Lead poisoning epidemiology

Overmann, S.R. and J.J. Krajicek. 1995. Snapping turtles (Chelydra serpentina) as biomonitors of lead contamination of the Big River in Missouri s old lead belt. Environ. Toxicol. Chem. 14 689-695. Osweiler, G.D. and G.A. Van Gelder. 1978. Epidemiology of lead poisoning in animals. Pages 143-177 in F.W. Oehme (ed.). Toxicity of Heavy Metals in the Environment. Part 1. Marcel Dekker, NY. 

A role for lead in hypertension gains further credence from epidemiologic studies of low-level lead exposure (i.e., exposure too low in intensity to produce the classic symptoms of acute lead poisoning). The Second National Health and Nutrition Examination Survey performed between 1976 and 1980 included blood lead and blood pressure measurements in almost... 

Philip, A.T. euid B. Gerson. (1994) Lead poisoning — Part I. Qin. Lab. Med. 14 423-44 Pocock, S.J., M. Smith and P. Baghurst. (1994) Environmental lead and children s intelligence A systematic review of the epidemiological evidence. Br. Med. J. 309 1189-1197 Press, M.F. (1977) Lead encephalopathy in neonatal long-evans rats Morphologic studies. J. Neuropathol. Exp. Neurol. 36 169-193... 

Jacobziner, H. (1966). Lead poisoning in childhood epidemiology, manifestations and prevention. Clin. Pediatr., 5, 277... 

U.S. lead paint control efforts. Regulation of lead paint exposures and control of poisonings, furthermore, focused on the owners of properties with a lead paint problem, i.e., numerous landlords dispersed throughout America s cities. In some cases, U.S. cities with a growing childhood lead poisoning problem confined their response efforts to epidemiological studies, case... 

No doubt there are such epidemiological associations but some of those suggested may be fanciful. There is some experimental evidence that industrial exposure to lead can have carcinogenic effects [15] but Westerman et al [95] have reported, on the basis of the analysis of tissues, blood and urine, that they found no association between lead poisoning and multiple sclerosis, either early or late in the disease. 

See Elwood, St. Leger, and Morton (1976) and Lauwerys et al. (1977). For Moore s analysis and response, see Moore et al. (1979), which showed that blood lead varied with the cubed root of water lead. See also the discussion in chapter 2 on the significance of nonlinear relationships in studying the epidemiology of lead poisoning. 

In summary, the PbB decay rates reported under experimental and epidemiological survey conditions indicate relatively short biological half-lives. The values of the half-lives vary with the type of study, e.g., length of survey and number of measurement points. For example, the lead-poisoned workers of Hryhorczuk et al (1985) showed a median PbB decay half-life of 619 days when followed for more than 5 years. The PbB curves for these subjects probably included more of the slow decay component than in any of the other reports. With an increase in lead exposure, adults appear to require ca. 60 days to return to exposure steady state, i.e., a rise in the PbB curve followed by a plateau. 

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