The role of thiocyanate in the etiology of goiter in an industrial metropolitan area

Abstract

Objective: Thiocyanate (SCN−) has concentration dependent antithyroid properties and a role in the etiology of goiter has been suggested in several studies. In 1991 an epidemiological survey conducted in the region of Halle/Leipzig (Saxony), an area with significant air pollution, suggested an inverse relationship between urinary iodine (I−)/SCN− excretion and goiter prevalence. 10 years later, we reinvestigated the same industrial area to clarify if the situation has changed after the elimination of most industrial waste products and moreover, if SCN− excretion levels alone or in combination with air pollution or smoking as a SCN− source are critical for thyroid function. Design and methods: We investigated a cohort of 708 probands for I−, SCN− and creatinine excretion in spot urine samples and determined the prevalence of goiter and thyroid nodules by high resolution ultrasonography. Results: Probands with goiter (n = 79, 11%) had significantly higher urinary SCN− excretions than probands without (3.9 ± 2.8 vs 3.1 ± 3.4 mg SCN−/g creatinine) and significantly lower urinary I−/SCN− ratios than patients without thyroid disorders (41 ± 38 vs 61 ± 71 μg I−/mg SCN−/l). Mean urinary I− excretions were not different between probands with or without goiter. Smokers showed significantly elevated urinary SCN−/creatinine ratios in comparison to non-smokers (4.3 ± 4.3 vs 2.4 ± 2.1 mg SCN−/g creatinine). ANOVA revealed a prediction of thyroid volume through age (P < 0.001), gender (P < 0.001), body weight (P < 0.05) and smoking (P < 0.05). Conclusions: In our investigation, age, gender and smoking (raising SCN− levels by CN− inhalation) were predictive for thyroid volume and the urinary I−/SCN− ratios were able to detect probands with an increased risk of developing goiter in contrast to urinary I− excretion levels alone. These data suggest, that in an era and area of decreased cyanide pollution, SCN− may remain a cofactor in the multifactorial aetiology of goiter.