Mercury Exposure

Lead Toxicity, Free Radicals and AIDS: Is There a Connection?

by Beldeu Singh

The subject of lead toxicity had been of great interest for some time. Lead was removed as an additive to gasoline and it was replaced with another highly toxic immunosuppressant.

Three generations of families have been found to have a cocktail of toxic industrial chemicals and it seems to be accumulating in children as young as nine.

Dairy milk was also analysed from cows that were raised near highways and they had lead in their milk. The human story about development is centered around pollutants that have contaminated our livestock, the human body and human breast milk as well. It seems to be a tragic story about contamination that in many cases is carcinogenic or immnunotoxic.

Bone analysis of very old skeletons indicates that modern humans have nearly 500-1,000 times more lead in our bones than did our ancient ancestors. Our total body content of lead nowadays is estimated at 125-200 mg. We can handle nearly 1-2 mg. daily with normal functioning, but the margin of safety is narrow.

One thesis studied the hypothesis that lead toxicity is associated with free radical oxidative damage in adult rat erythrocytes and neonatal rat brain tissue was tested.^This hypothesis was evaluated by studying: (1) the effect of lead toxicity on the formation of end products of lipid peroxidation both in vivo and in vitro, (2) the effect of lead toxicity on cellular oxidant defense biochemistry, and (3) the ability of lead to potentiate the toxicity of certain oxidant stressors. Lead toxicity leads toe free radical oxidation of biomembranes.

Lead is a neurotoxin and commonly generates abnormal brain and nerve function. It passes into the brain and can also contaminate the in-utero fetus and breast milk. Most lead, though, is stored in the bones. With lead intoxication, "lead lines" are visible in the bones on X-rays. Some is also stored in the liver and soft tissues. Infants have very little lead, but our body concentrations usually increase with age.

Metals have two main effects - direct metal binding and free-radical generation. Metal ions, such as copper, zinc, iron, and manganese, are integral, functional components of many enzymes and transcriptional regulatory proteins. On the other hand, when these or other metals with known toxicity (cadmium, mercury, lead) bind to macromolecules, there is often a perturbation of normal biological function. Metal-catalyzed formation of oxygen-derived free radicals has been implicated in promoting a multitude of pathological disorders, including mutagenicity, carcinogenicity, and aging. Metals are essential components of life, but are harmful when present in excess. Increases in the levels of bioavailable toxic metals in the environment are, therefore, of great concern to human health.

A free radical is any chemical species that contains one or more unpaired electrons.10 The presence of an unpaired electron often causes the free radical to be highly reactive because the free radical acts as an electron acceptor and essentially steals electrons from other molecules.10 This loss of electrons is called oxidation, and free radicals often are referred to as oxidizing agents because they tend to cause other molecules to donate their electrons to free radicals.10

The most common cellular free radicals are hydroxyl radical (OH•), superoxide radical (O2-•), and nitric oxide (NO•) (Fig. 1).7,9 Other molecules, such as hydrogen peroxide (H2O2) and peroxynitrate (ONOO-), are not free radicals but can lead to the generation of free radicals through various chemical reactions (outlined in Fig. 1). Free radicals and related molecules (eg, H2O2 and ONOO-) often are classified together as reactive oxygen species (ROS) to signify their ability to lead to oxidative changes within the cell.9

Free radicals and other ROS are by-products of cellular metabolism, and cells normally have a number of mechanisms to defend against damage induced by free radicals.5,9 Problems occur, however, when the production of ROS exceeds the ability of cells to defend against these substances. This imbalance between cellular production of ROS and the ability of cells to defend against them is referred to as oxidative stress.4,7,9 Oxidative stress can cause cellular damage and subsequent cell death because the ROS oxidize critical cellular components, such as lipids, proteins, and DNA.9 It follows that cells such as substantia nigra neurons would undergo degeneration and death if subjected to damage induced by free radicals. Free-radical toxicity may be the underlying cause of nigral cell deterioration in people with Parkinson's disease.

The problem arises where there are excessive free radicals in the body which damage the cells and tissues, and the over-abundance of the free radicals create even more free radicals in the body. In very high volumes free radicals can alter the genetic code material of cells themselves. Mutations that are formed by free radicals can lead to leukemia and other types of cancer as well as a host of other diseases.

When a free radical comes in contact with the inner lining of your arteries, microscopic injuries result. This process is called lipid peroxidation (the process that causes fats to become rancid) and is recognized as one of the underlying causes of atherosclerosis. Eventually the build-up of fat, cholesterol, toxic metals and other substances at the site of injury narrows the arteries.

Lead toxicity has been around for a long time. US medical authorities diagnosed childhood lead poisoning in 1887. Leaded gasoline went on sale in select markets in 1923. And in 1932, the British Medical Journal cited lead poisoning as "slow, subtle insidious saturation of the system by infinitesimal doses of lead extending over a long period of time."

