Hyperuricemia after exposure to polychlorinated dibenzo-p-dioxins and dibenzofurans near a highly contaminated area.

BACKGROUND

Hyperuricemia (too much uric acid in the blood) is the predisposing condition for gout and is associated with hypertriglyceridemia, diabetes mellitus, and coronary artery disease. Polychlorinated dibenzo-p-dioxins and dibenzo-furans (PCDD/Fs) cause renal toxicity and elevate uric acid. The aim of this analysis was to investigate and clarify the effect of moderate-to-high PCDD/F exposure on hyperuricemia risk.

METHODS

In this cross-sectional study, we recruited 1531 healthy participants living near a deserted pentachlorophenol factory. We measured serum levels of 17 2,3,7,8-substituted PCDD/Fs, and then examined associations between the main predictor variable, serum TEQ(DF-2005) (total PCDD/Fs 2005 World Health Organization [WHO] toxic equivalency [TEQ]), and dependent variables such as uric acid, glomerular filtration rates, and hyperuricemia risk.

RESULTS

We observed a strong monotonic inverse relationship between serum TEQ(DF-2005) quartiles and the estimated glomerular filtration rate after adjusting for confounding factors (Men: β were 0, -4.7, -6.2, and -14.8; Women: β were 0, -6.7, -12.9, and -21.5). In addition, we observed a suggestive positive trend between serum TEQDF-2005 quartiles and uric acid only in men after adjusting for confounding factors (Men: β were 0, 0.40, 0.36, and 0.59; P for trend <0.05). Men with serum TEQ(DF-2005) higher than the reference group's (<7.4 pg WHO(2005)-TEQ(DF/g) lipid) had a higher hyperuricemia risk after adjusting for confounding factors (25th to <50th percentile, adjusted odds ratio [AOR] = 2.20 [95% confidence interval {CI} = 1.30-3.73]; 50th to <75th percentile, AOR = 1.86 [95% CI = 1.08-3.22]; ≥ 75th percentile, AOR = 3.00 [95% CI = 1.69-5.31]).

CONCLUSIONS

We conclude that serum TEQ(DF-2005) is an important determinant of serum uric acid levels and heightens the risk of hyperuricemia in general populations.