Blood lead levels in children have fallen, but vigilance is still needed
Authors: Mark P Taylor and Bruce P Lanphear
Published online: 2 March 2020
Ongoing population‐level strategies are needed to further reduce lead exposure
The largest survey of blood lead levels in children in Australia outside high risk mining and smelting communities since the phasing out of leaded petrol was undertaken as part of the Barwon Infant Study in Victoria. As reported in this issue of the MJA,1 the investigators found that blood lead concentrations in children were considerably lower (geometric mean, 0.95 μg/dL) than those measured in the last major survey of Australian children, more than 25 years ago (geometric mean, 5.05 μg/dL).2 Blood lead levels have declined dramatically over the past 50 years,3,4 and Symeonides and colleagues have found that levels in children continue to fall. Nevertheless, they are still about 60 times higher than in pre‐industrial humans (0.016 μg/dL),5 and health agencies have declared that there is no safe level of lead for children.6,7
Low levels of lead exposure that only recently were thought to be safe or innocuous have been found to be associated with significant risks.8 For instance, it was estimated in 2013 that a blood lead level of 1.0 μg/dL was associated with a one‐point loss in IQ score,9 confirming that there is no lower safe threshold of exposure. Further, the adverse effects of exposure continue throughout life, affecting inter alia emotional10 and physical health11 and socio‐economic outcomes.12 It has recently been reported that risk of death from cardiovascular and ischaemic heart disease increases sharply in adults as their blood lead level rises from 1.0 to 6.7 μg/dL,11 further indicating that adverse health effects can be manifested at levels below 5.0 μg/dL.13
Several studies have reported that other toxic chemicals and pollutants, including radon, airborne particles, asbestos, tobacco, and benzene, have decelerating exposure–response curves (ie, steeper at the lowest dose or levels of exposure) and no safe threshold level.14 Most concerning is that these studies show that adverse effects are proportionately greater at the lowest levels of exposure. Consequently, current regulatory strategies for preventing exposure to lead and other pollutants include an inherent perversity of protection, as they rely on set thresholds before intervention is regarded as warranted; in the case of lead, this is a blood level exceeding 5.0 μg/dL.15 Moreover, although greater exposure is typically restricted to a small fraction of the overall population, a larger proportion of people can still be subject to chronic low level exposure.
The blood lead concentrations measured in 4‐year‐old children in the Barwon Infant Study are similar to those reported for other developed nations, such as the United States.16 By only testing 4‐year‐olds, however, the study authors probably underestimated the proportion of children who have ever had blood levels exceeding 5.0 μg/dL. Blood lead concentrations typically peak at 2–3 years of age, partly because of hand–mouth activity and mobility factors, and are declining by the time children reach their 4th birthdays.8
Given the reported dramatic declines in blood lead concentrations, together with technological advances that allow increasingly low lead concentrations to be measured, we should move from quantifying lead in μg/dL to μg/L (= parts per billion), consistent with how we quantify other metals, such as mercury and arsenic. The change would also acknowledge the proportionately greater risks per unit of exposure at lower levels.
Symeonides and colleagues explored associations of lead levels with several potential risk factors that could be modified to reduce lead exposure in young children, including contamination of older homes (lead‐containing paint), renovations, and contact with contaminated soil. Children living in older houses (50 years old or more) or from families of lower household income had higher blood lead levels, as did those living closer to Point Henry, the site of a now closed aluminium smelter.
While the study by Symeonides and colleagues focused on a population at low risk of exposure, for populations at higher risk, as in Broken Hill, Port Pirie and Mount Isa, exposure remains unacceptably high. Ongoing contamination needs to be reduced and unnecessary use of lead (eg, in high concentrations in lead‐brass in taps — up to 4.5% lead in Australia, compared with 0.25% in the USA17 — wheel weights, fishing sinkers) should be avoided. This is particularly important when the use of lead can easily lead to it entering the human food chain and ecological systems.
It is also time to accelerate the reduction of permissible levels of lead exposure in workplaces where it is typically much higher than for the general community.18,19 Emerging concerns for adults include a range of serious disorders linked with lead exposure, including kidney disease,20 heart disease,13 amyotrophic lateral sclerosis,21 and dementia.22
Unfortunately, Australia has not established a national biomonitoring surveillance program — unlike the USA16 and Canada23 — for monitoring changes in exposure to toxic chemicals such as lead, fluorosurfactants, flame retardants, and mercury. Surveillance programs provide valuable insights into new chemical exposures and opportunities for implementing new harm mitigation strategies.
