Current issues in the epidemiology and toxicology of occupational exposure to lead.

Landrigan, Philip J.

doi:10.1289/ehp.908961

Cited by 72 publications

(87 citation statements)

References 31 publications

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“…The elucidation of the adverse effects of lead [24] has led to the lowering of the formerly acceptable permissible lead levels (PEL) in adults from 40 µg/dL [25] to 20 µg/dL [26]. In this study, all exposed subjects (100%) had blood lead levels above 20 µg/dL, the PEL for blood lead in adults [26].…”

Section: Discussionmentioning

confidence: 90%

Liver and Renal Function Tests in Artisans Occupationally Exposed to Lead in Mechanic Village in Nnewi, Nigeria

Dioka

Orisakwe

Adeniyi

et al. 2004

IJERPH

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Additives in petroleum solvents have been reported to have adverse health implications. An evaluation study on some toxicological effects of occupational exposure to petroleum products (especially petrol which contains tetraethyl lead) amongst twenty five occupationally exposed artisans and twenty five graduate students of College of Health Sciences, Nnamdi Azikiwe University, Nnewi, Nigeria as controls, was carried out using the following biochemical markers: electrolytes, urea, uric acid, inorganic phosphorus, creatinine, zinc and blood lead, as well as the activities of alanine and aspartate aminotransferases, and alkaline phosphatase. The results showed that occupational exposure of human subjects to lead in petrol increases the concentrations of uric acid (357 ± 123µ mol/L) and phosphate (1.5 ± 0.5m mol/L) in exposed subjects compared with unexposed subjects (uric acid 228 ± 105µ mol/L, phosphate 1.2 ± 0.41m mol/L; p < 0.01 in both cases). Significantly lower activities were observed for alkaline phosphatase (66 ± 18.9 iu/L). The activities of alanine aminotransferase (11.4 ± 4.0 iu/L) and aspartate aminotransferase (15.8 ± 4.4 iu/L) in occupationally exposed artisans were higher compared with unexposed subjects (alkaline phosphatase = 78 ± 22.4 iu/L alanine aminotranferase = 6.8 ± 2.7 iu/L, aspartate aminotranferase = 9.6 ± 3.5i u/L; p < 0.01 in all cases). Occupational exposure of human subjects to lead significantly increased blood lead (59.6 ± 15.9 µg/dL) and decreased plasma zinc (71.3 ± 14.4 µg/L) in exposed compared with unexposed subjects (blood lead = 35 ± 7 µg/dL, zinc = 108.4 ± 16.9 µg/dL; p < 0.01). The results indicate that occupational exposure to lead in petrol may compromise liver and renal function.

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Section: Discussionmentioning

confidence: 90%

Liver and Renal Function Tests in Artisans Occupationally Exposed to Lead in Mechanic Village in Nnewi, Nigeria

Dioka

Orisakwe

Adeniyi

et al. 2004

IJERPH

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“…[1,2] Lead is an environmental chemical and one of the oldest occupational and environmental toxins known. [3][4][5] Lead in contrast to calcium is not an essential nutrient and has no established toxicity threshold concentration. [6] As a biochemical analogue of calcium, lead interferes with calcium metabolism and many of its physiological functions.…”

Section: Introductionmentioning

confidence: 99%

Decreased total and ionized calcium levels and haematological indices in occupational lead exposure as evidence of the endocrine disruptive effect of lead

