Beatriz Suárez1, Fernando Vela-Soria2, Francesca Castiello3, Alicia Olivas-Martinez4, Dario Acuña-Castroviejo5, José Gómez-Vida6, Nicolás Olea7, Mariana F Fernández8, Carmen Freire9. 1. Instituto de Investigación Biosanitaria de Granada (ibs.GRANADA), 18012 Granada, Spain; CIBER de Epidemiología y Salud Pública (CIBERESP), Spain; Biomedical Research Center (CIBM), University of Granada, 18100 Granada, Spain. Electronic address: beatriz.suarez@ciberesp.es. 2. Instituto de Investigación Biosanitaria de Granada (ibs.GRANADA), 18012 Granada, Spain. Electronic address: fervs@ugr.es. 3. Instituto de Investigación Biosanitaria de Granada (ibs.GRANADA), 18012 Granada, Spain; Unidad de Gestión Clínica (UGC) de Pediatría, Hospital Universitario San Cecilio, 18016 Granada, Spain. 4. Instituto de Investigación Biosanitaria de Granada (ibs.GRANADA), 18012 Granada, Spain; Biomedical Research Center (CIBM), University of Granada, 18100 Granada, Spain. Electronic address: aolivas@ugr.es. 5. Instituto de Investigación Biosanitaria de Granada (ibs.GRANADA), 18012 Granada, Spain; Biomedical Research Center (CIBM), University of Granada, 18100 Granada, Spain; Department of Physiology, School of Medicine, University of Granada, 18071 Granada, Spain. Electronic address: dacuna@ugr.es. 6. Unidad de Gestión Clínica (UGC) de Pediatría, Hospital Universitario San Cecilio, 18016 Granada, Spain. 7. Instituto de Investigación Biosanitaria de Granada (ibs.GRANADA), 18012 Granada, Spain; CIBER de Epidemiología y Salud Pública (CIBERESP), Spain; Biomedical Research Center (CIBM), University of Granada, 18100 Granada, Spain; Department of Radiology and Physical Medicine, School of Medicine, University of Granada, 18071 Granada, Spain. Electronic address: nolea@ugr.es. 8. Instituto de Investigación Biosanitaria de Granada (ibs.GRANADA), 18012 Granada, Spain; CIBER de Epidemiología y Salud Pública (CIBERESP), Spain; Biomedical Research Center (CIBM), University of Granada, 18100 Granada, Spain; Department of Radiology and Physical Medicine, School of Medicine, University of Granada, 18071 Granada, Spain. Electronic address: marieta@ugr.es. 9. Instituto de Investigación Biosanitaria de Granada (ibs.GRANADA), 18012 Granada, Spain; CIBER de Epidemiología y Salud Pública (CIBERESP), Spain; Biomedical Research Center (CIBM), University of Granada, 18100 Granada, Spain. Electronic address: cfreire@ugr.es.
Abstract
OBJECTIVE: To examine the association between urinary metabolites of organophosphate (OP) pesticides and serum concentrations of thyroid and reproductive hormones in male adolescents and to assess the potential effect of interactions between OP pesticides and paraoxonase 1 (PON1) polymorphisms on hormone levels. METHODS: Study subjects (N = 117) were male 16- to 17-year-olds from the Environment and Childhood (INMA)-Granada cohort in Spain. Concentrations of 3,5,6-trichloro-2-pyridinol (TCPy), a metabolite of chlorpyrifos/chlorpyrifos-methyl, 2-isopropyl-6-methyl-4-pyrimidinol (IMPy), a metabolite of diazinon, and diethylthiophosphate (DETP) and diethyldithiophosphate (DEDTP), non-specific metabolites of OP pesticides, were measured in a spot urine sample from each subject and adjusted for creatinine. Levels of reproductive hormones (total testosterone [TT], estradiol [E2], dehydroepiandrosterone sulfate [DHEAS], sex hormone binding globulin [SHBG], luteinizing hormone [LH], follicle stimulating hormone [FSH], anti-Müllerian hormone [AMH], insulin growth factor 1 [IGF-1], and prolactin), thyroid hormones (free thyroxine [FT4], total triiodothyronine [TT3], and thyroid stimulating hormone [TSH]), and PON1 Q192R and L55M polymorphisms were determined in blood drawn during the same clinical visit. RESULTS: Multiple linear regression models showed that detectable levels of TCPy were associated with an increase in DHEAS and decreases in E2, FSH, and AMH; detectable IMPy with increases in E2, DHEAS, FSH, AMH, and prolactin and decreases in SHBG and LH; and detectable DETP with marginally-significant increases in TT and TT3 and decreases in FSH, AMH, and prolactin. The effect of IMPy and DETP on DHEAS and TT levels, respectively, was higher in subjects that carried the PON1 55MM genotype, while the effect of TCPy, IMPy, and DETP on thyroid hormone levels was higher in PON1 192QR/RR or 55MM genotype carriers. CONCLUSIONS: In male adolescents, non-occupational exposure to OP pesticides was associated with several changes in reproductive and thyroid hormone levels, and the magnitude of some associations was greater in adolescents genetically more susceptible to OP pesticide exposure who carry the PON1 55MM genotype.
