This is going to be a short post from my viewpoint because I’m mostly going to quote from Safe Work Australia’ “Health monitoring – Guide for inorganic lead”. https://www.safeworkaustralia.gov.au/system/files/documents/2002/health_monitoring_guidance_-_lead.pdf Just the interesting bits though.

Remember, this document is the basis for the RSHQ regulations, but it has some interesting extra comments that you may not have seen. I’ve bolded the stuff I think you might find interesting. My comments will be in brackets.

Here are some quotes from the section on lead hazards which are supposed to be communicated to lead risk workers before they start lead risk work.

Health effects of lead

Workers should be informed of the potential health effects associated with exposure to inorganic lead including the different risks to men and women and people of younger age (i.e. less than18 years of age).
Workers should be informed of the bioaccumulation of lead and be advised to minimise exposure particularly for long term lead risk work.

(You knew this, right?. If you’ve read my previous blogs so you already knew that lead accumulates in the body, and I’m sure none of you have worked in Mt Isa for longer than 6 months?))

(I haven’t mentioned the effect of lead on reproductive function yet because it is so well known. That’s right isn’t it?)

Family planning
Workers who consider they have not completed their family should be counselled on the health effects of lead on male and female reproduction, as appropriate.

(I’m sure they would have warned you about the fact that some of the DNA damage caused by lead could muck things up in terms of eggs and sperm and offspring?)

Female workers working in lead risk jobs should be informed exposure to lead during pregnancy may be associated with pregnancy complications and may pose a risk to the development of the foetus. Female workers should be counselled on the effects of lead on foetal and childhood development, in particular cognitive development.

(May be? That ought to read WILL BE)

Females of reproductive capacity should be informed about the reproductive health risks where blood lead levels may exceed 10 μg/dL (0.48 μmol/L). It is highly recommended that in order to give maximum protection to the foetus, women who are planning a pregnancy should endeavour to limit lead exposure to a blood lead level well below 5 μg/dL (0.24 μmol/L) for a period of at least a year prior to pregnancy.

(That means don’t go anywhere near lead for at least 12 months. Bit hard in Mt Isa, and anyway, the lead you’ve accumulated is still there.)

Male workers should be informed that exposure to lead may adversely affect reproductive function.

(They told you that a vasectomy was a good idea before you signed up, didn’t they?)

Pregnancy and breastfeeding
Workers who are pregnant or breastfeeding should be advised to seek alternative duties (that do not involve lead exposure) from the person conducting the business or undertaking (PCBU).
Infants are more susceptible to the health effects of lead than adults. A breastfeeding worker should keep her blood lead level as low as possible.

(Blood lead is primarily lead bound to red blood cells). In a breastfeeding mother the calcium in her milk, and the lead, for the most part comes from her bones. Blood lead levels do not reflect bone lead except after several months of no exposure to lead. In Mt Isa?)

(How many babies have been harmed because we don’t have any accurate estimate of the amount of lead in a persons’ body, and the attendant risks? How many babies have been harmed because lead wasn’t removed, just left in place?)

Other health monitoring methods
The distribution and clearance of absorbed inorganic lead is such that urine lead levels are not considered a suitable indicator of inorganic lead exposure.
Lead inhibits the mitochondrial enzyme, ferrochelatase, and delta-aminolaevulinic acid dehydratase (ALAD); both are involved in haem synthesis. This inhibition results in the accumulation of protoporphyrin in red blood cells, which chelates with zinc instead of iron to form zinc protoporphyrin (ZPP), also resulting in increased urinary excretion of coproporphyrin.
Blood ZPP levels have been used as a measure of lead exposure to differentiate between recent exposure and chronic accumulation. As ZPP remains in erythrocytes for the average lifespan of the red blood cell, the blood ZPP level reflects averaged exposure over a three-month period. There is a wide range of inter-individual variability in the protoporphyrin response to lead absorption and it is suggested results are compared with previous results from the same individual with monitoring of the individual response rather than interpretation of a particular level. The protoporphyrin response lags behind the current blood lead level by two to three months as an increase only becomes measurable in the peripheral blood as affected erythrocytes mature and are released from the bone marrow. It is recommended testing for ZPP as a measure of lead exposure only be considered once removal limits have been reached. As with blood lead levels, continued exclusion from lead work is recommended until levels return to satisfactory levels.
There can be limitations of this method compared with measurement of blood lead levels:
– low sensitivity and potential false negatives, and
– lower specificity – ZPP levels can be influenced by conditions other than exposure to lead.

