I’ve talked a bit about this topic in the past and my personal opinion is a resounding yes. But convincing bureaucrats is another game entirely.

Australia doesn’t explicitly ban prophylactic chelation for lead risk workers, but it isn’t encouraged either. The United States on the other hand bans prophylactic chelation for lead risk workers, despite the fact that oral calcium EDTA was first used in 1956 by lead miners, and was sufficiently effective that unscrupulous employers were soon using prophylactic chelation as a way to avoid the often-costly exercise of minimising lead exposure in the workplace.

I should point out that even in a totally awful environment, lead exposure-wise, oral calcium EDTA still managed to drop workers blood lead levels, much to the outrage of the regulators. After not very careful reviewing of “current” information about prophylactic chelation they produced the following edict about prophylactic chelation (sorry I should have said regulation) in 1979:

Prophylactic chelation, however, is both the routine use of chelating drugs
to prevent elevated blood lead levels in workers who are occupationally
exposed to lead and the use of these drugs to routinely lower blood lead
levels to predesignated concentrations believed to be safe. This practice is
harmful to health and can produce serious side effects. An employer may
be practicing prophylactic chelation as an alternative to providing adequate
controls of lead in the air or otherwise overexposing the worker to lead.
Health hazards reported with prophylactic chelation include: removal of
vital trace minerals from the blood; increased absorption of intestinal lead;
hypocalcemia; kidney damage; reduction in WBC count; nausea,
exanthamate and fever; and exposure to a suspected carcinogen.

The comments about harm from chelation were at one time valid. In the late 1950s and 1960s IV chelation using disodium EDTA was carried out rather enthusiastically, and early use of too high a dose for too long did indeed cause the harmful symptoms listed above, but there was never a mention of cancer. By 1966 however, standard protocols had been developed to avoid these problems. I make this point because the OHSA regulations were published 13 years later, and yet they still used outdated data as an argument against chelation. They alos fail to make a distinction between the potential harm from IV administration of chelator, and oral administration.

I’d like to make the case for the use of calcium disodium EDTA (calcium EDTA).

As stated, the earliest published study of the industrial use of oral calcium EDTA appears in 1956. There are some valid concerns about using the high (4 grams/day) dose reported in this study, namely removal of
vital trace minerals from the blood and increased absorption of intestinal lead. EDTA binds many metals, including copper, magnesium, mercury, cadmium and lead. While magnesium and copper are essential trace elements, EDTA removing heavy metals that are known to cause harm can’t be viewed as a problem. However, a deficiency of essential trace metals could potentially cause health problems. If a lower dose of EDTA is used (600mg/day or less) with the occasional mineral supplement, no net depletion is seen.

Another argument against the use of oral chelators is that they can cause increased intestinal absorption of lead. Studies have shown this is a valid concern with some chelators, but EDTA yields a net decrease of body lead regardless.

The harmful effects attributed to IV chelation simply don’t apply to oral chelation and I’ll repeat that there has been no indication whatsoever that EDTA, either IV or oral is a suspected carcinogen. I haven’t covered one often quoted “failing” attributed to EDTA, namely it’s poor intestinal absorption. An early study using radioactively labelled EDTA indicated that slightly less than 5% of the EDTA was absorbed. Subsequent publications have misquoted the absorption at 4% or lower, and I’ve even come across a recent review that said EDTA was not absorbed. It was a review arguing against chelation but stating EDTA is not absorbed is bad science.

Later studies have indicated that provided enteric capsules are used, or the EDTA is taken with food, the absorption can be as high as 15-20%. That’s absolutely high enough.

It’s important to understand the rationale used by the US OHSA (Occupational Health and Safety) regulators who banned prophylactic chelation, and the situation as it stands today in Australia. As I’ve stated, while Australia doesn’t ban prophylactic chelation, it’s not part of the workplace safety net.

Part of the problem is the 70-year long resistance to any significant change in the regulations except for lowering the removal BLL. It’s in part due to no progress in the tools used to assess and manage the lead workers health risk.
Only one tool is now used for the bulk of WHS assessment of lead exposure, blood lead levels (BLL). Other good qualitative indicators of lead exposure are no longer used and BLL is pretty much it, the equivalent of a carpenter only having a hammer.

