Exposure to chemical found in personal care products may contribute to childhood obesity

[OKIsItJustMe]

Last edited Fri Jan 20, 2012, 12:16 PM - Edit history (1)

http://www.eurekalert.org/pub_releases/2012-01/tmsh-etc011912.php

[font face=Times,Times New Roman,Serif]Public release date: 20-Jan-2012

Contact: Mount Sinai Press Office
[e-mail]
212-241-9200
The Mount Sinai Hospital / Mount Sinai School of Medicine

[font size=5]Exposure to chemical found in personal care products may contribute to childhood obesity[/font]

[font size=3]Researchers from the Children's Environmental Health Center at The Mount Sinai Medical Center in New York have found an association between exposure to the chemical group known as phthalates and obesity in young children – including increased body mass index (BMI) and waist circumference.

Phthalates are man-made, endocrine-disrupting chemicals that can mimic the body's natural hormones. They are commonly used in plastic flooring and wall coverings, food processing materials, medical devices, and personal-care products. While poor nutrition and physical inactivity are known to contribute to obesity, a growing body of research suggests that environmental chemicals – including phthalates – could play a role in rising childhood obesity rates.

…

Mount Sinai researchers measured phthalate concentrations in the urine of 387 black and Hispanic children in New York City, and recorded body measurements including BMI, height, and waist circumference one year later. The urine tests revealed that greater than 97 percent of study participants had been exposed to phthalates typically found in personal care products such as perfume, lotions, and cosmetics; varnishes; and medication or nutritional supplement coatings. The phthalates included monoethyl phthalate (MEP) and other low molecular-weight phthalates. The team also found an association between concentrations of these phthalates with BMI and waist circumference among overweight children. For example, BMI in overweight girls with the highest exposure to MEP was 10 percent higher than those with the lowest MEP exposure.

"Research has shown that exposure to these everyday chemicals may impair childhood neurodevelopment, but this is the first evidence demonstrating that they may contribute to childhood obesity," said the study's lead author Susan Teitelbaum, PhD, Associate Professor in the Department of Preventive Medicine at Mount Sinai School of Medicine. "This study also further emphasizes the importance of reducing exposure to these chemicals where possible."

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http://dx.doi.org/10.1016/j.envres.2011.12.006

[MineralMan]

1. Association is not necessarily causation.

This study appears to be badly planned, if the information in the post is correct. If 97% of children have been exposed to phthalates, then it's very difficult to support that those phthalates are causally related to the obesity. There is no control group in the study, and other studies have demonstrated that certain groups have higher rates of obesity in children.

There may be a connection, but you'd never be able to tell from this flawed study.

[OKIsItJustMe]

2. Did you actually read the study? (Or just the excerpt from the press release?)

http://dx.doi.org/10.1016/j.envres.2011.12.006

[font face=Times, Serif]…

[font size=4]4. Discussion[/font]

[font size=3]Our main findings were associations of MEP and low MWP with BMI and waist circumference among overweight children. For example, there was a 2 unit increase in BMI and a 5 cm increase in waist circumference for both MEP and low MWP going from the 1st (<1 μm) to 3rd (>3 μm) micromolar biomarker quantiles. This corresponds approximately to a tenfold increase in concentrations (median MEP 100 μg/gC in <1 μm quantile and 1211 μg/gC in >3 μm quantile). Of note, MEP was the highest concentration individual metabolite in our study. We did not observe associations between the other phthalates and body size among normal weight girls and boys. To our knowledge, this is the first longitudinal study to examine the association between phthalate exposure and anthropometric measures of children.

Our results offer interesting comparisons with those from two cross-sectional NHANES studies that examined the urinary concentrations of several phthalates and body size ( |Stahlhut et al., 2007| and |Hatch et al., 2008|). Consistent with findings in adolescents and older women (Hatch et al., 2008), we found a positive association between MEP concentrations with both BMI and WC. Although our findings were not significant, the magnitude of associations were comparable to Hatch, who reported a difference of about 2 units in BMI for adolescent girls: 22.9–24.7 kg/m2 with a 2–3 μM change in MEP (quartile 1–4; 110–694 μg/gC). We observed a similar increase in our high BMI girls (21–23 kg/m2) for a 1–3 μM change. For waist circumference, they found an increase of about 4 cm (77.4 to 81.6 cm) with a 1–3 μM change in MEP (quartile 1–4); we also report about a 5 cm difference in our high BMI girls (see Fig. 1 and Table 4). However, among the most comparable NHANES female age group (children ages 6–11 years), no phthalate metabolite-body size characteristic associations were observed in boys (N=329) or girls (N=327) (Hatch et al., 2008). We saw no significant associations in boys, whereas among older NHANES males, positive associations between the concentrations of some phthalate metabolites and body size measures were observed, both in adolescents and adults ( |Stahlhut et al., 2007| and |Hatch et al., 2008|).

