Neither WHS nor most health professionals seem to understand that most of the lead you absorb stays in your bones, whether you’re a child or an adult and it accumulates over time.

The only quantitative measurement of body lead burden has been blood lead levels, so the whole understanding about lead toxicity is centred around blood lead, and that has led to some gloriously incorrect conclusions.

As a result we have clinicians that make their clinical decisions based on blood lead levels (BLL) that can be completely misleading. High BLL can be due to recent acute exposure to lead, or they can be due to the accumulation of lead over a long period, where the high BLL indicates a high body burden of lead. The treatment needed in those scenarios is rather different, but how can they know?

Since both Safe Work Australia AND the WHS bible, “Hunter’s Diseases of Occupations” both say the same thing, that most lead stays in the body and ends up in the bones, it’s hard to understand why after nearly 50 years that simple fact is still ignored in the WHS regulations for managing lead risk worker exposure. Lead does NOT rapidly leave the body. Lead risk workers are absolutely not safe working under the existing regulations. They are being harmed because of a lack of understanding about what happens to lead in the body.

What possible justification can there be for doing nothing to improve a harmful situation? Where is the “safety” that’s quoted in the names of our regulatory organizations?

Once informed of the true state of affairs, continuing as before can only be interpreted as deliberately ignoring their duty of care.

But I’d like to re-emphasize where things have gone wrong in the understanding around the effects of lead.

The most important concept to understand is that once lead is absorbed it enters the circulation and is distributed throughout the body. I will present a simplified summary of how lead is distributed in the body, but if you don’t mind a difficult read, this paper is the real deal (Toxicokinetics of Bone Lead by MB Rabinowitz, Environmental Health Perspectives, Vo. 91, pp 33-37, 1991). Please note that it was published over 30 years ago.

There are two scenarios that have to be considered with regard to body lead distribution: what happens in the case of acute exposure and what happens in the case of chronic exposure to lead.

In the event of acute exposure and absorption of lead, lead first appears in the blood and some of it binds to red blood cells. Most of the lead in blood will be in the red blood cells, but the larger portion remaining will have been distributed to the soft tissues, which represent a much larger pool, and then eventually to bone.

When BLL (blood lead level) is measured after acute exposure, you are measuring lead in red blood cells (RBC), which is only a fraction of the lead in the rest of the body, primarily in soft tissues. As an example, brain (astrocytes) bind lead quite avidly.

As the RBC are broken down, RBC-bound lead appears in the urine and faeces, and BLL drops, but the bulk of the lead remains in the body. Over time, bone lead will account for up to 90% of the body’s lead burden. Lead in bone has a half-life ranging from 2-9 years or longer depending on the age of the individual and bone type.

Bone lead represents a reservoir of lead that will maintains a low but chronic level of lead in the body, in the soft tissues and brain and in the circulation. In the absence of lead exposure, BLL will be maintained at a more or less constant level due to the slow release of lead from bone.

If you don’t remove the lead, it stays in the body for a very long time.

You can accelerate the loss of lead from the body by taking calcium and other food supplements, but it is still a very slow process. Chelation, using chemical agents that bind lead, is the only treatment that removes lead from the body in a reasonable time frame.

Chelation is most effective in removing lead from the body, from a quantity of lead removed per time viewpoint, while most of the lead is still in the soft tissue and circulation pools. In the case of chronic exposure to lead, the bulk of the body’s lead burden will be in bone, where it can only be removed much more slowly.

When you use a chelator, it removes lead from the soft tissue pool and circulation, which produces a drop in BLL. If there is significant bone lead, when chelation is stopped the soft tissue and blood lead levels will be replenished by lead released from the bones and the BLL will rise.

If we only use BLL as an indicator, chelation “appears” to produce an immediate effect, because it has removed lead from the soft tissue pool and circulation, but since bone lead can represent  up to 90% of body lead in adults, you have only removed at most a fraction of the total lead still in the body.

BLL isn’t really a very good indicator of the body’s lead burden.

A child being treated for high BLL, in the absence of symptoms of encephalopathy, will likely be given an oral chelator, DMSA (dimercaptosuccinic acid) to reduce BLL and hopefully avoid the more serious consequences of severe lead poisoning.

DMSA or Succimer, is the preferred pediatric chelator, despite the fact that it is metabolized in the body producing side effects, and is quite objectionable to children because of it’s smell. However it is well absorbed and is specific for metals that interact with sulphur such as lead, cadmium and mercury, and generally doesn’t appear to remove significant amounts of other divalent metals such as copper, zinc and magnesium.

