Introduction Several studies have linked heavy metal exposure to oxidative stress and alteration of immune response. We conducted a repeated measures study to examine the relationships between heavy metals in the blood and circulating markers of inflammation, and whether these associations were modified by participant characteristics.
Methods We assessed heavy metals in blood specifically cadmium (Cd), mercury (Hg) and lead (Pb) and studied measurements of C-reactive protein (CRP), soluble vascular cell adhesion molecule-1 (sVCAM-1), and soluble intracellular adhesion molecule-1 (sICAM-1) for 140 traffic enforcers of the Metropolitan Manila Development Authority (MMDA) health study. We fitted linear mixed-effects models with random subject-specific intercepts to estimate the effect of heavy metal exposure on the change in mean circulating inflammatory markers and adjusted for potential confounders. We also looked at effect modification by participant characteristics.
Results Blood Pb concentration was related to increased CRP. A 10% increase in Pb was associated with a 5.4% increase in CRP level [95% confidence interval (CI): 1.5–9.3]. The association between Pb and CRP was stronger among traffic enforcers who were nonsmokers (7.2% increase; 95% CI: 1.6–12.7) vs. smokers (3.8% increase; 95% CI: −1.4–9.1), traffic enforcers who were females (10.5% increase; 95% CI: −0.7–21.7) vs. males (4.6% increase; 95% CI: 0.5–8.8), or traffic enforcers who were not hypertensive (6.7% increase; 95% CI: −4.4–17.8) vs. hypertensive (5.2% increase; 95% CI: 1.0–9.4). However, no associations between all the three heavy metals, and sICAM-1 and sVCAM-1, and between Hg and Cd metals and CRP were found.
Conclusions Lead (Pb) is associated with increased CRP in the blood. Pb in blood may increase CRP among traffic enforcers who are female, traffic enforcers who are not hypertensive and nonsmoking traffic enforcers. Moreover, the study provides additional evidence that lead (Pb) via the inflammation pathway may have a important role in cardiopulmonary toxicity.
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