(ZPP used to be used confirm lead exposure, before that it was a stippled appearance of the blood. As lead detection methods improved, the older indicators were largely dropped. but they still don’t measure body[bone] lead), which is what really counts. )

(Talking about technologies that were used before the age of chemical and ICP-MS blood lead measurements may be an indicator of just how long it’s been since someone did a decent job of bringing these guidelines into the 21st century)

(But this gets better)

Target organ/effect
One of the main targets of inorganic lead toxicity in adults is the nervous system – central and peripheral. Severe exposures may cause encephalopathy and progressive degeneration of certain parts of the brain, coma or death.
Chronic high level workplace exposure to lead damages the peripheral nervous system, resulting in local paralysis, or ‘lead palsy’. Workers with lower levels of exposure may experience fatigue, irritability, depression, insomnia, headaches and subtle evidence of intellectual decline.
Exposure to inorganic lead may also damage the formation and functioning of red blood cells. Anaemia is one of the most characteristic symptoms of high level chronic lead exposure.

(Not quite. Once you’ve got enough lead on board anaemia is a given)

Low to moderate exposure may result in cardiovascular effects, including increased blood pressure and electrocardiographic abnormalities.
Once in the body, lead is transported in the bloodstream, entering all body tissues. Only two to five per cent of the total body lead is found in red blood cells. Approximately 94 per cent of the total body burden of lead is in the bones for adults. Lead is preferentially stored in the skeleton and in regions undergoing the most active calcification at the time of exposure – both cortical and trabecular bone.
Distribution of lead to various organs is variable as are elimination rates. Blood lead clearance after an exposure change is approximately 20 to 35 days, while red blood cells have a half-life of 120 days. Redistribution from bone is much slower and takes approximately three to 30 years. Due to the slow clearance rate from the body, lead can accumulate in various organs, including the bones.
Body recovery is slower each time exposure occurs and body burden continues to accumulate with repeated exposure. Clinical treatment using chelation therapy to reduce lead levels may decrease total lead body burden but not the risk of cognitive effects.
Lead affects people of all ages, but the effects of lead are considered most serious in young children.

Observed health effects and blood lead levels
The adverse health effects of lead have been well documented over the years in both occupational and non-occupational studies. A summary of health effects from occupational studies and their associated blood lead levels can be found in Figure 1 below.
Research in non-occupational settings has indicated:
– increased risk of spontaneous abortion and potential for postnatal developmental delay at maternal blood lead levels ≥ 5 μg/dL

– hypertension and kidney dysfunction at blood lead levels ≥ 5 μg/dL
– reduced birth weight and potential for subclinical neurocognitive deficits at maternal blood lead levels ≥ 10 μg/dL
– increased non-specific symptoms at blood lead levels ≥ 30 μg/dL
– neurocognitive effects, sperm abnormalities nephropathy, anaemia, colic, gout at blood lead levels ≥ 40 μg/dL, and
– encephalopathy and peripheral neuropathy at blood lead levels ≥ 80 μg/dL.
Medical conditions that may be exacerbated with continued exposure to lead include chronic renal dysfunction, hypertension, neurological disorders, and cognitive dysfunction.
Non-specific symptoms may include headache, fatigue, sleep disturbance, anorexia, constipation, arthralgia, myalgia, and decreased libido.

(Well that’s it from Safe Work Australia. That ought to be a reliable source. Did you get the mention about gout?)

(This is stuff you should have been advised about when you became a lead risk worker. Did they make you sign the document to prove you understood all this?)

The people (SWA) that make the broken regulations that don’t take accumulation of lead into account absolutely know what the bioaccumulation of lead will do to you. But they produced a regulatory model for lead risk workers that ignores almost everything they know. That’s an absolute travesty. How did they get away with this in the 21st century?