EDTA (ethylene diamine tetraacetic acid) has a much longer history of safe use, but it also has a degree of notoriety that is totally undeserved.

In the 1950s, there was a lot of indiscriminate use of EDTA, with doses that were too high or that represented too large a cumulative dose, and that could lead to renal damage and even death. Careful investigation of the renal damage and animal experiments (1962) showed that the renal changes reverted to normal when EDTA administration stopped. Provided a lower dose was used, with a pause between treatments, no renal damage was ever observed.

One other cause of notoriety in the Paediatric world was the death of a 5-year old autistic child with raised heavy metal levels, who died of heart failure due to hypocalcemia while receiving chelation therapy. The doctor had requested calcium disodium EDTA (Versenate) which cannot result in hypocalcemia, the pharmacy provided Na EDTA (Edetate), which unfortunately did.

As a result, it has become “common knowledge”, from many sources, “that the chelation therapy with EDTA is risky, can cause kidney damage and even death. In fact, chelation therapy with EDTA resulted in the death of a child.”

I’d like to present the case for EDTA.

EDTA is administered as a salt because pure EDTA is insoluble. That is also the reason why oral EDTA, as Ca Na EDTA or NA EDTA, is absorbed relatively poorly (about 5%). If you want to avoid the effects of stomach acids, Ca or Na EDTA should be taken with food, or administered in enteric capsules.

Three main salts of EDTA are used:

• Disodium EDTA is used to treat hypercalcemia and digitalis toxicity-associated ventricular arrhythmias. It removes calcium from the circuation, and is also used to effectively treat atherosclerosis. Uncontrolled administration of Na EDTA can result in hypocalcemia.
• Calcium Disodium EDTA is used to remove lead and other heavy metals from the body, and it conserves calcium in the body. You cannot induce hypocalcemia using Ca Na EDTA.
• Magnesium disodium EDTA can be used for intramuscular injection of EDTA in the case of acute lead toxicity, if IV CA Na EDTA is impractical. It is used because intramuscular injection of calcium disodium EDTA is extremely painful.

As mentioned earlier, the absorption of EDTA salts, while poor compared to DMSA, can be improved by the use of enteric capsules. EDTA has a far longer safety record, despite it’s “notoriety”, than DMSA. It is tasteless so doesn’t have any rejection problems with children, it isn’t metabolized in the body, so has few side effects with the exception of the removal of some other divalent metals, in particular zinc and magnesium/ Little copper is lost in humans as opposed to rats. zinc, magnesium and copper. If the oral dose is low enough the normal dietary content of essential metals is usually enough to maintain a healthy balance.

That brings me to the last point, which is the protocol for removing lead from the body. As I’ve stated, in the scenario of long-term or chronic exposure to lead most of the body’s lead is in the bones. If you want to remove lead from bones, in particular hard bone, it is a slow process.

You will see rapid release of lead from bone is in the presence of gestation, breast-feeding, osteoporosis, blood cancers, inflammatory disease and thyroid disease.

I’d like to propose that the best way to remove lead from the body is at the same rate as lead is released from bone, namely slowly. The idea is to continually deplete the soft tissue and blood pool, which will eventually cause depletion of the bone lead pool.

I would also argue that oral Ca Na EDTA, in enteric capsules, is far less likely to result in undesirable side effects when administered for longer periods, provided potential essential metal depletion is managed.

In adults (lead risk worker), 600mg of Ca Na EDTA in enteric capsules appears to prevent further net uptake of lead, and slowly deplete bone lead. If you weren’t dealing with constant exposure to lead, an even lower dose would probably be effective for an adult.

While the ideal scenario would be to measure bone lead with XFR, a steadily dropping BLL is a good indicator of positive progress. The target endpoint should be a BLL of under 5ug/dl or perhaps even lower in children.

Children would require a yet lower dose of chelator to avoid essential metal depletion. Here we are probably looking at 50-100 mg of Ca Na EDTA per day, interleaved with a vitamin supplement which includes trace metals. I believe that would result in a reduction in neurological effects of lead and in a significant reduction in the risk of long-term damage due to lead exposure.

That’s pretty simple, so why isn’t it happening?

Why are children that have BLL below 45ug/dl not treated to remove lead when we know that it will cause harm? Why are lead risk workers left to suffer a myriad of lead-related diseases, without any concern about the continued accumulation of lead in their bodies?

I can’t provide an answer to those questions without causing offence to someone, but we could definitely have better outcomes.