48 one assumes that the half-life and rates of intake and exeretion are constant. A single exponential model leads to the equation C= Call ~ &), CONCLUSION The data presented here on both stable lead a 210Pb are consistent with those of Horiuchi ét (1) where C’,, is the skeletal concentration of lead at long times, A is the decay constant (0.693/half-life), and ¢ is the time in years. An iterative procedure to estimate the parameters of the above equation (Davidon’s variable metric minimization) @® gives a half-life of 71 + 12 years and a content at long times of 91 + 13 pg/g ash for the “normal” subjects. This half-life is sub- stantiated to some extent in data on 71°Pb excretion rates in radium dial painters in which the biological half-life (which would appear to applyto stable lead, also) is about 57 years.“® The increase in stable lead with ageis also consistent with previously published data on 7!°Pb in 128 samples from about 100 subjects from an unexposed midwestern U.S. population.) A linear regression of the variation of specific activities in pCi 7!°Pb/g bone ash with age ¢ was Y = (0.068 + 0.024) + (0.0015 + 0.004)¢. (2) The rate of inerease is significant (P < 0.005), al- though as with stable lead in subjects over 30 years of age, the coefficient was smaller and not significant at the 5% level, in agreement with the data of Hunt et al.@. For the radioactive lead this decrease in slope is probably caused by the radioactive decay half-life of 21.4 years, which limits the effective (observed) halflife in the body to a maximum of about 15 years. Although the half-life estimated here is similar to that found previously, the large variances are a strong indication of the necessity for further examination of the assumptions, particularly those of constant intake, and of the model itself. Thus, the intake of Pb may vary drastically at various times in life or with social change. A particularly large increase may occur in the late teens, because of an increased exposure to cigarette smoke and auto exhaust. Smoking alone mayincrease the intakes of stable lead by 30%‘ and of 7#°Pb by 100%.20 In contrast to the possible increased exposure to young adults, a decreased exposure above age 70 seems likely. The fraction of male smokers drops from 55.9% m the 17 to 44-year group to 28.4% in the over 65-year group. For women, an even greater reduction in the percent smoking is observed.) This means that persons reaching the older ages would be partially selected by smoking habit from a lower lead intake group. This selectivity would result in the reduced numberof high values at the older ages as shown in Figure 39, and as noted by others. &-®) and of Schroeder and Tipton‘? and demonstrate . crease in the skeletal concentration of lead with : about 0.6 ug (g ash) —1 yr—!, This increase with a quires that 1% of the daily intake be perma bound by bone, and indicates that the body is 1 equilibrium with environmental lead. The soft concentrations of lead were constant with age in U.S. subjects.®) In contrast, Schroeder and 1] showed a positive correlation between skeleta soit tissue concentrations in U.S. subjects. Thus, the skeletal lead maynotbe toxic and bone may: a detoxifying “sink” in cases of lead poisoning,” skeletal concentration is an indication of the tot: posure. Smoking appears to increase the daily ints lead. Since the percentage of the human populat: exposed is lowest in the very young and the very smoking will affect the correlation between agr the concentration of lead in the bone. Further st of this nature combined with extensive, well-cont: metabolic balance studies are indicated. In parti the lead concentrations in bone from smokers and smokers need further investigation. REFERENCES 1. Patterson, C. C. Contaminated and Natural Lea vironments in Man. Arch. Environ. Health 11, 34 (1965). 2. Hardy, H. L. What is the Status of Knowledge of the | Effect of Lead on Identifiable Groups in the Popul: Clin. Pharmacol. Therap. 7, 7138-722 (1966). 3. The Working Group on Lead Contamination. Sur Lead in the Atmosphere of Three Urban Commu: Public Health Service Publication No. 999-AP-12. 4. Kehoe, R. A. The Metabolism of Lead in Man in H and Disease. (The Harben Lectures, 1960). J. Roy. Public Health Hyg. 24, 81-121, 129-143, 177-203 (19 &. Nusbaum, R. E., Butt, E. M., Gilmour, T. C., and DiDic. Relation of Air Pollutants to Trace Met: Bone. Arch. Environ. Heaith 10, 227-232 (965). 6. Schroeder, H. A. and Balassa, J. J.Abnormal Trace M. in Man: Lead. J. Chronic Diseases 14, 408-425 (16 7. Schroeder, H. A. and Tipton, I. H. The Human | Burden of Lead. Arch. Environ. Health 17, 965-978 (1°: 8. Horiuchi, K., Horiguchi, S., and Suekane, M. Studi the Industrial Lead Poisoning. I. Absorption, T) portation, Deposition and Exeretion of Lead. 6. Lead Contents in Organ-Tissues of the Normal Jap Osaka City Med. Journal 6, (1), 41-70 (1959). 9. Holtzman, R. B. Critique on the Half-Lives of Lead RaD in the Human Body. Argonne National Labora Radiological Physics Division Semiannual Re; July through December 1960. ANL-6297, pp. 67-80. 10. Tipton, I. H., Steiner, R. L., Foland, W. D., Cook, 3] Bowman, D. K., MeDaniel, K. K., Fentress, 8. D.,