OBJECTIVE: To examine the association between urinary metabolites of organophosphate (OP) pesticides and serum concentrations of thyroid and reproductive hormones in male adolescents and to assess the potential effect of interactions between OP pesticides and paraoxonase 1 (PON1) polymorphisms on hormone levels. METHODS: Study subjects (N = 117) were male 16- to 17-year-olds from the Environment and Childhood (INMA)-Granada cohort in Spain. Concentrations of 3,5,6-trichloro-2-pyridinol (TCPy), a metabolite of chlorpyrifos/chlorpyrifos-methyl, 2-isopropyl-6-methyl-4-pyrimidinol (IMPy), a metabolite of diazinon, and diethylthiophosphate (DETP) and diethyldithiophosphate (DEDTP), non-specific metabolites of OP pesticides, were measured in a spot urine sample from each subject and adjusted for creatinine. Levels of reproductive hormones (total testosterone [TT], estradiol [E2], dehydroepiandrosterone sulfate [DHEAS], sex hormone binding globulin [SHBG], luteinizing hormone [LH], follicle stimulating hormone [FSH], anti-Müllerian hormone [AMH], insulin growth factor 1 [IGF-1], and prolactin), thyroid hormones (free thyroxine [FT4], total triiodothyronine [TT3], and thyroid stimulating hormone [TSH]), and PON1 Q192R and L55M polymorphisms were determined in blood drawn during the same clinical visit. RESULTS: Multiple linear regression models showed that detectable levels of TCPy were associated with an increase in DHEAS and decreases in E2, FSH, and AMH; detectable IMPy with increases in E2, DHEAS, FSH, AMH, and prolactin and decreases in SHBG and LH; and detectable DETP with marginally-significant increases in TT and TT3 and decreases in FSH, AMH, and prolactin. The effect of IMPy and DETP on DHEAS and TT levels, respectively, was higher in subjects that carried the PON1 55MM genotype, while the effect of TCPy, IMPy, and DETP on thyroid hormone levels was higher in PON1 192QR/RR or 55MM genotype carriers. CONCLUSIONS: In male adolescents, non-occupational exposure to OP pesticides was associated with several changes in reproductive and thyroid hormone levels, and the magnitude of some associations was greater in adolescents genetically more susceptible to OP pesticide exposure who carry the PON1 55MM genotype.
Authors: Andrea Corrales Vargas; Jorge Peñaloza Castañeda; Emelie Rietz Liljedahl; Ana María Mora; Jose Antonio Menezes-Filho; Donald R Smith; Donna Mergler; Brian Reich; Andrew Giffin; Jane A Hoppin; Christian H Lindh; Berna van Wendel de Joode Journal: Sci Total Environ Date: 2021-10-28 Impact factor: 10.753
Authors: Jose V Tarazona; Maria Del Carmen González-Caballero; Mercedes de Alba-Gonzalez; Susana Pedraza-Diaz; Ana Cañas; Noelia Dominguez-Morueco; Marta Esteban-López; Irene Cattaneo; Andromachi Katsonouri; Konstantinos C Makris; Thorhallur I Halldorsson; Kristin Olafsdottir; Jan-Paul Zock; Jonatan Dias; Annelies De Decker; Bert Morrens; Tamar Berman; Zohar Barnett-Itzhaki; Christian Lindh; Liese Gilles; Eva Govarts; Greet Schoeters; Till Weber; Marike Kolossa-Gehring; Tiina Santonen; Argelia Castaño Journal: Toxics Date: 2022-06-09