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Synthesis/Regeneration 41   (Fall 2006)

Lead Toxicity

by Devin M Ceartas

Having lead in your body is like putting a CD-ROM in your DVD recorder — the shapes are similar but they don’t work the same. Lead, in the form in which it affects biological systems, has the same +2 charge and roughly the same size as calcium ions. Lead ions are also similar to zinc and iron ions. Lead ions take the place of calcium, zinc and iron ions in many overlapping biochemical pathways. By substituting for essential minerals, lead can do permanent and severe damage to humans and other animals.

Because it is an element, lead does not degrade or lose its toxic effect over time. Being toxic on such a basic level, it is important to note that there is no known level at which lead is safe.[1] There is no chemical or biological reason to expect there to be a safe level of lead.

By substituting for essential minerals, lead can do permanent and severe damage …

Greek physician Dioscorides is quoted as saying that lead makes the “mind give way” as long ago as the second century BCE.[2] It is clear that lead has a disruptive effect on the ability of cells in the brain and other parts of the nervous system to send and receive information.

Calcium ions play a critical role in this process, as an internal signal causing nerve cells to release chemicals known as neurotransmitters which carry signals between nerve cells. Researchers believe that early childhood brain activity builds pathways which lead to the development of mental abilities. The effect on this process appears to be one reason children exposed to even minute amounts of lead can suffer permanent negative effects to their reasoning and behavioral skills.[3] Lead has it’s strongest effects on children under the age of six.

Enzymes make many critical biochemical pathways possible, such as the conversion of food into energy and the cells needed for growth. Lead ions can substitute for iron, zinc or other metal ions in the chemically active core of several enzymes, blocking the functioning of the enzyme.

Lead could bind to naturally occurring RNA creating an enzyme-like activation for the cutting of chemical bonds in other RNA strands, thus destroying them.[4] The primary role of RNA is in taking genetic messages from cellular DNA to the parts of the cell which make enzymes and other protein molecules.

Lead is known to disrupt the normal biochemistry in the kidney, brain and bones by causing the excessive production of some proteins whose role is to bind specifically to other molecules.[5]

The tendency for the body to confuse lead for calcium accounts for the fact that lead is incorporated into bones and teeth.

Amino acids and other small molecules are converted to glucose sugar in the liver. Glucose plays an important role in our cells in transporting energy and as a building block for the construction of other molecules.[6] This conversion is disrupted by lead, apparently by damaging the functioning of mitochondria, sub-cellular components responsible for much of the cell’s energy related chemistry. [7]

The membranes of both mitochondria and the cells containing them are altered by lead, causing them to become more fragile.[8]

Vitamin D regulates the body’s use of calcium and phosphorus, as well as influencing the health of our skin. Abnormal processing and use of Vitamin D can result from interference by lead ions.[9]

The tendency for the body to confuse lead for calcium accounts for the fact that lead is incorporated into bones and teeth. This can be used as one way of measuring the amount of lead a person has been exposed to over time. Lead can also be released to the bloodstream from bones at a later time, especially during times of stress, fever, hyperthyroidism, prolonged inactivity, pregnancy and when breast feeding.[10]

Childhood symptoms of lead poising include “headaches, irritability, abdominal pain, vomiting, anemia, weight loss, poor attention span, noticeable learning difficulty, slowed speech development, and hyperactivity.” Long term-effects of childhood exposure include “reading and learning disabilities, delays in physical and mental development, shortened attention span, speech and language handicaps, lowered IQ, neurological deficits, behavior problems, mental retardation, kidney disease…” and in extreme cases heart attacks or death.[11]

… adult exposure to lead could account for some characteristics commonly attributed to old age.

All children have an increased susceptibility to lead’s effects due to their forming nervous and other systems, low body weight, and tendency to get into household hazards such as lead paint dust. Adding to this burden, children from disadvantaged households may have even greater risk. A US Food and Drug Administration publication states that, “Calcium deficiency especially increases lead absorption, as does iron deficiency, which can also increase lead damage to blood cells. A high-fat diet increases lead absorption, and so does an empty stomach.”[12]

A very recently published Washington University study finds that adult workplace exposure to lead results in ongoing deterioration of verbal memory, visual memory and hand-eye coordination.[13] The study found a decrease in brain size and increased brain tissue abnormalities in direct proportion to lead exposure. The authors suggest that cumulative adult exposure to lead could account for some characteristics commonly attributed to old age. Adult exposure to lead is also known to be related to increases in blood pressure.

The body cannot break down lead to make it less dangerous.

Lead plays no positive role in human biochemistry. The considerable complexity of humans and the many factors we are exposed to make it difficult to determine the exact effects of very small amounts of lead. Even so, the consequences of low-level lead exposure have become increasingly clear and the “action level” at which lead should be considered dangerous suggested by government agencies has dropped several times over the years. The body cannot break down lead to make it less dangerous.

Devin Ceartas is a forest activist in the Heartwood network and self-employed computer programmer.


1.  David C. Bellinger, Lead. Pediatrics, April 2004, 113(4) 1016–1022.

2.  Toxicity, Lead. e-medicine from WebMD, http://www.emedicine.com/MED/topic1269.htm

3.  Mark J. Schuld, Lead toxicity: Its effects on fetal and infant development. http://www.indstate.edu/thcme/anderson/MJS.html

4.  Miroslawa Z. Barciszewska, Eliza Wyszko, Rolf Bald, Volker A. Erdmann & Jan Barciszewski. 5S rRNA Is a Leadzyme. A Molecular Basis for Lead Toxicity. J. Bio-chem, 2003, 133(3) 309–315; http://jb.oxfordjournals.org/cgi/content/abstract/133/3/309

5.  J. Patocka & K. Cerny, Inorganic lead toxicology. Acta Medica 2003,42(2) 65–72, http://www.pubmed.gov

6.  Wikipedia, http://en.wikipedia.org/wiki/Glucose

7.  J M Amatruda, A J Staton, & L A Kiesow, Inhibition of carbon dioxide fixation by lead acetate in rat liver mitochondria. Biochem J. 1977 July 15; 166(1): 75–79. http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1164958&blobtype=pdf

8.  Toxicity, Lead. cited above [2].

9.  Physician's Handbook on Childhood Lead Poisoning Prevention (NY), http://www.health.state.ny.us/nysdoh/lead/handbook/phc3.htm

10.  Lead Toxicology. http://www.corrosion-doctors.org/Elements-Toxic/Lead-toxicology.htm

11.  Lead Toxicology. cited above.

12.  Dangers of Lead Still Linger. U S Food and Drug Administration, FDA Consumer, January–February 1998. http://www.cfsan.fda.gov/~dms/fdalead.html

13.  Past adult lead exposure is linked to neurodegeneration measured by brain MRI, W.F. Stewart, B. S. Schwartz, C. Davatzikos, D. Shen, D. Liu, X. Wu, A. C. Todd, W. Shi, S. Bassett & D. Youssem, Neurology 2006, 66, 1476–1484. http://www.neurology.org/cgi/content/full/66/10/1476

[20 sep 06]

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