C de Felice, G Presta, A del Vecchio, I Paris, F Ruggieri and P
Mazzeo. 2003. In utero exposure to di-(2-ethylhexyl)-phthalate
and human pregnancy duration. Environmental
Health Perspectives, on line 19 August 2003.
et al. confirm significant and widespread presence of the
phthalate DEHP and its metabolite, MEHP, in the blood of newborn
infants in an Italian hospital. 88% of cord blood samples had DEHP
and/or MEHP. They also report a small but statistically significant
increase in risk of preterm birth associated with exposure to MEHP.
link between MEHP and preterm birth is important. Premature
birth has risen 23% in the US since the 1980s. Infants born
prematurely are more at risk to infant mortality and then, if they
survive, to a pattern of health problems throughout life.
consensus has been reached about why preterm birth is increasing,
although contamination in the womb has been identified as a potential
factor. A recent
study, for example, showed an increased risk of preterm birth
associated with DDE levels. DDE exposures, however, have dropped
over the past 20 years since DDT was banned. Hence DDE cannot be
causing the current rise. Thus this new link to a ubiquitous contaminant
identifies a new avenue of research for understanding preterm birth's
did they do? Latini et al. took cord blood from
babies at birth in a hospital in Brindisi, Italy. They then analyzed
the blood for the phthalate di-(2-ethylhexyl)-phthalate (DEHP) and
mono-ethylhexyl-phthalate (MEHP). In a statistical analysis, they
then examined the relationships between several aspects of the infants'
health at birth and exposure to DEHP and MEHP
did they find? The study focused on babies born in 84 consecutive
births in the Brindisi hospital. Of them, 39 were male, 45 female.
Eleven out of the 84 were preterm, with only 3 very low birth weight
infants. Four of them were considered "small
for gestational age." None were the result of in vitro
found DEHP and/or MEHP present in 88% of the cord serum samples
they measured. Both were present in 77%. The concentrations averaged
1.19±1.15 µg/ml DEHP and 0.52±0.61 µg/ml
with MEHP had a significantly lower gestational age than those
without MEHP exposures, averaging 38 vs 39 weeks. This difference
was statistically significant, based on a regression analysis
(p=0.019). The chance of preterm birth was increased by 50%
in babies with MEHP exposure (odds ratio= 1.5; 95% confidence
graph on the right compares gestational age of babies with
MEHP exposure (red) to those without (green). Not only are
there no babies with extremely short gestation periods in
the sample of of babies without MEHP, there are proportionally
fewer with gestation lengths of 34 to 38 weeks compared to
the babies with MEHP exposure.
other infant characteristics, including sex, birth weight and neonatal
jaundice showed no association with phthalate exposure.
does it mean? These results open up new chapters in (1)
the search for why preterm birth rates are increasing in the US,
and (2) the possible health consequences of exposure to the phthalate
DEHP. Given the relatively small sample size, this work bears repeating
before firm conclusions can be reached. But the striking difference
it reveals in the distribution of gestational ages of babies with
MEHP exposure vs. those without (figure above) should command the
attention of medical researchers trying to explain the pre-term
birth epidemic. As the US Centers for Disease has established, phthalate
exposure is widespread in American women. Now this study reveals
a link between one phthalate, DEHP, and preterm birth.
is worth noting that DEHP, like DDE (discussed above), is an anti-androgen
(it interferes with the ability of androgen to bind with the androgen
receptor and turn on the suite of genes that androgen normally activates).
Whether this common mode of action is a clue to the causation of
preterm birth remains to be established.
they resolve whether these results are real or artifactual, it would
be sensible to avoid DEHP/MEHP exposures during pregnancy.