In its defiance, BLL is a great way to assess acute exposure to lead, but regulators have ignored 2 critically important facts: (1) BLL falls relatively quickly (30-day half-life) after exposure is halted. This was interpreted as meaning that lead rapidly leaves the body, and this erroneous conclusion is responsible for the harmful stupidity of managing lead worker safety risk by removing them from lead work until the BLL drops. This safety management process ignores the fact that (2) in the case of chronic exposure lead accumulates in the bones, and it is bone lead that correlates best with disease risk.

When a worker leaves lead risk work, they carry the legacy of future harm from lead with them. Then again, early dementia, cognitive decline, increased risk of heart disease and trivial things like gout aren’t the employer’s concern. They should be, because they impact the worker’s future health and life but once you walk out the door, you’re on your own.

It’s also worth stressing that if BLL is only measured every 2-3 months or longer, it no longer indicates anything useful from a lead worker’s lead exposure safety viewpoint. Accidents happen, but if BLL isn’t measured often enough, they get missed.

I’d better relate this back to the real world where people get paid to do lead risk work.

Glencore is a Swiss Multinational that is Australia’s largest employer of lead risk workers. They operate the mines and smelter in MOunt Isa where my nephew was working. AFter talking to him about the working condition and workplace safety, I spent some time looking at the workplace health and safety regulations, and came to the realisation they provided no safety whatsoever for workers. As a result, I had a meeting with Glencore in Brisbane expressing my concerns about lead risk worker harm from existing workplace health and safety (WHS) measures, and I proposed using x-ray fluorescence spectrometry (XRF) to measure lead accumulation in bone, and prophylactic oral calcium EDTA to manage body lead levels.

I was told by the Health and Hygiene Principal that Glencore were in full compliance with state, national and international regulations and safety measures. I then received a letter from Glencore which stated that XRF exposed Glencore workers to an unacceptable level of radiation (about the same as a tooth x-ray) and that oral chelation with calcium disodium EDTA was experimental and too risky.

XFR has been used since the 1980s, including on children where far less risk is tolerated than in adults. As I mentioned in the introduction on chelation, oral calcium EDTA has been used for prophylactic control of body lead content since the mid 1950s.

But there was one WHS regulation missed or ignored by Glencore, according to a sample of workers asked. One of the WHS regulations for lead risk work requires the employer to disclose the full risks of lead exposure before an employee begins lead risk work. It appears to have been forgotten for the onboarding in Mount Isa. That’s perhaps understandable if you don’t want new employees walking out.

There is another point that has to be made. The legal consequences from workers and former workers finding out they are carrying a burden of lead in their bones from working for Glencore that will shorten their lives, is perhaps one reason why a progressive change has not been implemented.

Having failed with Glencore I started up the regulatory chain and contacted the state regulator, who denied any responsibility, and directed me to Safe Work Australia (SWA), who provide the model regulations used by most state WHS regulators.

But there is a massive problem. Changes to WHS regulations use a consensual method which means that if a change isn’t acceptable to employers, it’s unlikely to happen. One recent change which proposed dropping the BLL which was used to trigger worker removal, was passed on the basis that BLL measurement could be less frequent.

I need to make this clear. If you wait too long after a worker has been exposed to high lead levels, the BLL will not indicate high exposure because it has dropped back down. A worker might have had a BLL way higher than the removal limit (30ug/dL) due to accidental exposure but by the time it’s measured, it could be back at an “acceptable” limit (below 20ug/dL).

That’s verging on pretty useless, and the same word probably describes the employers and WHS regulators when it comes to the safety of workers exposed to lead. Lead is a slow poison and many of the ill effects are unlikely to be apparent while the worker is still working at lead risk work.

Employers and regulators either don’t care that lead workers are exposed to long term harm, or don’t want to know. After all, the effects lead are mostly invisible, unlike a crushed foot or hand. If a worker dies 5 years earlier than they ought to because of the effects of lead, who besides their families are going to notice or care?

Lead risk workers aren’t the only ones at risk. Workers manufacturing batteries face a hideous long-term prognosis because their working conditions are often even less well policed than the miners. Painters and decorators get severely lead poisoned renovating old houses painted with lead paint.

We could fix this. XRF spectrometers are somewhat expensive but still a lot less than a CT scanner. Calcium EDTA costs a few cents (not dollars) a day and will prevent the accumulation of lead in the body. Why can’t we make this happen?