Dr. Claire Patterson of the California Institute of Technology did a study in 1965 called "Contaminated and Natural Lead Environments of Man," which offered first hand proof that high lead levels in industrial nations are man-made and endemic. In fact, the study showed that the average bone lead level of a deceased person today averages approximately 1000 times higher than that of deceased people who lived 400-500 years ago.

Symptoms of heavy metal exposure can include a wide range of problems from neurological disorders, such as Parkinson's disease and Multiple Sclerosis, to attention deficit disorders and learning disabilities … to excessive free radical production and dangerous blockages in the arteries, which lead to cardiovascular disease. Even the rise in fatigue disorders, cancers and autoimmune diseases could be related to a toxic burden of heavy metals in the body.

Symptoms of heavy metal exposure can include a wide range of problems from neurological disorders, such as Parkinson's disease and Multiple Sclerosis, to attention deficit disorders and learning disabilities. They are in all likelyhood due to excessive free radical production and dangerous blockages in the arteries, which lead to cardiovascular disease, including perhaps also the rise in fatigue disorders, cancers and autoimmune diseases could be related to a toxic burden of heavy metals in the body.

Lead is thought to interfere with functions performed by essential minerals such as calcium, iron, copper, and zinc. Lead does interrupt several red blood cell enzyme systems, including delta-aminolevulinic dehydratase and ferrochelatase. In brain chemistry, lead may create abnormal function by inactivating important zinc-, copper-, and iron-dependent enzymes. (When body levels of these three minerals are high, there is first less absorption of lead and then more competition with lead for enzyme-binding sites.) Lead affects both the brain and the peripheral nerves. It may also diminish hemoglobin synthesis and can react with cell membranes. This may cause increased permeability of the cells and damage or even death of those cells. Lead can displace calcium in bone, deposit there, and form softer, denser spots that can be seen on X-rays as "lead lines." Lead also binds with the sulfhydryl bonds and inactivates the cysteine-containing enzymes, thus allowing more internal toxicity from free radicals, chemicals, and other heavy metals.

Excess free radical formation is associated with many disease states. Inflammation, poor blood flow, degenerative diseases, and toxin exposures among other mechanisms all lead to oxidative stress. A wide variety of diseases have evidence of excess generation of free radicals, oxidative stress and inadequate antioxidant activity. Some examples are neuro-degenerative diseases, heart disease, HIV disease, chronic fatigue syndrome, hepatitis, cancer, autoimmune diseases. These reactions between cellular components and free radicals lead to DNA damage, mitochondrial malfunction, cell membrane damage and eventually cell death (apoptosis - which is the term for programmed cell death).

Now the press reports that dozens of the nation's largest drinking water utilities have tried to hide lead contamination and failed to correct problems.

An examination of 65 of the 3,000 largest utilities found cities such as Philadelphia, Boston, New York City, Providence, R.I., and Portland, Ore., are "manipulating the results of tests used to detect lead in water, violating federal law and putting millions of Americans at risk," The Washington Post said.

State and federal regulators helped utilities avoid expensive ways of reducing lead in drinking water, the paper said.

Pregnant women and infants are the most vulnerable to lead, which can cause kidney and brain damage and, in some cases, death.

The Environmental Protection Agency has required drinking water utilities since 1991 to reduce contamination if lead concentrations exceed 15 parts per billion in more than 10 percent of taps sampled.

About 54,000 community water systems supply water to 268 million Americans, or about 90 percent of the U.S. population, according to American Water Works Association, a trade group.

The Post said its analysis of EPA data identified 274 water systems, serving 11.5 million people, that had reported unsafe lead levels since 2000.

Problems with lead in drinking water surfaced in 2002 for thousands of residents in Washington, D.C., but only gained widespread attention this year. Residents complained that the District of Columbia Water and Sewer Authority did little to alert them.

Early signs of lead toxicity may be overlooked, as they are fairly vague: headache, fatigue, muscle pains, anorexia, constipation, vomiting, pallor, anemia. These can be followed by agitation, irritability, restlessness, memory loss, poor coordination and vertigo, and depression.

Lead is also an immunosuppressant; it lowers host resistance to bacteria and viruses, and thus allows an increase in infections. It may also influence our cancer risk. Lead affects the gastrointestinal tract causing symptoms, including a coliclike pain. Acute lead toxicity symptoms include abdominal pain similar to colic, nausea and vomiting, anemia, muscle weakness, and encephalopathy.

There appears to be an overlapping of symtoms of AIDS with symptoms of lead toxicity. This ought to be expected because lead toxicity is accompanied by free raidical damage including dabage to the biomembranes and quite possibly depletion of mDNA associated with muscle weakness or chronic fatigue and due to the fact that it is an immunosuppressant.

So, since lead toxicity leads to free radical damage of biomembranes and a host of diseases or chronic conditions including diseases of the autoimmune system and therefore AIDS and opportunistic infections, the areas that were supplied with water with high lead content must be studied for a higher than average incidence of AIDs and AIDS related conditions.

TV Radio: Independent Media TV

Copyright: Independent Media TV

Published: 18 October 2004

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