Phthalate Exposure Allegedly Linked to Fast-Food Consumption
A study has allegedly linked fast-food consumption to higher urinary
phthalate-metabolite levels but not to increased bisphenol A (BPA)
levels. Ami Zota, et al., “Recent Fast Food Consumption and Bisphenol
A and Phthalates Exposures among the U.S. Population in NHANES,
2003–2010,” Environmental Health Perspectives, April 2016. Using
24-hour dietary recall data obtained from 8,877 participants from the
National Health and Nutrition Examination Survey (NHANES 2003-
2010), researchers with George Washington University’s Milken Institute
School of Public Health apparently “observed evidence of a positive,
dose-response relationship between fast food intake and exposure
to phthalates.”
The study authors report that, compared to participants who did not
consume fast food, those who received more than 34 percent of their
total energy intake from fast food had 23.8 percent and 39 percent
higher levels of metabolites of di(2-ethylhexyl) phthalate (ΣDEHPm)
and diisononyl phthalate (DiNPm), respectively. In particular, the data
suggested that (i) “fast food-derived fat intake was also positively associated
with ΣDEHPm and DiNPm”; (ii) “ΣDEHPm was associated with
grain and other intake”; and (iii) “DiNPm was associated with meat and
grain intake.”
“Participants with high fast food intake had 20-40% higher urinary
concentrations of phthalate metabolites than non-consumers,” notes
the study. “The complexity and variability of fast food production makes
it difficult to identify the sources of high-molecular-weight phthalates,
though some likely sources have been suggested, including PVC gloves,
PVC tubing, and plastic packaging.”
Meanwhile, a separate study has apparently found no evidence associating
prenatal phthalate exposure with childhood fat mass in a New York
City cohort. Jessie Buckley, et al., “Prenatal Phthalate Exposures and
Childhood Fat Mass in a New York City Cohort,” Environmental Health
Perspectives, April 2016. The authors analyzed the phthalate metabolite
concentrations in the third-trimester maternal urine of approximately
400 women, as well as their children’s body composition during multiple
follow-up visits. After adjusting for multiple covariates, researchers
found “prenatal phthalate exposures were not associated with increased
body fat among children 4–9 years of age, though high prenatal DEHP
exposure may be associated with lower fat mass in childhood.”
“The finding that high prenatal DEHP exposure was associated with
lower body fat in children runs counter to the hypothesis that phthalates
are environmental obesogens,” explains a concurrent editorial.
“This hypothesis is based in part on evidence that phthalates interact
with peroxisome proliferator-activated receptors, which are involved in
metabolism. However, says first author Jessie Buckley, a postdoctoral
research associate in the Department of Epidemiology at the University
of North Carolina, ‘This finding is to some extent supported by animal
studies of relatively high dose postnatal DEHP exposure that report lower
body fat.’”
Issue 601
