Toxic Injury & Things to Avoid

Toxic injury is a type of injury caused by toxins.  As such, they can cause teratogenic effects, gastrointestinal effects, cardiovascular effects, hepatic effects, renal effects, and neurological effects.

In fact, they can also lead to various forms of cancer, learning disabilities, infertility.  Effects can occur after a short term exposure (acute), ir it can occur after long-term exposure (chronic).  These effects, moreover, may depend on the toxicity of the substance, but more often, it may be only a whiff by a chemically-injured person to go into shock or death.

Those who suffer from Multiple Chemical Sensitivity are at greater risk of toxic injury.

As posted in Wikipedia, in America, May is recognized as Multiple Chemical Sensitivity and Toxic Injury Awareness Month.  If what you read below scares you, it should.  Action needs to be taken NOW by refusing to purchase and use consumer products that are injurious to your health and others.

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http://chemicalinjury.net/

This website is dedicated to providing both the public and the medical community with the latest research and information on chemical injury. You’ll find articles, lists, and links covering the prevention, evaluation, and treatment of chemical sensitivity and related conditions caused by the thousands of poorly tested or untested, hazardous chemicals you are exposed to every day.  Each section features articles specifically written for the general public and articles specifically written for medical professionals.

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From THE WOMEN’S VOICES FOR THE EARTH (WVE)

“Dirty Secrets: What’s Hiding in Your Cleaning Products?” (November 2011)

What WVE Found–

  •  some products contained reproductive toxins such as toluene and phthalates, carcinogens such as 1,4-dioxane and chloroform, and a hormone disrupting synthetic musk;
  •  several known allergens were also detected in these products, the highest levels of which appeared in fragranced air fresheners;
  •  allergens were found in products marketed as fragrance-free; and
  •  none of these chemicals were listed on the product’s label.
  • FEBREZE was mentioned six times

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List of harmful toxins:

http://science.naturalnews.com/index-Harmful_Toxins.html

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TERATOGENIC EFFECTS:  In general, birth defects.  Teratogenic agents are wide-range chemicals and environmental factors suspected or known to be tertogenic in humans and in animals.  Here are a selected few:

Other compounds are known as severe teratogens based on veterinary work and animal studies, but aren’t listed above because they have not been studied in humans, e.g. cyclopamine. Teratogenic effects also help to determine the pregnancy category assigned by regulatory authorities; in the United States, a pregnancy category of X, D, or C may be assigned if teratogenic effects (or other risks in pregnancy) are documented or cannot be excluded.

Isotretinoin (13-cis-retinoic-acid; brand name Roaccutane), which is often used to treat severe acne, is such a strong teratogen that just a single dose taken by a pregnant woman may result in serious birth defects. Because of this effect, most countries have systems in place to ensure that it is not given to pregnant women, and that the patient is aware of how important it is to prevent pregnancy during and at least one month after treatment. Medical guidelines also suggest that pregnant women should limit vitamin A intake to about 700 μg/day, as it has teratogenic potential when consumed in excess.

Exposure to teratogens can result in a wide range of structural abnormalities such as cleft lip, cleft palatedysmeliaanencephalyventricular septal defect. Exposure to a single agent can produce various abnormalities depending on the stage of development it occurs. Specific birth defects are not characteristic of any single agent.

GASTROINTESTINAL EFFECTS:  There are a number of diseases and conditions affecting the gastrointestinal system, including:

he gastrointestinal tract is also a prominent part of the immune system.[11] The surface area of the digestive tract is estimated to be the surface area of a football field. With such a large exposure, the immune system must work hard to prevent pathogens from entering into blood and lymph.[12]

The low pH (ranging from 1 to 4) of the stomach is fatal for many microorganisms that enter it. Similarly, mucus (containing IgA antibodies) neutralizes many of these microorganisms. Other factors in the GI tract help with immune function as well, including enzymes in saliva and bile.Enzymes such as Cyp3A4, along with the antiporter activities, also are instrumental in the intestine’s role of detoxification of antigens and xenobiotics, such as drugs, involved in first pass metabolism.

