Perinatal dioxin exposure and neurodevelopment of 2-year-old Vietnamese children in the most contaminated area from Agent Orange in Vietnam

Pham, Ngoc Thao; Nishijo, Muneko; Tran, Ngoc Nghi; Lê, Văn Quân; Tran, Hai Anh; Phan, Huy Anh Vu; Nishino, Yoshikazu; Nishijo, Hisao

doi:10.1016/j.scitotenv.2019.04.425

Cited by 24 publications

(20 citation statements)

References 46 publications

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“…The intrauterine environment has been linked to multiple aging-related diseases, and maternal chemical exposures during pregnancy are risk modifiers for these diseases. For example, AHR activation by TCDD or related chemicals in the fetus has been linked to increased risk for eczema ( Ye et al, 2018 ), autoimmune diseases ( Gogal and Holladay, 2008 ), neurodevelopmental disorders ( Pham et al, 2019 ) and impairment of mammary gland differentiation ( Vorderstrasse et al, 2004 ), as well as others. To test whether fetal TCDD exposure changes urinary function in adult male mice, a single dose of TCDD (1 µg/kg, oral maternal dose) was given at embryonic day (E)13.5 (resulting in continuous exposure beginning in utero and throughout lactation), and urinary function was evaluated by cystometry in anesthetized male mice on postnatal day (P)90-P98.…”

Section: Resultsmentioning

confidence: 99%

A mechanism linking perinatal 2,3,7,8 tetrachlorodibenzo-p-dioxin exposure to lower urinary tract dysfunction in adulthood

Turco

Oakes

Stietz

et al. 2021

Disease Models &Amp; Mechanisms

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Benign Prostatic Hyperplasia / Lower Urinary Tract Dysfunction (BPH/LUTD) is a classic disease of aging which affects nearly all men. Symptoms typically present in the fifth or sixth decade and progressively worsen over the remainder of life. Here, we identify a surprising origin of this disease that traces back to the intrauterine environment of the developing male, challenging existing paradigms about when this disease process begins. We delivered a single bolus dose of a widespread environmental contaminant, present in the serum of most Americans (2,3,7,8 tetrachlorodibenzo-p-dioxin, TCDD, 1 µg/kg), and representative of a broader class of environmental contaminants, to pregnant mice and observed an increase in the abundance of a neurotrophic factor, artemin, in the developing mouse prostate. Artemin is required for noradrenergic axon recruitment across multiple tissues and TCDD rapidly increases prostatic noradrenergic axon density in the male fetus. The hyperinnervation does not resolve, but rather persists into adulthood, when it is coupled to autonomic hyperactivity of prostatic smooth muscle and abnormal urinary function, including increased urinary frequency, a bothersome symptom in men. We offer new evidence that prostate neuroanatomical development is malleable and that intrauterine chemical exposures can permanently reprogram prostate neuromuscular function to cause male LUTD in adulthood.

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Section: Resultsmentioning

confidence: 99%

A mechanism linking perinatal 2,3,7,8 tetrachlorodibenzo-p-dioxin exposure to lower urinary tract dysfunction in adulthood

Turco

Oakes

Stietz

et al. 2021

Disease Models &Amp; Mechanisms

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“…Sex-related difference in the sensitivity to the toxicity of dioxin have been reported in various species including mice, rats, and humans (Pohjanvirta et al., 2012). Perinatal dioxin exposure has affected the development of language and gross motor skins only in boys exposed to Agent Orange in Vietnam (Pham et al., 2019). In a national survey in the United States, the negative association between serum levels of PCBs and cognitive scores was stronger in women than in men (Bouchard et al., 2014).…”

Section: Discussionmentioning

confidence: 99%

Influence of dioxin-related compounds on physical function in Yusho incident victims

Fukushi

Tsushima

Matsumoto

et al. 2019

Heliyon

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Few studies have examined the influence of dioxin-related compounds on human physical function, and existing results are inconsistent. In 1968, accidental human exposure to rice oil contaminated with dioxin-related compounds resulted in the development of Yusho oil disease in Japan. We aimed to determine whether the degree of exposure to dioxin-related compounds was associated with physical function in Yusho patients. Methods: In 2016, 65 men (average age: 65.7 years) and 77 women (average age: 64.7 years) participated in a nationwide health examination in Fukuoka prefecture. Functional reach, gait speed, hand grip strength, and toe grip strength were evaluated as part of physical function. The serum levels of polychlorinated dibenzo-p-dioxin, polychlorinated dibenzofurans, and non-ortho polychlorinated biphenyls were measured using high-resolution gas chromatography and high-resolution mass spectrometry. We examined the association between physical function tests and serum toxic equivalency (TEQ) values. Results: A 10-fold increase in serum TEQ levels was negatively associated with functional reach (adjusted b ¼-4.07, p ¼ 0.017) and hand grip strength (adjusted b ¼-2.20, p ¼ 0.0245) in men. No association was observed between serum TEQ level and physical function in women. Conclusion: Our findings suggest that dioxin-related compounds have a negative influence on physical function in men. However, these findings should be interpreted carefully. Future studies examining additional data on musculoskeletal disorders are warranted.

