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Air Quality Criteria for Lead Volume II of II - (NEPIS)(EPA) - US ...

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AX6-83<br />

Table AX6-4.2 (cont’d). Renal Effects <strong>of</strong> <strong>Lead</strong> in the Occupational Population<br />

Reference, Study<br />

Location, and<br />

Period Study Description Pb Measurement Findings, Interpretation<br />

Europe (cont’d)<br />

Coratelli et al. (1988)<br />

Study location and<br />

date not provided;<br />

authors from Italy<br />

Fels et al. (1994)<br />

Study location and<br />

date not provided<br />

Garçon et al. (2004)<br />

France<br />

Study date not<br />

provided<br />

20 Pb battery factory workers.<br />

20 controls.<br />

12 mo longitudinal study.<br />

Renal outcomes = urinary alanine aminopeptidase, NAG<br />

and lysozyme.<br />

81 male Pb workers; 45 age matched controls.<br />

Extensive exclusionary criteria.<br />

Renal outcomes<br />

Serum creatinine<br />

Glomerular markers = 6-keto-prostaglandin F 1 alpha,<br />

thromboxane B 2, and fibronectin.<br />

Proximal tubular markers = brush border antigens (BBA,<br />

BB50, HF5) and intestinal alkaline phosphatase.<br />

Distal nephron markers = prostaglandin E2, prostaglandin<br />

F 2 alpha.<br />

35 male nonferrous metal smelter workers.<br />

Renal outcomes = α1-microprotein, ∃ 2-microglobulin,<br />

retinol binding protein, α and π glutathione S transferases<br />

(GST).<br />

Oxidative stress markers also measured.<br />

All variables log trans<strong>for</strong>med.<br />

Initial mean blood Pb<br />

47.9 µg/dL (workers)<br />

23.6 µg/dL (controls)<br />

Median blood Pb<br />

42.1 µg/dL (workers)<br />

7.0 µg/dL (controls)<br />

Mean blood Pb<br />

39.6 µg/dL<br />

Mean blood cadmium<br />

5.8 µg/L<br />

Mean urine cadmium<br />

4.7 µg/g creatinine<br />

NAG and lysozyme higher in exposed compared to<br />

controls throughout study. A statistically significant<br />

decline in urinary NAG was noted in association with a<br />

one mo period <strong>of</strong> decreased occupational exposure in the<br />

Pb workers. NAG correlated with time <strong>of</strong> exposure<br />

(nonlinear) but not blood Pb. Clinical renal function<br />

measures were not studied.<br />

Serum creatinine similar in exposed compared to controls.<br />

Medians <strong>of</strong> several markers statistically greater in workers<br />

compared to controls. After adjustment <strong>for</strong> age and<br />

erythrocyte protoporphyrin, several renal marker outcomes<br />

showed “some relation” to blood Pb. The table <strong>of</strong> these<br />

data shows r and r 2 but not beta coefficients making the<br />

actual statistical method used unclear.<br />

Study limitations include lack <strong>of</strong> adjustment in statistical<br />

analysis, potential <strong>for</strong> healthy worker bias.<br />

Correlations between urine Pb and cadmium and the renal<br />

outcomes assessed (not blood Pb or cadmium).<br />

Significant positive correlations included:<br />

urine Pb and α GST (p < 0.01)<br />

urine cadmium and RBP (p < 0.05)<br />

Also, urine cadmium and 8-OHdG negatively correlated.<br />

Limitations = use <strong>of</strong> urine Pb, lack <strong>of</strong> adjustment <strong>for</strong> other<br />

covariates, sample size.<br />

Significant correlations between blood Pb and two<br />

markers <strong>of</strong> oxidative stress were observed along with a<br />

correlation between blood cadmium and one marker <strong>of</strong><br />

oxidative stress.

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