http://www.med.akita-u.ac.jp/~eisei/english.html

Commentary
Critical level of lead resulting in adverse health effects in adults and children
Lead is a toxic element causing a variety of adverse effects such as encephalopathy, peripheral neuropathy,
anemia, and renal failure in humans, although it is used in the manufacture of batteries, paints, metal products, andceramic glazes. The Scientific Committee on Neurotoxicology and Psychophysiology and the Scientific Committee on
the Toxicology of Metals of the International Committee on Occupational Health in 2006 recommended that the standard
for blood lead (BPb) levels be reduced to 30 g/dL for industrial workers and 5 g/dL for children. To examine
whether the critical level of lead producing adverse effects truly differs between workers and children, we provided an
overview of studies addressing the critical level of lead in workers, together with a perspective on lead toxicity inchildren. In 25 reports published in English with keywords of “benchmark dose (BMD),” “lead” and “humans,” only
five studies proved to be relevant to lead toxicity. Four more studies with figures illustrating significant relationships
between lead and neurotoxic outcomes were selected. Baed on data from previous reports using a BMD approach, thecritical organ of lead in workers was thought to be the nervous system and the critical BPb level (number-weightedmean) was between 10.7 and 17.5 g/dL. The neurotoxic effects of lead exposure at such levels seemed reversible.
The BPb level at which lead-associated intellectual deficits occurred in children was as low as the critical level of BPb(below 5 g/dL) for inhibited heme synthesis in workers. The neurotoxic effects of lead in adults appear to be initiatedat BPb levels of 10 g/dL, which are somewhat higher than the critical level of lead neurotoxicity in children. Eachnational institute for risk management should take evidence-based preventive action against subclinical lead poisoning in
adults, as well as in children (Murata et al., 2009).
By the way, Menke et al. (2006) measured BPb in a nationally representative sample of 13,946 adultparticipants of the National Health and Nutrition Examination Survey recruited in 1988 to 1994 and the cohort was
followed-up for 12 years for cardiovascular mortality. The BPb range of the cohort was between 1 and 10 g/dL(geometric mean, 2.58 g/dL). After multivariate adjustment, the hazard ratio for comparisons of participants in thehighest tertile of BPb (>3.63 g/dL) at mean age of 50.7 years with those in the lowest tertile (<1.93 g/dL) at mean ageof 36.7 years was 1.55 (95% CI, 1.08 to 2.24) for cardiovascular mortality. On the other hand, Shankar et al. (2008)
performed a prospective cohort study among 58,044 participants aged >45 years (55.9% women) without preexisting
cardiovascular disease. Compared with persons with a sleep duration of 7 hours (referent), the multivariable relativerisk of coronary heart disease mortality for a sleep duration of <5 hours was 1.57 (95% CI, 1.32 to 1.88); for a sleep
duration of >9 hours, it was 1.79 (1.48 to 2.17). Also, similar risks due to sleep duration in postmenopausal American
women have been reported by Chen et al. (2008). In the study carried out by Menke et al., the range of BPb was
extremely narrow (i.e., the past critical level was not included within the whole range of BPb); and, nevertheless thehighest tertile group of BPb was 14 years older than the lowest tertile group, sleep duration depending on lifestyle was
not used as a crucial confounder in the data analysis. Therefore, which of lead exposure and sleep duration affectedcardiovascular mortality and whether the hazard ratio for cardiovascular mortality can increase with elevated BPb (i.e.,>10 g/dL) remain unclear. Further research with a wide range of BPb is required to establish the critical level of leadin adults.
References
Murata K, Iwata T, Dakeishi M, Karita K. Lead toxicity: does the critical level of lead resulting in adverse effects differ between adults
and children? J Occup Health 2009; 51: 1-12
Menke A, Muntner P, Batuman V, Silbergeld EK, Guallar E. Blood lead below 0.48 mol/L (10 g/dL) and mortality among US adults.
Circulation 2006; 114: 1388-94
Shankar A, Koh WP, Yuan JM, Lee HP, Yu MC. Sleep duration and coronary heart disease mortality among Chinese adults in
Singapore: a population-based cohort study. Am J Epidemiol 2008; 168: 1367-73
Chen JC, Brunner RL, Ren H, Wassertheil-Smoller S, Larson JC, Levine DW, Allison M, Naughton MU, Stefanick ML. Sleep duration
and risk of ischemic stroke in postmenopausal women. Stroke 2008; 39: 3185-92

K Murata, Environmental Health Sciences, Akita University School of Medicine