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“…More recently, the Centers for Disease Control (CDC, 2019) and the Global Burden of Disease study, supervised by the Institute for Health Metrics and Evaluation (Shaffer et al, 2019), also urgently recommended additional studies on environmental health risk factors of disease including developmental neurotoxicants. These recommendations are supported by studies demonstrating negative effects on brain development and increased risk for neurodevelopmental disorders after environmental exposure to lead (Lanphear et al, 2005), mercury (Axelrad et al, 2007;Oken et al, 2008), air pollution (Chiu et al, 2013;Siddique et al, 2011;Suglia et al, 2008), organophosphorus pesticides (Bouchard et al, 2011;Engel et al, 2011), brominated flame retardants (Lam et al, 2017), polychlorinated biphenyls (PCBs; Pessah et al, 2019), polybrominated diphenyl ethers (PBDEs; Gibson et al, 2018), and dioxin (Ames et al, 2019;Nishijo et al, 2012;Pham et al, 2019;Tai et al, 2013). Additionally, the relative contributions of environmental exposures to the prevalence of neurodevelopmental disorders have been reported to be more substantial than nonchemical risk factors such as preterm birth, type 1 diabetes, and congenital heart disease as well as socioeconomic, nutritional, and psychosocial factors (Bellinger, 2012).…”

Section: Environmental Exposures and Neurodevelopmentmentioning

confidence: 98%

“…Populations with known exposure to TCDD have body burdens ranging from 96 to 7,000 ng/kg body weight, while the general population is estimated to have an average background TCDD concentration of approximately 58 ng/kg serum lipid, corresponding to a body burden of 13.5 ng/kg body weight (DeVito et al, 1995;Hojo et al, 2002). While there is evidence in humans correlating high-level, acute exposures with deficits in various metrics of neurodevelopment (Ames et al, 2019;Nishijo et al, 2012;Pham et al, 2019;Tai et al, 2013), the effects of lower, environmentally relevant levels of TCDD exposure are less well understood. Experimental studies in rodents, however, have linked gestational exposure to environmentally relevant levels of TCDD with impaired spatial learning and memory (Markowski et al, 2002), altered executive | 627 LATCHNEY ANd MAJEWSKA functions (Endo et al, 2012;Haijima et al, 2010;Kakeyama et al, 2014), and abnormal development of multiple brain areas including the cortex (Mitsuhashi et al, 2010) and the hippocampus (Latchney et al, 2011;Nguyen et al, 2013).…”

Section: Polychlorinated Dibenzodioxinsmentioning

confidence: 99%

Persistent organic pollutants at the synapse: Shared phenotypes and converging mechanisms of developmental neurotoxicity

Latchney

Majewska

2021

Developmental Neurobiology

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The developing nervous system is sensitive to environmental and physiological perturbations in part due to its protracted period of prenatal and postnatal development.Epidemiological and experimental studies link developmental exposures to persistent organic pollutants (POPs) including polychlorinated biphenyls, polychlorinated dibenzop-dioxins, polybrominated diphenyl ethers, and benzo(a)pyrene to increased risk for neurodevelopmental disorders in children. Mechanistic studies reveal that many of the complex cellular processes that occur during sensitive periods of rapid brain development are cellular targets for developmental neurotoxicants. One area of research interest has focused on synapse formation and plasticity, processes that How to cite this article: Latchney SE, Majewska AK. Persistent organic pollutants at the synapse: Shared phenotypes and converging mechanisms of developmental neurotoxicity.

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Perinatal dioxin exposure and neurodevelopment of 2-year-old Vietnamese children in the most contaminated area from Agent Orange in Vietnam

Cited by 24 publications

References 46 publications

A mechanism linking perinatal 2,3,7,8 tetrachlorodibenzo-p-dioxin exposure to lower urinary tract dysfunction in adulthood

A mechanism linking perinatal 2,3,7,8 tetrachlorodibenzo-p-dioxin exposure to lower urinary tract dysfunction in adulthood

Influence of dioxin-related compounds on physical function in Yusho incident victims

Persistent organic pollutants at the synapse: Shared phenotypes and converging mechanisms of developmental neurotoxicity

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