain barrier in very small amounts, if at all, and does not concentrate in the heart muscle, as demonstrated after oral administration of HG203-Cl salt. A strikingly higher toxicity after exposure to an atmosphere containing only mercury vapors as compared to one with mercury and chlorine vapors should be emphasized.” The effect of chlorine on mercury vapor intoxication. Autoradiographic study Viola PL & Cassano GB Med Lavoro 59 1968 437-44
32.
33. Wilson’s Disease (copper overload) and Hemochromatosis (iron overload) are good model diseases to understand mercury’s variable toxic effects
35. Differences in ApoE proteins, glutathione protein synthesis and metallothioneins are all being reported by clinicians dealing with mercury-poisoned patients
36. Pink Disease – “acrodynia” – established two incontrovertible facts: 1) health care providers can unwittingly poison large swaths of the population with mercury, and 2) the susceptibility to mercury poisoning is, indeed, HIGHLY variable. Some get poisoned by amounts that leave others unscathed. The successful termination of Pink Disease in the 1950’s, when mercury-containing infant medicines were voluntarily withdrawn from the marketplace by drug companies, SHOULD have been the death knell to mercury dental amalgams. Alas . . . Individual Sensitivity to Toxic Effects is Key
42. Kark RAP (1994) Handbook of Clinical Neurology. Modern Allopathic Medicine says: Old Homeopathic Medicine says: Certain dentists are themselves aware of the popular dread of mercury and hence the false term of “Silver Filling” which is a deliberate swindle and a disgrace to the dental occupation. It is not claimed that mercury worn in the mouth is universally detrimental to health. My own experience, which includes hundreds of observations, leads to the conclusion that injurious effects are detected in only a small percent of those who wear red rubber and silver fillings. But the exceptions are frequent and the results are no doubt often disastrous. So disastrous, in fact, as to warrant the absolute and unqualified condemnation of the practice. Howard Drutcher, MD, Hahnemanian Advocate, Vol. 35 #8 1896 The problem of susceptibility to mercury is essentially that doses of mercury harmless to most people produce a dramatic neurological disease in a few. Apparently the few had been healthy before exposure to mercury. Could they be susceptible because they had an otherwise harmless polymorphism which led to excessive mercury being retained, distributed to the brain, or unrestrained from damaging essential neurochemical reactions, or which led to critical reactions being unusually prone to inhibition by mercury? This is the situation in which people would be with the gene defect for Wilson’s disease if they had been raised in an environment entirely free of copper and if they were suddenly moved into ordinary surroundings. Health would quickly change into disease. Vallee’s group raised the possibility that polymorphisms of metallothionein or a related protein could account for the susceptibility, but there was no direct support for this hypothesis. Neal et al. (1941) had pointed out that hatters ill with mercury toxicity often had much lower urinary mercury levels than their healthy workmates. The susceptibility might represent an inability to excrete the metal at an adequate rate. In modern terms, this may be due to a polymorphism.
43. What brain structures are being poisoned? Alfred Stock’s Theory: the pituitary Eleven autopsies: 6 Hg-free, 5 amalgam bearing. Elevated levels were found in the pituitary. Hg-free: u=78.75 ng/g wet weight, range 40-133 ng/g Hg Amalgam Wearers: u=140, range 40-232 “ The observation that the pituitary gland, which despite its small size, is of such importance for the regulation of the hormonal status, accumulates mercury to levels similar to the kidneys, should be of extreme importance for the mechanism of chronic mercury poisoning. If an above normal Hg-level disturbs the functioning of the pituitary gland as it is known to do with the kidneys (inflammation, anuria, uremia, etc.) then almost all symptoms of the up to now quite mysterious chronic mercury vapor poisoning can be explained. [Understanding the mechanisms at work here] might, in addition to mercury poisoning, be of value also for the treatment of other types of poisoning.” Stock, A, The Mercury Content of the Human Body, Biochemische Zeitschrift 304 1940 73-80
44.
45. Whole-body imaging of the distribution of mercury released from dental fillings into monkey tissues Hahn LJ, Kloiber R, Leininger RW, Vimy MJ & Lorscheider FL FASEB J 4 1990 3256-60
46.
47. Correlation betwen selenium and mercury in man following exposure to inorganic mercury Kosta I, Byrne AR, Zelenko V Nature 254 1975 238-9
48. Mercury, selenium, and cadmium in human autopsy samples from Idrija residents and mercury mine workers. Falnoga I; Tusekznidaric M; Horvat M; Stegnar P Environmental Research; 84 (3) p211-218 NOV 2000
49. Dental "silver" tooth fillings: a source of mercury exposure revealed by whole-body image scan and tissue analysis Hahn, LJ, Kloiber R, Vimy MJ, Takahashi Y & Lorscheider FL FASEB J 3 1989 2641-6
50. This unlucky monkey got 16 radio-active mercury fillings placed in his teeth, and was killed on day 28. Whole-body imaging of the distribution of mercury released from dental fillings into monkey tissues Hahn LJ, Kloiber R, Leininger RW, Vimy MJ & Lorscheider FL FASEB J 4 1990 3256-60
51. Sheep Tissue Accumulation Monkey Tissue Accumulation Notice how, in comparison to all the brain regions tested, the pituitary accumulates several-fold higher amounts of mercury. Interestingly, this disparity is even MORE pronounced in the monkey, an animal that chews less than a sheep.
52. 3-5 Fetal Lambs exposed in utero after mother’s amalgam placement 5 adult ewes autopsied at different times after amalgam placement Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings Vimy MJ, Takahashi Y & Lorscheider FL Am J Physiol 258 1990 R939-945 Mothers Detox Dental Mercury Into their Babies
53.
