Vulnerability of the developing brain to thyroid abnormalities: environmental insults to the thyroid system.

Porterfield, Susan P.

doi:10.1289/ehp.94102125

Cited by 160 publications

(64 citation statements)

References 59 publications

(69 reference statements)

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“…Irreversible neurologic damage resembling that seen in those exposed to thyroid hormone deficiency in utero and/or in infancy was also observed (2,11). In occupationally exposed workers, an increased prevalence of thyroid disorders and thyroid cancer (12,13) has been reported.…”

Section: Introductionmentioning

confidence: 85%

Increased thyroid volume and prevalence of thyroid disorders in an area heavily polluted by polychlorinated biphenyls

Langer

Tajtáková

Fodor³

et al. 1998

European Journal of Endocrinology

101

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Objective: To evaluate whether long-term exposure to heavy environmental pollution with polychlorinated biphenyls (PCBs) could result in impairment of thyroid status as evaluated by an epidemiological field survey. Methods: Thyroid volume (ThV) was measured by ultrasound in 238 employees of a factory (EMP) which previously produced PCBs and 454 adolescents from the surrounding area polluted by PCBs. Controls (C) were 572 adults and 965 adolescents from much less polluted areas. In the 238 EMP and various numbers (shown in parentheses) of adult C the levels of thyroid-stimulating hormone (TSH) (n ¼ 498), thyroxine (n ¼ 498), thyroglobulin (n ¼ 278) and thyroid antibodies (anti-peroxidase (TPO Ab), n ¼ 517; anti-thyroglobulin (Tg Ab), n ¼ 455; anti-TSH receptor (TSHR Ab), n ¼ 238) were estimated in serum, while only TSH and TPO Ab were measured in 269 and 171 adolescents from polluted and control areas respectively. In several subjects in whom thyroid disease was suspected, total tri-iodothyronine or free thyroxine and tri-iodothyronine were measured. In a total of 362 adults and adolescents the urinary iodine was estimated. Results: Using the Mann-Whitney test, ThV in EMP (mean Ϯ S.E. ¼ 18.85 Ϯ 0.69 ml, median ¼ 17.3 ml, upper quartile ¼ 22.9 ml, n ¼ 238) was significantly higher (P < 0.001) than that in C (13.47 Ϯ 0.48 ml, 11.5 ml, 15.3 ml, n ¼ 486 respectively). Similarly, ThV in adolescents from the polluted area (9.37 Ϯ 0.17 ml, 8.9 ml, 11.0 ml, n ¼ 454 respectively) was significantly higher (P < 0.001) than that in C (8.07 Ϯ 0.10 ml, 7.6 ml, 9.6 ml, n ¼ 965 respectively).In adults, a significantly increased prevalence of TPO Ab (P<0.05) was found (using the chi-square test) in EMP women of all ages (54/190) vs C women (70/282), in EMP women aged 31-50 years (40/117 vs 70/282 respectively) and those aged 41-50 years (28/77 vs 54/215 respectively). Compared with C, there was also a higher prevalence of Tg Ab in EMP women aged 31-60 years (36/169 vs 50/342 respectively) and of TSHR Ab (P < 0.001) in the group of EMP men and women (25/238) vs sex-and age-matched C (6/238).No difference between EMP and C was found in the level of thyroxine (mean Ϯ S.D. ¼ 116.1 Ϯ 31.2 nmol/l, n ¼ 238 vs 112.2 Ϯ 37.0 nmol/l, n ¼ 460 respectively), TSH in the range 0.1-4.5 mU/l (1.56 Ϯ 0.86 mU/l, n ¼ 219 vs 1.51 Ϯ 0.84 mU/l, n ¼ 460 respectively), prevalence of TSH >4.5 (14/238 vs 28/498 respectively) and <0.1 mU/l (5/238 vs 10/498 respectively). The prevalence of individuals without any defined clinical or laboratory signs of thyroid disorders among EMP who had worked in the factory for 21-35 years (43/128, 33.6%) was significantly lower than that in twice as many matched C (118/256, 46.1%, P < 0.025) or in EMP who had worked for only 11-20 years (36/73, 49.3%, P < 0.05).In adolescents, no difference was found in the prevalence of TPO Ab or TSH >4.5 mU/l between the polluted (17/269, 6.3% and 2/243, 0.8% respectively) and C areas (15/171, 8.5% and 4/140, 2.8% respectively). The median values of urinary iodine were in the op...