The study by Symeonides and colleagues provides further evidence that the high exposure to lead during the 20th century has now been reduced, particularly in developed nations.16 The authors contend that their findings indicate that “regulatory measures for reducing the lead exposure of children in the general Australian population have been effective”.1 The authors did not find any evidence that the reductions in blood lead levels, which mirror the rapid decline in concentrations in environmental sources such as aerosols and dusts in the post‐leaded petrol era,3 were attributable to behavioural changes. Ongoing population‐level strategies for further reducing lead exposure are needed.24
Competing interests
References
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- Donovan J. Lead in Australian children. Report on the national survey of lead in children. Canberra: Australian Institute of Health and Welfare, 1996. https://www.aihw.gov.au/getmedia/b6d0e6d2-09f1-4ef1-b62b-a0930557509b/lead-in-australian-children.pdf.aspx?inline=true (viewed Aug 2019).
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- Robbins N, Zhang Z‐F, Sun J, et al. Childhood lead exposure and uptake in teeth in the Cleveland area during the era of leaded gasoline. Sci Total Environ 2010; 408: 4118–4127.
- Flegal AR, Smith DR. Lead levels in preindustrial humans. N Engl J Med 1992; 326: 1293–1294.
- Centers for Disease Control and Prevention. Childhood lead poisoning prevention. July 2019. https://www.cdc.gov/nceh/lead/prevention/default.htm (viewed Nov 2019)
- World Health Organization. Lead poisoning and health. Aug 2019. https://www.who.int/news-room/fact-sheets/detail/lead-poisoning-and-health (viewed Nov 2019).
- Canfield RL, Henderson CR, Cory‐Slechta DA, et al. Intellectual impairment in children with blood lead concentrations below 10 μg per deciliter. N Engl J Med 2003; 348: 1517–1526.
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- Lanphear BP, Rauch S, Auinger P, et al. Low‐level lead exposure and mortality in US adults: a population‐based cohort study. Lancet Public Health 2018; 3: e177–e184.
- Reuben A, Caspi A, Belsky DW, et al. Association of childhood blood lead levels with cognitive function and socioeconomic status at age 38 years and with IQ change and socioeconomic mobility between childhood and adulthood. JAMA 2017; 317: 1244–1251.
- National Toxicology Program. Health effects of low‐level lead (NTP monograph). U.S. Department of Health and Human Services, June 2012. https://ntp.niehs.nih.gov/ntp/ohat/lead/final/monographhealtheffectslowlevellead_newissn_508.pdf (viewed Aug 2019).
- Lanphear BP. Low‐level toxicity of chemicals: no acceptable levels? PLoS Biol 2017; 15: e2003066.
- National Health and Medical Research Council. Managing individual exposure to lead in Australia: a guide for health practitioners. Canberra: NHMRC, 2016. https://www.nhmrc.gov.au/about-us/publications/managing-individual-exposure-lead-australia (viewed Nov 2019.
- Centers for Disease Control and Prevention. National Health and Nutrition Examination Survey (NHANES): blood lead levels in the US population. Updated July 2019. https://www.cdc.gov/nceh/lead/data/nhanes.htm (viewed Aug 2019).
- Taylor MP, Harvey PJ, Morrison AM. Lead in plumbing products and materials. June 2018. https://www.abcb.gov.au/Resources/Publications/Consultation/Lead-in-Plumbing-Products-and-Materials (viewed Sept 2019).
- Shaffer RM, Gilbert SG. Reducing occupational lead exposures: strengthened standards for a healthy workforce. NeuroToxicology 2018; 69: 181–186.
- Safe Work Australia. Lead. Updated July 2019. https://www.safeworkaustralia.gov.au/topic/lead (viewed Aug 2019).
- Navas‐Acien A, Tellez‐Plaza M, Guallar E, et al. Blood cadmium and lead and chronic kidney disease in US adults: a joint analysis. Am J Epidemiol 2009; 170: 1156–1164.
- Kamel F, Umbach DM, Hu H, et al. Lead exposure as a risk factor for amyotrophic lateral sclerosis. Neurodegener Dis 2005; 2: 195–201.
- Bakulski KM, Rozek LS, Dolinoy DC, et al. Alzheimer's disease and environmental exposure to lead: the epidemiologic evidence and potential role of epigenetics. Curr Alzheimer Res 2012; 9: 563–573.
- Health Canada. Fourth Report on human biomonitoring of environmental chemicals in Canada. Aug 2017. https://www.canada.ca/en/health-canada/services/environmental-workplace-health/reports-publications/environmental-contaminants/fourth-report-human-biomonitoring-environmental-chemicals-canada.html (viewed Sept 2019).
- Nussbaumer‐Streit B, Yeoh B, Griebler U, et al. Household interventions for preventing domestic lead exposure in children. Cochrane Database Syst Rev 2016; CD006047.
Provenance: Commissioned; externally peer reviewed.