Over the 20-year period since the first issue of Environmental Health Perspectives was published, there has been considerable progress in the understanding of the potential toxicity of exposure to lead. Many of these advances have been reviewed in published symposia, conferences, and review papers in EHP. This brief review identifies major advances as well as a number of current concerns that present opportunities for prevention and intervention strategies. The major scientific advance has been the demonstration that blood lead (PbB) levels of 10-15 micrograms/dL in newborn and very young infants result in cognitive and behavioral deficits. Further support for this observation is being obtained by prospective or longitudinal studies presently in progress. The mechanism(s) for the central nervous system effects of lead is unclear but involve lead interactions within calcium-mediated intracellular messenger systems and neurotransmission. Effects of low-level lead exposure on blood pressure, particularly in adult men, may be related to the effect of lead on calcium-mediated control of vascular smooth muscle contraction and on the renin-angiotensin system. Reproductive effects of lead have long been suspected, but low-level effects have not been well studied. Whether lead is a carcinogen or its association with renal adenocarcinoma is a consequence of cystic nephropathy is uncertain. Major risk factors for lead toxicity in children in the United States include nutrition, particularly deficiencies of essential metals, calcium, iron, and zinc, and housing and socioeconomic status. A goal for the year 2000 is to reduce prevalence of blood lead levels exceeding 15 micrograms/dL.

Lead toxicity: current concerns.

CHAPTER 7 – The toxicity of arsenic and its compounds

Environmental contamination by lead has greatly increased as more and more lead is used for petrol (gasoline) and in various industrial products, although severe cases of lead intoxication, as often seen in former times, have become rare owing to better health care. These facts have drawn attention to effects of lead which may arise, possibly without a threshold, at low exposure levels. Among the classical manifestations of lead intoxication are, anemia, gastro-intestinal, renal and nervous symptoms. Those in the nervous system and perhaps also in the kidney may have consequences even at subclinical levels of lead exposure. Thus, the possibility that such exposure may cause mental alterations in children, induced late renal damage or affect nerve conduction is now much debated. The mechanisms of action of lead on the developing central nervous system is still uncertain. They may be related to a composition between lead and calcium on the synaptosomal level. Among the typical stochastic risks, tumors have been found in lead-intoxicated rodents, but do not seem to occur in man, and the situation with respect to genetic risks is not entirely clear. Certain effects of lead on genetic material have been observed in simple organisms, and it appears that lead exposure in vivo or in vitro can induce light chromosomal aberrations such as gaps and fragments. Under conditions of calcium deficiency, severe aberrations such as dicentrics may also arise, but the data on man are controversial because lead is almost never the only potentially mutagenic agent to which people are exposed in an industrial environment. Nevertheless, the efficiency of lead in causing such aberrations appears low compared with that of other mutagenic agents so that genetic effects of lead do not appear of primary concern for human health. Lead can prevent implantation of the embryo, delay its growth during later stages of pregnancy and, when injected during organogenesis particularly under conditions of calcium deficiency, cause malformations. The risks to the developing human organism are difficult to evaluate owing to the large differences in lead metabolism between man and rodent, so studies on species resembling man are desirable.

Toxicity, mutagenicity and teratogenicity of lead

https://deepblue.lib.umich.edu/bitstream/handle/2027.42/27099/0000091.pdf;sequence=1

Richter Gw

Papers

Cell proliferation in mouse kidney induced by lead. I. Synthesis of deoxyribonucleic acid.