Thyroid function and exposure to styrene.
BACKGROUND
Many natural substances and drugs have long been known to cause goiter or thyroid dysfunction. More recently, several environmental pollutants, such as pesticides and industrial compounds, have been investigated for their thyroid-disrupting activity and related adverse effects on human health. The aim of this study was to evaluate the effects of styrene on the thyroid axis in occupationally exposed workers.


METHODS
Thirty-eight exposed (E) and 123 nonexposed (NE) male workers (controls) were assessed. Serum concentrations of thyrotropin (TSH; basal and after thyrotropin-releasing hormone [TRH] administration.), free thyroxine (FT(4)), free triiodothyronine (FT(3)), anti-thyroglobulin, thyroid peroxidase antibody, and calcitonin were measured. Thyroid ultrasound examination was also performed. In E workers, urinary creatinine, mandelic acid (MA), and phenylglyoxylic acid (PGA) were also measured.


RESULTS
No significant differences between E and NE workers were demonstrated, as far as thyroid volume, nodularity, serum thyroid antibodies, and calcitonin were analyzed. However, in the E group a positive correlation between duration of exposure and thyroid volume was detected. After exclusion of subjects with nodular or autoimmune thyroid diseases, serum concentrations of FT(4), FT(3), and TSH did not differ between the two groups. In E workers there was a positive correlation between the urinary concentrations of styrene metabolites (MA plus PGA) and FT(4) or FT(4)/FT(3) ratio (p < 0.05; r = 0.45 and p < 0.005; r = 0.61, respectively), while no correlation was observed between urinary concentrations of MA plus PGA and serum TSH (either basal and stimulated).


CONCLUSIONS
Chronic exposure to styrene is not associated with an increase in nodular or autoimmune thyroid diseases. However, styrene could interfere with peripheral metabolism of thyroid hormones by inhibiting T(4) to T(3) conversion. Whether this is a direct effect on iodothyronine deiodinases or a consequence of a general distress, such as in nonthyroidal illnesses, remains to be established. Further studies in a larger population of exposed workers are needed to confirm these preliminary observations.
Santini
Ferruccio
F
Department of Endocrinology and Kidney, University Hospital of Pisa, Pisa, Italy. fsantini@endoc.med.unipi.it
Mantovani
Alberto
A
Cristaudo
Alfonso
A
Rago
Teresa
T
Marsili
Alessandro
A
Buselli
Rodolfo
R
Mignani
Aldo
A
Ceccarini
Giovanni
G
Bastillo
Rosalinda
R
Taddei
Donatella
D
Ricco
Ilaria
I
Vitti
Paolo
P
Pinchera
Aldo
A
D000328:Adult; D000906:Antibodies / Q000097:blood; D002116:Calcitonin / Q000097:blood; D003404:Creatinine / Q000652:urine; D006038:Glyoxylates / Q000652:urine; D006801:Humans; D007453:Iodide Peroxidase / Q000276:immunology; D008297:Male; D008333:Mandelic Acids / Q000652:urine; D008875:Middle Aged; D016273:Occupational Exposure / Q000009:adverse effects*; D020058:Styrene / Q000009:adverse effects* / Q000378:metabolism / Q000652:urine; D013954:Thyroglobulin / Q000276:immunology; D013961:Thyroid Gland / Q000187:drug effects / Q000502:physiology*; D013972:Thyrotropin / Q000097:blood; D013973:Thyrotropin-Releasing Hormone; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
D000906:Antibodies; D006038:Glyoxylates; D008333:Mandelic Acids; D014284:Triiodothyronine; C012482:phenylglyoxylic acid; D020058:Styrene; D013973:Thyrotropin-Releasing Hormone; D013972:Thyrotropin; D002116:Calcitonin; D013954:Thyroglobulin; D003404:Creatinine; D007453:Iodide Peroxidase; C037938:mandelic acid; D013974:Thyroxine