Embryotoxic effects of di-2-ethylhexyl phthalate (DEHP) and di-n-butyl phthalate (DBP) in mice

Shiota, Kohei; Chou, Ming-Jen; Nishimura, Hideo

doi:10.1016/0013-9351(80)90136-x

Cited by 85 publications

(39 citation statements)

References 26 publications

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“…Furthermore, administration of DBP and DEHP to pregnant rats interferes with normal fetal development in male offspring (15). Regarding reproductive and developmental effects, phthalates vary in potency, with DEHP being the most potent and DBP and BzBP roughly an order of magnitude less potent (8)(9)(10)(11)(12)(13)(14)(15).Based on the varied toxicities of phthalates, internal dose measurements of specific phthalates and their monoester metabolites (16) are important for exposure assessment, and ultimately for accurate human risk assessment. Previous methods for assessing human exposure to phthalates have been subject to laboratory and sample-collection contamination problems from these environmentally ubiquitous compounds (17)(18)(19)(20).…”

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“…Di-(2-ethylhexyl) phthalate (DEHP) is a rodent liver carcinogen through a mechanism thought to involve peroxisome proliferation (5); however, carcinogenicity by this mechanism is unlikely to be relevant to humans (6,7). Several phthalates, DEHP, dibutyl phthalate (DBP), and benzyl butyl phthalate (BzBP), are teratogenic in animals (8)(9)(10). DBP is also toxic to the testes, possibly through its metabolite, monobutyl phthalate (MBP) (11,12); other phthalate metabolites, monobenzyl phthalate (MBzP) and mono-2-ethylhexyl phthalate (MEHP), are Sertoli cell toxicants and teratogens in animals (13,14).…”

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Levels of Seven Urinary Phthalate Metabolites in a Human Reference Population

Blount¹,

Silva²,

Caudill³

et al. 2000

Environmental Health Perspectives

117

147

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Dialkyl or alkyl aryl esters of 1,2-benzenedicarboxylic acid, commonly called phthalates, are ubiquitous industrial chemicals with a wide range of chemical and toxicologic characteristics. Phthalates are used primarily as plasticizers in flexible polyvinyl chloride (PVC) products such as blood bags and children's toys. Nonpolymeric uses of phthalates as fixatives, detergents, lubricating oils, and solvents lead to their inclusion in numerous and diverse products such as cosmetics and wood finishes. The widespread use of phthalates results in multiple human exposure routes (oral, dermal, inhalation, and intravenous). Phthalates are lipophilic compounds that appear not to bioaccumulate (1). Phthalates are rapidly metabolized to their respective monoesters and further oxidative products, which are glucuronidated and excreted through the urine and feces (1-4).Animal toxicology of several phthalates has been studied. Di-(2-ethylhexyl) phthalate (DEHP) is a rodent liver carcinogen through a mechanism thought to involve peroxisome proliferation (5); however, carcinogenicity by this mechanism is unlikely to be relevant to humans (6,7). Several phthalates, DEHP, dibutyl phthalate (DBP), and benzyl butyl phthalate (BzBP), are teratogenic in animals (8-10). DBP is also toxic to the testes, possibly through its metabolite, monobutyl phthalate (MBP) (11,12); other phthalate metabolites, monobenzyl phthalate (MBzP) and mono-2-ethylhexyl phthalate (MEHP), are Sertoli cell toxicants and teratogens in animals (13,14). Furthermore, administration of DBP and DEHP to pregnant rats interferes with normal fetal development in male offspring (15). Regarding reproductive and developmental effects, phthalates vary in potency, with DEHP being the most potent and DBP and BzBP roughly an order of magnitude less potent (8)(9)(10)(11)(12)(13)(14)(15).Based on the varied toxicities of phthalates, internal dose measurements of specific phthalates and their monoester metabolites (16) are important for exposure assessment, and ultimately for accurate human risk assessment. Previous methods for assessing human exposure to phthalates have been subject to laboratory and sample-collection contamination problems from these environmentally ubiquitous compounds (17)(18)(19)(20). For this reason, previous measurements of internal phthalate dose have focused on highly exposed people (21,22). As the primary urinary metabolite, phthalate monoesters are useful biomarkers of specific phthalate exposure.We report the urinary phthalate monoester levels for a human reference population using a new, highly selective technique (23). This analytical approach allows us to directly measure the individual phthalate metabolites responsible for the reproductive and developmental toxicity of phthalates in animals while avoiding contamination from the ubiquitous parent compound. The metabolites measured are monoethyl phthalate (MEP), MBP, MBzP, mono-n-octyl phthalate, MEHP, and mono-3-methyl-5-dimethylhexyl phthalate (monoisononyl, MINP). Commercially used di-isononyl p...

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confidence: 99%

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Levels of Seven Urinary Phthalate Metabolites in a Human Reference Population

Blount¹,

Silva²,

Caudill³

et al. 2000

Environmental Health Perspectives

117

147

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“…In addition, rural women of childbearing age had higher levels of benzyl butyl phthalate compared with those of older rural women. This is of concern because both of these phthalate isomers have been implicated in animal studies of reproductive toxicity (Gray 1998;Jobling et al 1995;Shiota et al 1980;Wilkinson and Lamb 1999). Human studies are scarce, but a recently published case-control study examined the association between premature thelarche (premature breast development) and phthalate exposure among girls 6 months to 8 years of age (Colon et al 2000).…”

Section: Compounds In the Femalementioning

confidence: 99%

Off to a good start: the influence of pre- and periconceptional exposures, parental fertility, and nutrition on children's health.

Chapin

Robbins

Schieve

et al. 2004

Environ Health Perspect

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The scientific community is developing a compelling body of evidence that shows the importance of the in utero environment (including chemical and hormonal levels) to the ultimate health of the child and even of the aging adult. This article summarizes the evidence that shows this impact begins with conception. Only a full life-cycle evaluation will help us understand these impacts, and only such an understanding will produce logically prioritized mitigation strategies to address the greatest threats first. Clearly, the time for analysis begins when the next generation is but a twinkle in the eye.

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“…Yagi et al (21) When DEHP or di-n-butyl phthalate (DBP) was administered in the diet of pregnant mice, the major teratogenic effects observed were neural tube defects (exencephaly and spina bifida) (23,24). DEHP and DBP caused intrauterine growth retardation and delayed ossification.…”

Section: Teratologymentioning

confidence: 99%

Effects of Phthalic Acid Esters (PAEs) on the Neonate and Aspects of Teratogenic Actions

Thomas¹,

Wienckowski²,

Gillies³

et al. 1986

Environmental Health Perspectives

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A review of the literature reveals that several different phthalic acid esters (PAEs) are capable of causing testicular damage. Phthalate-induced zinc deficiency is consistent with germinal epithelial damage. Among experimental animals, mice perhaps show the greatest sensitivity to phthalate-induced terata, but high doses/exposure are required. Little toxicologic information is available with regard to phthalate-induced effects upon the neonate.

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Embryotoxic effects of di-2-ethylhexyl phthalate (DEHP) and di-n-butyl phthalate (DBP) in mice

Cited by 85 publications

References 26 publications

Levels of Seven Urinary Phthalate Metabolites in a Human Reference Population

Levels of Seven Urinary Phthalate Metabolites in a Human Reference Population

Off to a good start: the influence of pre- and periconceptional exposures, parental fertility, and nutrition on children's health.

Effects of Phthalic Acid Esters (PAEs) on the Neonate and Aspects of Teratogenic Actions

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