Phthalates in the <scp>NICU</scp>: Is it safe?

Fischer, Cyril; Graz, Myriam Bickle; Muehlethaler, Vincent; Palmero, David; Tolsa, Jean-François

doi:10.1111/jpc.12244

Cited by 34 publications

(20 citation statements)

References 51 publications

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“…The dose of 10 mg/kg was more relevant to the environmental exposure for children undergoing medical interventions and for adult blood transfusion patients (Fischer et al, 2013; Loff et al, 2000; Lyche et al, 2009; Schettler, 2006; Wittassek and Angerer, 2008). …”

Section: Discussionmentioning

confidence: 99%

“…Because phthalates have been described as anti-androgenic compounds, males are considered a particularly susceptible population (David, 2003; Fisher, 2004; Frederiksen et al, 2007; Knez, 2013; Lyche et al, 2009; Ventrice et al, 2013). While the measured exposure to phthalates in the general population has been considered below tolerable levels of intake, children undergoing medical interventions may be exposed to significantly higher quantities of phthalates through equipment and medical devices (Fischer et al, 2013; Lyche et al, 2009; Wittassek and Angerer, 2008). The dose of phthalate exposure in these children has been estimated up to 10 – 20 mg/kg/day (Loff et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

“…However, another study did not show any association between phthalate metabolites and reproductive biomarkers (Jonsson et al, 2005). Thus, due to the limitations of epidemiological studies, there is yet no definite answer to whether phthalate exposure in humans imposes a significant health risk (Fischer et al, 2013; Johnson et al, 2012; Kamrin, 2009; Lyche et al, 2009). …”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Phthalate esters affect maturation and function of primate testis tissue ectopically grafted in mice

Rodriguez‐Sosa

Bondareva

Tang

et al. 2014

Molecular and Cellular Endocrinology

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Di-n-Butyl (DBP) and Di-(2-EthylHexyl) (DEHP) phthalates can leach from daily-use products resulting in environmental exposure. In male rodents, phthalate exposure results in reproductive effects. To evaluate effects on the immature primate testis, testis fragments from 6-month-old rhesus macaques were grafted subcutaneously to immune-deficient mice, which were exposed to 0, 10, or 500 mg/kg of DBP or DEHP for 14 weeks or 28 weeks (DBP only). DBP exposure reduced the expression of key steroidogenic genes, indicating that Leydig cell function was compromised. Exposure to 500 mg/kg impaired tubule formation and germ cell differentiation and reduced numbers of spermatogonia. Exposure to 10 mg/kg did not affect development, but reduced Sertoli cell number and resulted in increased expression of inhibin B. Exposure to DEHP for 14 week also affected steroidogenic genes expression. Therefore, long-term exposure to phthalate esters affected development and function of the primate testis in a time and dosage dependent manner.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Phthalate esters affect maturation and function of primate testis tissue ectopically grafted in mice

Rodriguez‐Sosa

Bondareva

Tang

et al. 2014

Molecular and Cellular Endocrinology

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“…This source of exposure presents a general public health concern. Indeed, the metabolites of these plasticizers are found in the urine of many hospitalized patients, particularly neonates in intensive care units (Mallow & Fox, ; Fischer, Bickle Graz, Muehlethaler, Palmero, & Tolsa, ). Some of these chemicals are likely to be hazardous for patients, as has been demonstrated for di‐(2‐ethylhexyl)phthalate (DEHP), which is now classified as CMR 1B (carcinogenic, mutagenic or toxic for reproduction) under the CLP Regulation due to its effect on reproduction and fertility (Regulation (EU) 1272/2008, ).…”

Section: Introductionmentioning

confidence: 99%

In vitro and in silico hormonal activity studies of di‐(2‐ethylhexyl)terephthalate, a di‐(2‐ethylhexyl)phthalate substitute used in medical devices, and its metabolites

Kambia

Séverin

Farce

et al. 2019

J of Applied Toxicology

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Plasticizers added to polyvinylchloride used in medical devices can be released into patients’ biological fluids. The substitution of di‐(2‐ethylhexyl)phthalate (DEHP) by alternative plasticizers is essential but their safety must be demonstrated. DEHP, di‐(2‐ethylhexyl)terephthalate (DEHT) and their metabolites were investigated using level 2 Organization for Economic Co‐operation and Development bioassays to screen for in vitro hormonal changes. Differences between the DEHP and DEHT metabolites were observed. Albeit weak, the hormonal activities of DEHT‐derived metabolites, e.g., 5‐OH metabolite of mono‐(ethylhexyl)terephthalate (5‐OH‐MEHT), were detected and the results of docking experiments performed on estrogen receptor alpha and androgen receptor agreed with the biological results. A co‐stimulation of human estrogen receptor alpha and human androgen receptor was also observed. With regard to steroidogenesis, a 16‐fold increase in estrogen synthesis was measured with 5‐OH‐MEHT. Therefore, even if DEHT remains an interesting alternative to DEHP because of its low migration from medical devices, it seems important to verify that multi‐exposed patients in neonatal intensive care units do not have urinary levels of oxidized metabolites, in particular 5‐OH‐MEHT, suggesting a potential endocrine‐disrupting effect.

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“…Exposure continues through the newborn’s environment (61), baby formula, or breast milk (62). Concerns have been raised about the risks of phthalates in newborns and infants, because they have the highest levels of exposure, whether from the environment or perinatal medical interventions (63–65). …”

Section: The Plasticizer Dehp Pollutes Our Environmentmentioning

confidence: 99%

Mechanisms Mediating Environmental Chemical-Induced Endocrine Disruption in the Adrenal Gland

Martinez–Arguelles

Papadopoulos

2015

Front. Endocrinol.

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Humans are continuously exposed to hundreds of man-made chemicals that pollute the environment in addition to multiple therapeutic drug treatments administered throughout life. Some of these chemicals, known as endocrine disruptors (EDs), mimic endogenous signals, thereby altering gene expression, influencing development, and promoting disease. Although EDs are eventually removed from the market or replaced with safer alternatives, new evidence suggests that early-life exposure leaves a fingerprint on the epigenome, which may increase the risk of disease later in life. Epigenetic changes occurring in early life in response to environmental toxicants have been shown to affect behavior, increase cancer risk, and modify the physiology of the cardiovascular system. Thus, exposure to an ED or combination of EDs may represent a first hit to the epigenome. Only limited information is available regarding the effect of ED exposure on adrenal function. The adrenal gland controls the stress response, blood pressure, and electrolyte homeostasis. This endocrine organ therefore has an important role in physiology and is a sensitive target of EDs. We review herein the effect of ED exposure on the adrenal gland with particular focus on in utero exposure to the plasticizer di(2-ethylehyl) phthalate. We discuss the challenges associated with identifying the mechanism mediating the epigenetic origins of disease and availability of biomarkers that may identify individual or population risks.

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Phthalates in the NICU: Is it safe?

Abstract: Clinicians must be aware of the potential risks due to phthalate exposure in the NICU. Di(2-ethylhexyl)phthalate containing materials should be identified and alternative devices should be considered. There is a need to improve knowledge in this area.

Cited by 34 publications

References 51 publications

Phthalate esters affect maturation and function of primate testis tissue ectopically grafted in mice

Phthalate esters affect maturation and function of primate testis tissue ectopically grafted in mice

In vitro and in silico hormonal activity studies of di‐(2‐ethylhexyl)terephthalate, a di‐(2‐ethylhexyl)phthalate substitute used in medical devices, and its metabolites

Mechanisms Mediating Environmental Chemical-Induced Endocrine Disruption in the Adrenal Gland

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