Health-enhancing intestinal bacteria serve to prevent the overgrowth of potentially harmful bacteria in the gut. These two types of bacteria compete for space and “food,” as there are limited resources within the intestinal tract. A ratio of 80-85% beneficial to 15-20% potentially harmful bacteria generally is considered normal within the intestines. Microorganisms also are kept at bay by an extensive immune system comprising the gut-associated lymphoid tissue (GALT).

CARDIOVASULCAR EFFECTS:   Particulate matter has been studied for its short- and long-term exposure effects on cardiovascular disease. Currently, PM2.5 is the major focus, in which gradients are used to determine CVD risk. For every 10 μg/m3 of PM2.5 long-term exposure, there was an estimated 8-18% CVD mortality risk. Women had a higher relative risk (RR) (1.42) for PM2.5 induced coronary artery disease than men (0.90) did. Overall, long-term PM exposure increased rate of atherosclerosis and inflammation. In regards to short-term exposure (2 hours), every 25 μg/m3 of PM2.5 resulted in a 48% increase of CVD mortality risk. Additionally, after only 5 days of exposure, a rise in systolic (2.8 mmHg) and diastolic (2.7 mmHg) blood pressure occurred for every 10.5 μg/m3 of PM2.5. Other research has implicated PM2.5 in irregular heart rhythm, reduced heart rate variability (decreased vagal tone), and most notably heart failure. PM2.5 is also linked to carotid artery thickening and increased risk of acute myocardial infarction.

Epidemiology suggests a number of risk factors for heart disease:  age, gender, high blood pressure, high serum cholesterol levels, tobacco smoking, excessive alcohol consumption, family history, obesity, lack of physical activity, psychosocial factors, diabetes mellitus, AIR POLLUTION.  While the individual contribution of each risk factor varies between different communities or ethnic groups, the consistency of the overall contribution of these risk factors to epidemiological studies is remarkably strong.  Some of these risk factors are immutable.  However, many important cardiovascular risk factors are modifiable by lifestyle change or social change.

HEPATIC EFFECTS:   The liver is a vital organ present in vertebrates and some other animals. It has a wide range of functions, including detoxificationprotein synthesis, and production of biochemicals necessary for digestion. The liver is necessary for survival; there is currently no way to compensate for the absence of liver function in the long term, although new liver dialysis techniques can be used in the short term.

This organ plays a major role in metabolism and has a number of functions in the body, including glycogen storage, decomposition of red blood cells, plasma protein synthesis, hormone production, and detoxification. It lies below the diaphragm in the abdominal-pelvic region of the abdomen. It produces bile, an alkaline compound which aids in digestion via the emulsification of lipids. The liver’s highly specialized tissues regulate a wide variety of high-volume biochemical reactions, including the synthesis and breakdown of small and complex molecules, many of which are necessary for normal vital functions.[2]

the liver supports almost every organ in the body and is vital for survival. Because of its strategic location and multidimensional functions, the liver is also prone to many diseases.

Chemicals produce a wide variety of clinical and pathological hepatic injury. Biochemical markers (e.g. alanine transferasealkaline phosphatase and bilirubin) are often used to indicate liver damage. Liver injury is defined as a rise in either (a) ALT level more than three times of upper limit of normal (ULN), (b) ALP level more than twice ULN, or (c) total bilirubin level more than twice ULN when associated with increased ALT or ALP.[18][19] Liver damage is further characterized into hepatocellular (predominantly initial Alanine transferaseelevation) and cholestatic (initial alkaline phosphatase rise) types. However they are not mutually exclusive and mixed types of injuries are often encountered.

RENAL EFFECTS:   Acute kidney failure usually occurs when the blood supply to the kidneys is suddenly interrupted or when the kidneys become overloaded with toxins. Causes of acute failure include accidents, injuries, or complications from surgeries in which the kidneys are deprived of normal blood flow for extended periods of time. Heart-bypass surgery is an example of one such procedure.

Drug overdoses, accidental or from chemical overloads of drugs such as antibiotics or chemotherapy, may also cause the onset of acute kidney failure. Unlike chronic kidney disease, however, the kidneys can often recover from acute failure, allowing the patient to resume a normal life. People suffering from acute failure require supportive treatment until their kidneys recover function, and they often remain at increased risk of developing future kidney failure.

