Abstract
The aim of this study was to assess the correlation between blood lead levels and both serum uric acid and hyperuricemia in adult residents living within an area of China with lead pollution. We conducted a cross-sectional analysis of 2120 subjects (1180 of whom were male) between the ages of 20 and 75 years who had undergone health examinations at the Centers for Disease Control and Prevention (CDC) in a lead-polluted area of China between January 2013 and August 2014. Blood lead was positively correlated with serum uric acid in both males (r = 0.095, p = 0.001) and females (r = 0.134, p < 0.001). Multivariate linear regression analysis demonstrated that for males, blood lead (p = 0.006), age (p = 0.001), current smoking (p = 0.012), education (p = 0.001), triglycerides (TG) (p < 0.001), and serum creatinine (p < 0.001) were independently associated with serum uric acid. For females, blood lead (p < 0.001), body mass index (BMI) (p = 0.009), and TG (p < 0.001) were independently associated with serum uric acid. After multiple adjustments, blood lead was significantly associated with a higher prevalence of hyperuricemia when female subjects were categorized into quartiles (for the highest quartile vs. the lowest quartile, odds ratio (OR) = 2.190; 95% confidence interval (CI): 1.106–4.338; p = 0.025); however, no such association was observed for male subjects. Continuous lead exposure has an independent impact on serum uric acid for both males and females, although this impact is more pronounced for females than for males. Lead exposure is significantly associated with hyperuricemia for females but not for males.
Highlights
Uric acid is the end-product of endogenous and dietary purine metabolism in humans
The exclusion criteria were as follows: (1) the absence of data pertaining to age, gender, smoking, drinking, education, body weight, height, blood lead, uric acid, blood pressure, fasting glucose, total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), serum creatinine, or blood urea nitrogen (BUN); (2) a history of malignancy, severe cardiovascular diseases, stroke, liver diseases, and pregnant females; (3) currently had kidney autoimmune diseases or infectious diseases or currently exposed to other known renal toxicants; (4) who were taking medications such as uric acid-lowering agents; and
The percentages of current smoking, drinking, and the body mass index (BMI), SBP, DBP, TG, serum creatinine, uric acid, blood lead levels were significantly higher in males than in females (p < 0.05); the females were older and had a higher TC level than males
Summary
Uric acid is the end-product of endogenous and dietary purine metabolism in humans. It is formed by the liver and mainly excreted by the kidneys (65%–75%) and intestines (25%–35%) [1].Any factors that caused either higher synthesis or lower excretion of uric acid can make serum uric acid levels dramatically increase. Uric acid is the end-product of endogenous and dietary purine metabolism in humans. It is formed by the liver and mainly excreted by the kidneys (65%–75%) and intestines (25%–35%) [1]. Increasing evidence has demonstrated that mild to moderate increase in the serum uric acid levels, even within the normal range, is considered as a risk factor for cardiovascular diseases [5,6]. Plenty of evidence suggests that hyperuricemia is a prerequisite for gout and is associated with renal calculi, metabolic syndrome, cardiovascular events and all causes of mortality [7,8,9,10]
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