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Section: Introductionmentioning

confidence: 85%

Increased thyroid volume and prevalence of thyroid disorders in an area heavily polluted by polychlorinated biphenyls

Langer

Tajtáková

Fodor³

et al. 1998

European Journal of Endocrinology

101

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“…45 TH plays a crucial role during brain development, and disturbances in TH homeostasis can cause serious impairment in neurological development. 46,47 Therefore, it has been proposed that a disruption of TH homeostasis may explain the neurotoxicity of PBDEs. 12 Our previous study demonstrated that 150 days of exposing zebrafish embryos to DE-71 (1, 3, 10 μg/L) can elevate TH levels in adults and that increased TH levels are also transferred to F1 eggs.…”

Section: Environmental Science and Technologymentioning

confidence: 99%

Prenatal Transfer of Polybrominated Diphenyl Ethers (PBDEs) Results in Developmental Neurotoxicity in Zebrafish Larvae

Chen

Huang

et al. 2012

Environ. Sci. Technol.

156

100

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Parental exposure to polybrominated diphenyl ethers (PBDEs) in animals has been found to be transferred to the offspring. The environmental health risk and toxicity to the offspring are still unclear. The objective of the present study was to identify environmentally relevant concentrations of PBDEs for parental exposure that would cause developmental neurotoxicity in the offspring. Adult zebrafish were exposed to environmentally relevant concentrations of 0.8, 4.0 μg/L) via water. The results showed that PBDE exposure did not affect larvae hatching, malformation, or survival. The residue of PBDEs was detected in F1 eggs upon parental exposure. Acetylcholinesterase (AChE) activity was significantly inhibited in F1 larvae. Genes of central nervous system development (e.g., myelin basic protein, synapsin IIa, α1-tubulin) were significantly downregulated in larvae. Protein levels of α1-tubulin and synapsin IIa were also reduced. Decreased locomotion activity was observed in the larvae. This study provides the first evidence that parental exposure to environmentally relevant concentrations of PBDEs could cause adverse effects on neurodevelopment in zebrafish offspring.

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“…The latter hypothesis is based on the fact that brain development is highly dependent on thyroid hormones (114). PCBs and PCDDs that, like PBDEs, alter the thyroid hormone homeostasis have been suggested to disrupt brain development, resulting in permanent neurologic damage (115,116).…”

Section: Experimental Studies In Animalsmentioning

confidence: 99%

“…Because the development of the central nervous system is highly dependent on thyroid hormones, alterations in thyroid homeostasis may result in permanent neurobehavioral defects (114,115). It may also be the primary cause of neurodevelopmental toxicity of PBDEs.…”

Section: Experimental Studies In Animalsmentioning

confidence: 99%

Polybrominated diphenyl ethers: occurrence, dietary exposure, and toxicology.

Darnerud

Eriksen

Johannesson

et al. 2001

Environ Health Perspect

685

263

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Polybrominated diphenyl ethers (PBDEs) are used as flame retardants in plastics (concentration, 5--30%) and in textile coatings. Commercial products consist predominantly of penta-, octa-, and decabromodiphenyl ether mixtures, and global PBDE production is about 40,000 tons per year. PBDEs are bioaccumulated and biomagnified in the environment, and comparatively high levels are often found in aquatic biotopes from different parts of the world. During the mid-1970--1980s there was a substantial increase in the PBDE levels with time in both sediments and aquatic biota, whereas the latest Swedish data (pike and guillemot egg) may indicate that levels are at steady state or are decreasing. However, exponentially increasing PBDE levels have been observed in mother's milk during 1972--1997. Based on levels in food from 1999, the dietary intake of PBDE in Sweden has been estimated to be 0.05 microg per day. Characteristic end points of animal toxicity are hepatotoxicity, embryotoxicity, and thyroid effects as well as maternal toxicity during gestation. Recently, behavioral effects have been observed in mice on administration of PBDEs during a critical period after birth. Based on the critical effects reported in available studies, we consider the lowest-observed-adverse-effect level (LOAEL) value of the PBDE group to be 1 mg/kg/day (primarily based on effects of pentaBDEs). In conclusion, with the scientific knowledge of today and based on Nordic intake data, the possible consumer health risk from PBDEs appears limited, as a factor of over 10(6) separates the estimated present mean dietary intake from the suggested LOAEL value. However, the presence of many and important data gaps, including those in carcinogenicity, reproduction, and developmental toxicity, as well as additional routes of exposure, make this conclusion only preliminary. Moreover, the time trend of PBDEs in human breast milk is alarming for the future.

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Vulnerability of the developing brain to thyroid abnormalities: environmental insults to the thyroid system.

Cited by 160 publications

References 59 publications

Increased thyroid volume and prevalence of thyroid disorders in an area heavily polluted by polychlorinated biphenyls

Increased thyroid volume and prevalence of thyroid disorders in an area heavily polluted by polychlorinated biphenyls

Prenatal Transfer of Polybrominated Diphenyl Ethers (PBDEs) Results in Developmental Neurotoxicity in Zebrafish Larvae

Polybrominated diphenyl ethers: occurrence, dietary exposure, and toxicology.

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