54. Mercury produces pathological changes in the pituitary – It's not an essential trace mineral, and it’s not just harmlessly hanging around playing paddycake.
55. Different forms of Mercury all have d ifferent tissue distributions and do different nasty things to you. Dental Fillings release a lot of ELEMENTAL MERCURY, also called METALLIC MERCURY or simply MERCURY VAPOR, denoted chemically as: Hg0. Exposure to the vapor results in more than 10x as much Hg accumulating in the brain compared to exposure to equal amounts of injected mercury salts, Hg2+. Once mercury vapor has circulated through your blood stream for a while it is taken up by the red blood cells and the enzyme catalase oxidizes it into one of the two forms of INORGANIC MERCURY, both being Hg2+.
56. “ In animal experiments, mercury concentrates in the cerebellum, hypothalamus, and areas adjacent to the lateral ventricles and the area postramus.” -- Arena JM, Ed., Poisoning: Toxicology . Symptoms . Treatments, 5 th edition, Thomas Books, 1974 “ Mercury vapor readily crosses cell membranes, including the blood-brain barrier. Autoradiographic studies show that inorganic mercury (Hg2+) does not penetrate the blood-brain barrier but accumulates in areas such as the pituitary gland and area postrema where the anatomical barrier is normally absent.” -- Verity MA and Sarafian TA, Mercury and Mercury Compounds, p. 763, in: Experimental and Clinical Neurotoxicology, 2 nd edition, Spencer & Schaumberg, Eds., Oxford U. Press, 2000 After mercury vapor oxidizes into inorganic mercury it still hits the brain.
57.
58. Another group was exposed to 400 ug/M3, 6 hours a day, 5 days a week, for 2 weeks only.
59.
60. The Median Eminence is a major “switching station” where releasing hormones that are produced in the hypothalamus are transferred to the anterior pituitary where they stimulate the release of adrenal, thyroid and sex hormones, along with prolactin.
88. Low Oxytocin Reported Symptom in Hg Poisoning Hormonal Correlate or Modulator of Symptom
89. Hypothalamic Structures Hypothalamic Lesions There’s more damage to be done. . . Melmud, Shlomo, The Pituitary, 2 nd Edition, Blackwell Publishing, 2002 Mercury is a glutaminergic excitotoxin, meaning that it can make neurons fire to death by allowing too much glutamate to accumulate.
92. Mercury vapor without Booze (above) After inhaling Hg0 for one hour, this mouse was killed an hour later. High concentrations of mercury were encountered in the nasal mucosa, trachea, lung, myocardium, adrenal cortex, kidney, brown fat and especially in the brain . Mercury vapor with Booze (right) This mouse was treated with ethyl-alcohol (2 g/kg body weight, intra-peritoneally injected) 30 minutes before it inhaled mercury vapor for one hour, then was killed an hour later. While the mercury concentration increased in the liver as compared to the “dry” mouse, mercury decreased in the lung, myocardium, brown fat , and very conspicuously in the brain . Experimental evidence to support the therapeutic, neuroprotective, benefits of alcoholism . . . Khayat A, Dencker L, Whole Body and Liver Distribution of Inhaled Mercury Vapor in the Mouse: Influence of Ethanol and Aminotriazole Pretreatment. J Applied Toxicology 3 1983 66-74 “ A 44 year old dentist presented with marked finger tremor, visual deterioration, poor memory for recent events and a tendency to be irritable and argumentative. In the previous year he had felt vaguely unwell with headaches, muscle pains, 14 kg weight loss and a disturbed sleep pattern. Alcohol improved the symptoms leading to unfounded suspicions that alcoholism was the underlying problem.” Symington IS, Cross DC, Dale IM, Lenihan JMA, “Mercury Poisoning in Dentists” J. Soc. Occup. Med. (1980) 30, 37-39
93. The Joys of Working in a Dental Office Uzzell BP & Oler J, Chronic low-level mercury exposure and neuropsychological functioning J Clin Exp Neuropsychology 8 1986 581-93
94. The Great Tennessee Mercury Vapor Accident (how to give your patients inadequate care and still get published) Elemental Mercury Vapour Toxicity, Treatment, and Prognosis After Acute, Intensive Exposure in Chloralkali Plant Workers. Part I: History, Neuropsychological Findings and Chelator Effects. Bluhm RE, Bobbit RG, Welch LW, Wood AJJ, Bonfiglio JF, Sarzen C, Heath AJ, Branch RA Human & Experimental Toxicology 11 (3) p201-210 MAY 1992 After an acute exposure, these guys were treated for a total of less than 3 weeks with DMSA, a chelater that doesn’t cross the blood-brain-barrier to remove metals from the CNS
95. Erethism Cured with Aggressive Chelation Therapy Chronic elemental mercury intoxication: neuropsychological follow-up case study. Hua MS, Huang CC, Yang YJ, Brain Inj 1996 May 10(5):377-84 A few years later, in Taiwan, a more severely poisoned lampsocket worker was treated for 2 months with NAP, a chelator that crosses the blood-brain-barrier. Unlike the workers studied by the doctors in America, this man got better.
96. “ There is a principle which is a bar against all information, which is proof against all argument, and which cannot fail to keep man in everlasting ignorance. “ That principle is condemnation without investigation.” Herbert Spencer “ Don’t worry about what the world wants from you, worry about what makes you come more alive. Because what the world really needs are people who are more alive.” Lawrence Le Shan “ One must have teeth. Then love’s like biting into an orange when the juice squirts in your teeth.” Bertolt Brecht “ A test of what is real is that it is hard and rough. Joys are found in it, not pleasure. What is pleasant belongs to dreams.” Simone Weil