Conducted by Kim Harley and Brenda Eskenazi, from the University of California, Berkeley, and published in the journal Human Reproduction, the study shows an association between certain phthalates, parabens and phenols and precocious puberty in girls. [1]
Starting with the observation that girls are experiencing pubertal onset at progressively younger ages, study leader Professor Harley and her team analyzed data from 338 mothers and their children who were monitored from birth to adolescence.
Mothers and children
Researchers have enrolled pregnant women in 1999-2000. Mothers were mostly Latina, living below the federal poverty threshold and without a high school diploma. The mothers were first interviewed during pregnancy.
The researchers then measured concentrations of a variety of chemical substances in urine collected from mothers during pregnancy and from children at age 9. Three types of substances were targeted:
– three phthalate metabolites (monoethyl phthalate [MEP], mono-n-butyl phthalate and mono-isobutyl phthalate);
– methyl and propyl paraben;
– and four other phenols (triclosan, benzophenone-3 and 2,4- and 2,5-dichlorophenol).
The three compounds cited above were present in 90 percent of samples, with the exception of triclosan (a type of phenol) which was detected in 73 percent of samples collected from expectant mothers and 69 percent of samples from the 9-years-old children.
In parallel, pubertal timing was assessed among 179 girls and 159 boys every 9 months between ages 9 and 13 using clinical Tanner staging.
Prenatal exposition
The research found that girls prenatally exposed to these compounds are more likely to experience earlier puberty, and this risk is particularly high for the daughters of mothers exposed to monoethyl phthalate MEP concentrations and triclosan (TCS) and 2,4-dichlorophenol (2,4-DCP) concentrations.
The researchers found that higher concentrations of MEP and triclosan in prenatal urine was associated with changes in the timing of children’s development milestones. The higher the concentrations, the earlier puberty signs appear. A problematic situation in a context where the differences of exposure, within the women enlisted in the study, could vary from 1 to 20 according to the substances.
Possible reverse causality
Previous researches on rats (Bateman and Patisaul, 2008 and Rasier et al., 2006) have shown that phenols, parabens and phthalates might have endocrine disruptors effects. However, no studies have examined the effects of these substances on humans, both during the prenatal period and in the period before puberty. “This complicates our comparison with other studies,” explain the authors.
The researchers also warn that their “findings with peripubertal exposure to methyl and propyl parabens could reflect reverse causality if, for example, girls and boys who entered puberty early were more likely to use personal care products containing these preservatives compared to children entering puberty later.”
Indeed, these chemicals are quickly metabolized and are found very quickly in the urine (in 24 to 48 hours). Therefore, one to two urinary measurements per developmental point may not accurately reflect usual exposure.
The authors also mention another limitation of their study. The population which was observed is limited to Latino children of low socioeconomic status living in a farmworker community. The role of other environmental exposures, such as pesticides, cannot be excluded.
Despite these limitations, the authors consider their study is methodologically strong, with a longitudinal design, measurements of exposure biomarkers during two critical windows of development. It “contributes to a growing literature that suggests that exposure to certain endocrine disrupting chemicals may impact timing of puberty in children.”
