LEAD

TRACE ELEMENTS FACT SHEET

Introduction

Atomic mass 207. A ubiquitous constituent of the environment, lead has been, and to a lesser degree still is, used as a component of paints and as a petrol additive. Other settings that may result in exposure are lead mining and smelting, storage battery manufacturing and recycling, brass foundries, glass industries and plastics industries. Significant exposure to lead may occur in some hobbies.

Exposure

Acute and chronic poisoning may occur in places of heavy contamination. These places are typically near to mines and smelters. Heavy, localised contamination may result from stripping leaded paint or be associated with lead using industries. General exposure to lead is related to airborne fume emitted from motor vehicles and industrial emissions. Airborne lead eventually drops-out to contaminate soil, dust, sediments and waterways. Lead particles in dust and soil are small, requiring high performance vacuum devices to ensure effective removal. Where the contamination is related to vehicle exhaust, gross elevation of soil and dust lead concentration is restricted to the area within 25 metres of the road. Water and food contamination has not been found a widespread problem in Australia.

Absorption

Human exposure is almost always associated with inhalation or ingestion. Approximately 40-50 percent of particles of less than 1 micron are retained in the lung and absorbed. Children and fasted adults absorb more lead from the gut than normally fed adults. Iron deficiency is thought to enhance absorption.

Distribution

Lead accumulates in bone and teeth where it displays a half-life of years. A much smaller proportion of the body burden is distributed to the soft tissues including red blood cells. The half-life of this compartment is 1 month. Therefore, the determination of blood lead content demonstrates recent exposure to the metal, levels rising within hours of exposure. 95% of lead in whole blood is associated with the red cells.

Excretion

Lead is mainly eliminated from the body in the urine by glomerular filtration and tubular secretion.

Pathology

Altered haem synthesis is found early after lead exposure and is due to inhibition of delta aminolevulinic acid dehydratase. Lead is also a neurotoxin. Neurobehavioral deficits have been described in children with blood leads in the range 0.5 to 1.4 umol/L. Long term exposure to lead has been reported to result in renal disease, abdominal colic and disturbance in reproductive function.

Monitoring

Whole blood lead is the sample of choice for the investigation of lead exposure. It is a short-term marker of exposure and also reflects redistribution of lead from the skeleton. Urine lead levels are not recommended for monitoring exposure as, at these low concentrations, results are highly variable even when corrected for creatinine concentration. Urine lead determination is, however, valuable in determining the efficacy of chelation therapy. The use of a variant of chelation, the EDTA mobilisation test, is not recommended by this site due to the toxicity of the drugs, the potential for eliciting acute lead toxicity and the difficulty in interpreting the result of the test.

The investigation of the lead content of deciduous teeth allows the retrospective estimation of lead exposure. Lead accumulates at different rates within the tooth. Analysis of secondary dentine is the most valuable test and this requires careful preparation of the tooth, restricting the determination to specialist laboratories.

Determination of plasma lead is not possible because the concentration of the metal in this compartment is below the detection limit of current instrumentation.

Determination of lead in hair is not recommended because of the confounding variable of environmental contamination. Historically, lead exposure has been monitored through the determination of haem metabolites. These tests are insensitive to the lead exposures now known to cause neurobehavioral deficits and so cannot be recommended.

Treatment

Various groups have established action guidelines related to various blood lead concentrations in different scenarios. In occupational exposure each state promotes its own guidelines that are similar to the Western Australian version cited below; Lead <1.9umol/L repeat within 12 months, 1.9-2.9umol/L repeat within 3-6 months, >2.9umol/L investigate source of contamination, assess exposure, consider removing worker from lead area, repeat within 1 month. For exposure in children, the National Health Medical Reasearch Council (NHMRC) recommends the following responses to lead determinations.

Lead < 0.7umol/L no response
Lead 0.7-1.2umol/L identify exposure source and remediate, counselling, repeat test to evaluate effect of actions
Lead > 1.2umol/L take medical history, identify exposure source and remediate, counselling, repeat teat in 3 months
Lead > 2.6umol/L as for >1.2umol/L and include urgent clinical assessment.
The NHMRC promotes a goal blood lead for all Australians of <0.5umol/L.

Analysis

Collection of blood for the determination of lead should be made with care as the sample is prone to environmental contamination. Capillary sampling is not recommended. Please consult PaLMS Trace Elements Service prior to the collection so that the appropriate collection system is used and the samples handled correctly. Various atomic absorption spectrometric methods have been promoted for the determination and are available at this site. Routine blood lead determination at this site is made by inductively coupled plasma-mass spectrometry. Determinations in other biological and environmental matrices in support of investigation and remediation are also available at this site.

For further information please contact Graham Hams, PaLMS Trace Elements on (02) 9926 7682.
Last updated: Nov 98