Occupational lead exposure, nephropathy, and renal cancer

Baker, Edward L.; Goyer, Robert A.; Fowler, Bruce A.; Khettry, Urmila; Bernard, David B.; Adler, Stephen; White, Ralph W. deVere; Babayan, Richard K.; Feldman, Robert G.

doi:10.1002/ajim.4700010204

Cited by 49 publications

(20 citation statements)

References 17 publications

(8 reference statements)

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“…This accumulation has been shown to compromise some ability of bone cells to respond to hormones and also may result in alterations in the plasma levels of 1,25-dihydroxy-vitamin D 3 (Goyer, 1993;Pounds et al, 1991). Long-term exposure to Pb 2+ may also result in a nephropathy or renal adenocarcinoma (Baker et al, 1980;Buchet et al, 1980;Cooper et al, 1985;Fowler, 1993;Lilis, 1981;Goyer, 1982Goyer, , 1993Selevan et al, 1985).…”

Section: Leadmentioning

confidence: 99%

Molecular and ionic mimicry and the transport of toxic metals

Bridges

Zalups

2005

Toxicology and Applied Pharmacology

667

460

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Despite many scientific advances, human exposure to, and intoxication by, toxic metal species continues to occur. Surprisingly, little is understood about the mechanisms by which certain metals and metal-containing species gain entry into target cells. Since there do not appear to be transporters designed specifically for the entry of most toxic metal species into mammalian cells, it has been postulated that some of these metals gain entry into target cells, through the mechanisms of ionic and/or molecular mimicry, at the site of transporters of essential elements and/or molecules. The primary purpose of this review is to discuss the transport of selective toxic metals in target organs and provide evidence supporting a role of ionic and/or molecular mimicry. In the context of this review, molecular mimicry refers to the ability of a metal ion to bond to an endogenous organic molecule to form an organic metal species that acts as a functional or structural mimic of essential molecules at the sites of transporters of those molecules. Ionic mimicry refers to the ability of a cationic form of a toxic metal to mimic an essential element or cationic species of an element at the site of a transporter of that element. Molecular and ionic mimics can also be sub-classified as structural or functional mimics. This review will present the established and putative roles of molecular and ionic mimicry in the transport of mercury, cadmium, lead, arsenic, selenium, and selected oxyanions in target organs and tissues.

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Section: Leadmentioning

confidence: 99%

Molecular and ionic mimicry and the transport of toxic metals

Bridges

Zalups

2005

Toxicology and Applied Pharmacology

667

460

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“…However, a similar relationship between nephropathy in workers with occupational exposure to lead and renal cancer has not been clearly established from epidemiological studies, although two case reports have been published (60,61). The potential carcinogenesis of lead has been reviewed recently by EPA because ofthe uncertainty ofthis relationship (62).…”

Section: Nephrotoxicity and Carcinogenesis Lead Nephropathymentioning

confidence: 99%

Lead Toxicity: Current Concerns

Goyer¹

1993

Environmental Health Perspectives

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160

166

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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 pLg/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 lowlevel lead exposure on blood pressure, particularly in adult men, may be related to the effect oflead 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 ofessential 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 Ag/dL.

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“…Such tumors have been produced in experimental animals by near-lethal doses of lead (6,7,8,28,40,44,45,46,51,52,53). There are reports (5,22) describing single cases of renal cancer in long-term smelter workers. Selevan et al (41) found six renal cancer deaths where 2.94 were expected in a cohort of 1 987 male smelter workers in Idaho.…”

Section: Renal Cancermentioning

confidence: 99%

Mortality among employees of lead battery plants and lead-producing plants, 1947-1980.

Cooper¹,

Wong²,

Kheifets³

1985

Scand J Work Environ Health

121

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Mortality among employees of lead battery plants and lead-producing plants, . Scand J Work En viron Health II (1985) 331-345. Two cohorts of male lead workers, 4 519 battery plant workers and 2 300 lead production workers, all of whom had been employed for at least one year during the period I January 1946 through 31 December 1970, were observed for mortality during the 34 years from 1 Januar y 1947 through 31 December 1980. Vital status as of the closing date was determined for 94.7 lifo of the former group and 91.6 lifo of the latter. There were 1 718 deaths in the first cohort and 621 in the second. Mortality from all causes combined was significantly greater than expected in each cohort, the standardized mortality ratio (SMR) being 107 and 113, respectively. Among the battery plant workers the greater than expected mortality rate resulted in large part from a significant number of excess deaths from malignant neoplasms (SMR 113), other hypertensive disease (mainly renal) (SMR 320), chronic nephritis (SMR 222), and a group of ill-defined conditions (SMR 355). Among the lead production workers the pattern was similar, with a significant number of excess deaths from other hypertensive disease (SMR 475), hypertensive heart disease (SMR 203), chronic nephritis (SMR 265), and ill-defined conditions (SMR 214). There was also a significant excess of deaths from external causes (SMR 143). The SMR for total malignancies was 113, but this value was not significantly elevated at the 5 % level. In neither cohort were deaths from cerebrovascular disease in significant excess, the SMR being 93 and 132, respectively. A proport ionate mortality analysis showed that the excess deaths from cerebrovascular diseaseand from hypertensive heart disease among smelter workers were in part due to the high proportion of nonwhites in the smelter populations. The stomach, liver, and lungs were the sites responsible for most excess cancer deaths in both cohorts, but the elevated SMR values were statistically significant only for gastric and lung cancers in battery plant workers. There were no excess deaths from malignancies of the kidney, brain, or Iymphopoeitic system in either cohort. It is impossible to relate the observed mortality to levels of lead exposure; because of meager quantit ative information prior to 1960. It is known that past exposures had been very high. Ethnicity, diet, alcohol, and cigarette smoking could not be ruled out as possibleconfounding etiologic factors for the cancer deaths.

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Occupational lead exposure, nephropathy, and renal cancer

Cited by 49 publications

References 17 publications

Molecular and ionic mimicry and the transport of toxic metals

Molecular and ionic mimicry and the transport of toxic metals

Lead Toxicity: Current Concerns

Mortality among employees of lead battery plants and lead-producing plants, 1947-1980.

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