Prenatal Phenol and Phthalate Exposures and Birth Outcomes
Prenatal Phenol and Phthalate Exposures and Birth Outcomes
Background: Many phthalates and phenols are hormonally active and are suspected to alter the course of development.
Objective: We investigated prenatal exposures to phthalate and phenol metabolites and their associations with body size measures of the infants at birth.
Methods: We measured 5 phenol and 10 phthalate urinary metabolites in a multiethnic cohort of 404 women in New York City during their third trimester of pregnancy and recorded size of infants at birth.
Results: Median urinary concentrations were > 10 µg/L for 2 of 5 phenols and 6 of 10 phthalate monoester metabolites. Concentrations of low-molecular-weight phthalate monoesters (low-MWP) were approximately 5-fold greater than those of high-molecular-weight metabolites. Low-MWP metabolites had a positive association with gestational age [0.97 day gestational age per ln-biomarker ; 95% confidence interval (CI) , 0.07-1.9 days, multivariate adjusted] and with head circumference. Higher prenatal exposures to 2,5-dichlorophenol (2,5-DCP) predicted lower birth weight in boys (-210 g average birth weight difference between the third tertile and first tertile of 2,5-DCP ; 95% CI, 71-348 g) . Higher maternal benzophenone-3 (BP3) concentrations were associated with a similar decrease in birth weight among girls but with greater birth weight in boys.
Conclusions: We observed a range of phthalate and phenol exposures during pregnancy in our population, but few were associated with birth size. The association of 2,5-DCP and BP3 with reduced or increased birth weight could be important in very early or small-size births. In addition, positive associations of urinary metabolites with some outcomes may be attributable partly to unresolved confounding with maternal anthropometric factors.
Phthalates and phenols include a number of chemicals that are hormonally active and therefore might be expected to alter the course of fetal development. Fetal exposure is indicated by their detection in amniotic fluid (Bradman et al. 2003; Engel et al. 2006). Phthalates are widely dispersed in the environment, coming mainly from personal products (low- and high-molecular-weight phthalates) and household items (high molecular weight). Extensive experimental research on reproductive effects of phthalates has underscored their antiandrogenic activity. Changes in birth weight or early body weight in rodents after prenatal exposure to various phthalates have been reported (Sharpe et al. 1995; Tanaka 2002, 2003, 2005), but reports of no effects also exist (Arcadi et al. 1998; Hoshino et al. 2005). Of interest, butylbenzyl phthalate given to rats at high doses leads to lower birth weight and shorter anogenital distance in male pups (Tyl et al. 2004). Data in humans are sparse, but reports in male infants are consistent with the animal literature (Main et al. 2006; Swan et al. 2005), as are effects on male reproductive function (Hauser et al. 2006). Both low- and high-molecular-weight phthalates have been implicated in these biologic effects.
Less is known about phenols and their precursors. Bisphenol A (BPA) has elicited great interest because of its hormonal activity; it is found in resins and polymers used for dental sealants and container linings. BPA is hormonally active in rodents exposed in early life (Lee et al. 2005). Prenatal alkylphenol exposures have been linked with both reduced and increased birth weight in rodents (Ferguson et al. 2000; Latendresse et al. 2001; Sharpe et al. 1995). 2,5-Dichlorophenol (2,5-DCP), another phenol, is a metabolite of 1,4-dichlorobenzene (1,4-DCB), which causes lower birth weight and decreased maternal weight gain in the rat (Marsman 1995).
Among U.S. residents, urinary concentrations of biomarkers derived from phthalates and phenols have been relatively high compared with pesticides (Centers for Disease Control and Prevention 2005; Silva et al. 2004). The highly prevalent exposures in humans and their broad hormonal activity in experimental models led us to hypothesize that they might impair fetal development. Therefore, we investigated prenatal exposures to these agents and their relationships with birth outcomes, including birth weight and gestational age, in a multiethnic cohort of women enrolled during pregnancy.
Background: Many phthalates and phenols are hormonally active and are suspected to alter the course of development.
Objective: We investigated prenatal exposures to phthalate and phenol metabolites and their associations with body size measures of the infants at birth.
Methods: We measured 5 phenol and 10 phthalate urinary metabolites in a multiethnic cohort of 404 women in New York City during their third trimester of pregnancy and recorded size of infants at birth.
Results: Median urinary concentrations were > 10 µg/L for 2 of 5 phenols and 6 of 10 phthalate monoester metabolites. Concentrations of low-molecular-weight phthalate monoesters (low-MWP) were approximately 5-fold greater than those of high-molecular-weight metabolites. Low-MWP metabolites had a positive association with gestational age [0.97 day gestational age per ln-biomarker ; 95% confidence interval (CI) , 0.07-1.9 days, multivariate adjusted] and with head circumference. Higher prenatal exposures to 2,5-dichlorophenol (2,5-DCP) predicted lower birth weight in boys (-210 g average birth weight difference between the third tertile and first tertile of 2,5-DCP ; 95% CI, 71-348 g) . Higher maternal benzophenone-3 (BP3) concentrations were associated with a similar decrease in birth weight among girls but with greater birth weight in boys.
Conclusions: We observed a range of phthalate and phenol exposures during pregnancy in our population, but few were associated with birth size. The association of 2,5-DCP and BP3 with reduced or increased birth weight could be important in very early or small-size births. In addition, positive associations of urinary metabolites with some outcomes may be attributable partly to unresolved confounding with maternal anthropometric factors.
Phthalates and phenols include a number of chemicals that are hormonally active and therefore might be expected to alter the course of fetal development. Fetal exposure is indicated by their detection in amniotic fluid (Bradman et al. 2003; Engel et al. 2006). Phthalates are widely dispersed in the environment, coming mainly from personal products (low- and high-molecular-weight phthalates) and household items (high molecular weight). Extensive experimental research on reproductive effects of phthalates has underscored their antiandrogenic activity. Changes in birth weight or early body weight in rodents after prenatal exposure to various phthalates have been reported (Sharpe et al. 1995; Tanaka 2002, 2003, 2005), but reports of no effects also exist (Arcadi et al. 1998; Hoshino et al. 2005). Of interest, butylbenzyl phthalate given to rats at high doses leads to lower birth weight and shorter anogenital distance in male pups (Tyl et al. 2004). Data in humans are sparse, but reports in male infants are consistent with the animal literature (Main et al. 2006; Swan et al. 2005), as are effects on male reproductive function (Hauser et al. 2006). Both low- and high-molecular-weight phthalates have been implicated in these biologic effects.
Less is known about phenols and their precursors. Bisphenol A (BPA) has elicited great interest because of its hormonal activity; it is found in resins and polymers used for dental sealants and container linings. BPA is hormonally active in rodents exposed in early life (Lee et al. 2005). Prenatal alkylphenol exposures have been linked with both reduced and increased birth weight in rodents (Ferguson et al. 2000; Latendresse et al. 2001; Sharpe et al. 1995). 2,5-Dichlorophenol (2,5-DCP), another phenol, is a metabolite of 1,4-dichlorobenzene (1,4-DCB), which causes lower birth weight and decreased maternal weight gain in the rat (Marsman 1995).
Among U.S. residents, urinary concentrations of biomarkers derived from phthalates and phenols have been relatively high compared with pesticides (Centers for Disease Control and Prevention 2005; Silva et al. 2004). The highly prevalent exposures in humans and their broad hormonal activity in experimental models led us to hypothesize that they might impair fetal development. Therefore, we investigated prenatal exposures to these agents and their relationships with birth outcomes, including birth weight and gestational age, in a multiethnic cohort of women enrolled during pregnancy.
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