Among the accidental causes of renal failure is the crush syndrome, when large amounts of toxins are suddenly released in the blood circulation after a long compressed limb is suddenly relieved from the pressure obstructing the blood flow through its tissues, causing ischemia. The resulting overload can lead to the clogging and the destruction of the kidneys. It is a reperfusion injury that appears after the release of the crushing pressure. The mechanism is believed to be the release into the bloodstream of muscle breakdown products – notably myoglobinpotassium, andphosphorus – that are the products of rhabdomyolysis (the breakdown of skeletal muscle damaged by ischemic conditions). The specific action on the kidneys is not fully understood, but may be due in part to nephrotoxic metabolites of myoglobin.

Other acquired kidney diseases that could be caused by toxic injury:

NEUROLOGICAL EFFECTS:  Chronic solvent encephalopathy is a degenerative neurologic disorder caused by exposure to toxic substances like organic solvents. Exposure to toxic substances can lead to a variety of symptoms, characterized by an altered mental status,memory loss ,visual problems,etc etc.Toxic encephalopathy can be caused by various chemicals, some of which are commonly used in everyday life. Toxic encephalopathy can permanently damage the brain and currently, treatment is mainly just for the symptoms.

“Encephalopathy” is a general term describing brain malfunctions and “toxic” asserts that the malfunction is caused by toxins on the brain.The most prominent characteristic of toxic encephalopathy is an altered mental status. Toxic encephalopathy has a wide variety of symptoms, which can include memory loss, small personality changes/increased irritability, insidious onset of concentration difficulties, involuntary movements, fatigueseizures, arm strength problems, and depression.Neurobehavioural effects of occupational exposure to organic solvents among construction painters . The condition may also be referred to as substance-induced persistent dementia. Acute intoxication symptoms include lightheadedness, dizziness, headache and nausea, and regular cumulative exposure to these toxic solvents over a number of years puts the individual at high risk for developing toxic encephalopathy.

Magnetic Resonance Imaging (MRI) analyses have also demonstrated increased rates of dopamine synthesis in the putamen, reduced anterior and total corpus callosum volume, demyelination in the parietal white matter, basal ganglia, and thalamus, as well as atypical activation of frontal areas of the brain due to neural compensation. A thorough and standard diagnostic process is paramount with toxic encephalopathy, including a careful occupational history, medical history, and standardized imaging/neurobehavioral testing.

In addition, chemicals, such as lead, that could instigate toxic encephalopathy are sometimes found in everyday products such as cleaning products, building materials, pesticides, air fresheners, and even perfumes. These harmful chemicals can be inhaled (in the cause of air fresheners) or applied (in the case of perfumes). The substances diffuse into the brain rapidly, as they are lipophilic and readily transported across the blood–brain barrier. This is a result of increased membrane solubility and local blood flow, with central nervous system (CNS) solvent uptake being further increased with high levels of physical activity. When they are not detoxified immediately, the symptoms of toxic encephalopathy begin to emerge. However, in chronic situations, these effects may not become severe enough to be noticed until much later. Increased exposure time and increased concentration of the chemical solvents will worsen the effects of toxic encephalopathy, due to the associated structural CNS damage and direct functional impairment consequences.

RESPIRATORY EFFECTS:  Acute inhalation injury may result from frequent and widespread use of household cleaning agents and industrial gases (including chlorine and ammonia) or from bioterrorism-related events. Depending on the type and amount of irritant gas inhaled, victims can experience symptoms ranging from minor respiratory discomfort to acute airway and lung injury and even death. A common response cascade to a variety of irritant gases includes inflammation, edema and epithelial sloughing which, left untreated, can result in scar formation and pulmonary and airway remodeling. Currently, mechanical ventilation remains the therapeutic mainstay for pulmonary dysfunction following acute inhalation injury. There is therefore an urgent need to develop airway and pulmonary protective and reparative strategies for mitigation of this injury. A number of in vitro and in vivo models are available for preclinical testing and development of novel therapeutics. A clinically feasible therapeutic would be one that is effective when administered several hours after inhalation and which can be administered by first responders in a mass casualty setting. Development of such therapeutics will attenuate the morbidity and mortality associated with acute inhalation injury.

We need more people to go to their State governors to get Proclamations passed as the one below in 2009.

Toxic Injury Awareness Month
Toxic Injury Awareness Month (Photo credit: live w mcs)

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From a Yellow Canary of the 21st century, living in our disabling biosphere

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