Anetor

Akingbola

Adeniyi

et al. 2005

Indian J Occup Environ Med

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The multisystem and prime environmental and occupational toxin, lead (Pb) is seldom included in the list of endocrine disruptors group like bisphenols A, B and F, nonylphenol, benzoquine, equiline etc. One hundred and thirty-seven subjects consisting of 86 lead workers and 51 unexposed individuals (as controls) participated in the study. Dietary intake including dairy products and micronutrients as assessed by 24-hour dietary recall was similar between lead workers and controls. Calcium homeostasis and haematological indices were evaluated in all subjects. Blood lead level was significantly higher in the lead workers than in controls (P<0.001). Total and ionized calcium levels were in contrast significantly decreased in lead workers compared with controls (P<0.01, P<0.001 respectively). Inorganic phosphate level though slightly raised compared to controls did not reach statistical significance (P>0.05). The haematological indices, haemoglobin, haematocrit, and mean cell haemoglobin concentration like calcium levels were all significantly reduced (P<0.001) in all cases. Semi-quantitative assessment of erythrocyte protoporphyrin was trace (±) in both lead workers and controls (i.e. similar). Serum copper level was significantly higher in Pb workers than in controls (P<0.005). These decreases are consistent with a repression of the endocrine systems regulating both erythropoiesis and calcium homeostasis resident in the proximal convoluted tubule(PCT) of the kidney; the most vulnerable site to Pb damage. Our findings therefore, appear to provide evidence or a reminder that Pb satifies the conditions defining EDCs and should be recognized as one, especially in developing countries where high environmental Pb and malnutrition co-exist and may magnify this effect.

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“…While work to date has focused primarily on its toxic effects in the developing peripheral and central nervous system, lead also affects a number of other developmental processes, including those that occur in the hematological and musculoskeletal systems [15,22,26,46]. The skeleton has long been recognized as a major reservoir for ingested lead [3] and delayed skeletal development has been described in children exposed to lead in utero [31].…”

Section: Introductionmentioning

confidence: 99%

Lead alters parathyroid hormone‐related peptide and transforming growth factor‐β1 effects and AP‐1 and NF‐κKB signaling in chondrocytes

Zuscik

Pateder

Puzas

et al. 2002

Journal Orthopaedic Research

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The skeletal system is an important target for lead toxicity. One of the impacts of lead in the skeleton, the inhibition of axial bone development, is likely due to its effect on the normal progression of chondrocyte maturation that is central to the process of endochondral ossification, Since little is known about the effect of lead on chondrocyte function/maturation, its impact on ( I ) growth factor-induced proliferation, (2) expression of maturation-specific markers type X collagen and BMP-6, and (3) the activity of AP-1 and NF-KB was examined in chick growth plate and sternal chondrocyte models. Exposure to lead alone (1-30 pM) resulted in a dose-dependent inhibition of thymidine incorporation in growth plate chondrocytes. Lead also blunted the stimulation of thymidine incorporation by parathyroid hormone-related peptide (PTHrP) and transforming growth factor-Dl (TGF-PI), two critical regulators of chondrocyte maturation. Lead (1 and 10 pM), TGF-01 (3 ng/ml) and PTHrP (lo-' M) all significantly inhibited the expression of type X collagen, a marker of chondrocyte terminal differentiation. However, when in combination, lead completely reversed the inhibition of rype X collagen by PTHrP and TGF-01. The effect of lead on BMP-6, an inducer of terminal differentiation, was also examined. Independently, lead and TGF-PI were without effect on BMP-6 expression, but PTHrP significantly suppressed it. Comparatively, lead did not alter PTHrP-mediated suppression of BMP-6, but in combination with TGF-PI, BMP-6 expression was increased 3-fold. To determine if lead effects on signaling might play a role in facilitating these events, the impact of lead on NF-tiB and AP-1 signaling was assessed using luciferase reporter constructs in sternal chondrocytes. Lead had no effect on the AP-1 reporter, but it dose-dependently inhibited the NF-tiB reporter. PTHrP, which signals through AP-1, did not activate the NF-KB reporter and did not affect inhibition of this reporter by lead. In contrast, PTHrP activation of the AP-1 reporter was dosedependently enhanced by lead. These findings, which establish that chondrocytes are important targets for lead toxicity, suggest that the effects of lead on bone growth are derived from its impact on the modulation of chondrocyte maturation by growth factors and second messenger signaling responses.

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Current issues in the epidemiology and toxicology of occupational exposure to lead.

Cited by 72 publications

References 31 publications

Liver and Renal Function Tests in Artisans Occupationally Exposed to Lead in Mechanic Village in Nnewi, Nigeria

Liver and Renal Function Tests in Artisans Occupationally Exposed to Lead in Mechanic Village in Nnewi, Nigeria

Decreased total and ionized calcium levels and haematological indices in occupational lead exposure as evidence of the endocrine disruptive effect of lead

Lead alters parathyroid hormone‐related peptide and transforming growth factor‐β1 effects and AP‐1 and NF‐κKB signaling in chondrocytes

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