Our failure to see other similar relationships with those found in NHANES may be due to differences in the distribution of the exposure, assessed from the magnitude and range of the urinary concentrations, and body size measures resulting from the lack of similarity between the populations studied. Our sample had a narrow range of exposures (ex. MEP range in quartiles: 67–948 μg/gC) and outcome (ex. our percentage of girls in the overweight and obese categories compared to the general population 40.2% vs. 32.6%). Furthermore, associations seen in Stahlhut and Hatch were not monotonic increases. Reports of nonmonotonic (e.g., U-shaped) dose–response relationships, ultra-low dose effects and nonthreshold effects for endocrine disrupting chemicals continue to challenge some of the basic assumptions of toxicology and risk assessment (Hotchkiss et al., 2008). It is possible that these low level exposures could be spurious associations due to residual confounding (see below discussion).

With biomarkers of phthalates having limited range of exposure, population-based quartiles may not create a sufficient gradient as biomarker concentrations are low (95%<1 μM) (Table 2, Supplemental Table 1). The exposure range exhibited in our children may have been too low to elicit biologic effects. Population quartiles are assumed to represent increasing dose, when it is possible that there is no real biologic difference in concentration across the low quartiles. We created biologically relevant exposure categories based on molar concentrations to provide a possible parallel with biological doses in experimental studies. In our study and NHANES, few individuals have biomarker levels above 1 μM.

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[MineralMan]

3. Why, yes I did.

Again, only associations were reported, not causation. They could not report causation because the study was too small and the parameters too insignificant to even mention causation. There is association between many things and obesity. The actual causation is not known.

Just as I said, association is not necessarily causation, something recognized by these researchers as well.

[OKIsItJustMe]

4. Something recognized by these researchers as well.

Right. This was my point. The researchers were aware of the limitations of their study.

However, while association does not necessarily prove causation, a lack of association is pretty good indication of a lack of causation.

[MineralMan]

5. Yes, well, there are hundreds, if not thousands of associations

one can make with childhood obesity. Starting with milk and ending with almost anything they have in common as children. These days, it would be tough to find kids without phthalates in their bodies. I'm in no way convinced that they're a cause of obesity, although they may be a cause of other things. A lousy diet and lack of exercise is also associated in most of these kids. That is a much more likely cause than phthalates, I think, and that's already known to cause obesity.

Sometimes, the answer is simple. Phthalates should not be present in children, but obesity isn't the reason, I'm betting. There are many other reasons.

[OKIsItJustMe]

6. ”These days, it would be tough to find kids without phthalates in their bodies.“

Right, but the association was not simply with the presence of phthalates:

… As shown in Table 2, for six of the phthalate metabolites, more than 90% of the children had analyte concentrations below 1 μM, while MEP was the only metabolite where more than 10% of the children had concentrations greater than 3 μM. …

… Among overweight/obese girls (≥85th BMI percentile), MEP and low MWP exhibited dose response relationships with BMI. For example BMI increased 2.2 kg/m[font size="1"]²[/font] when comparing overweight girls in the uppermost quartile of MEP to those in the lowest quartile. …

Our main findings were associations of MEP and low MWP with BMI and waist circumference among overweight children. … Of note, MEP was the highest concentration individual metabolite in our study. We did not observe associations between the other phthalates and body size among normal weight girls and boys. …

[hedgehog]

7. Quite seriously - can you find a study that proves that lousy diets and lack of exercise

cause child obesity? Or is it that we look at obese children and find these things, while ignoring the non-obese children who have the same diets and exercise?

[Celebration]

8. good point n/t

[hedgehog]

9. I don't mean it as total snark - there have always been fat people around.

For a long time - people were identified as having Pickwick syndrome - sleepy and overweight - from a character in the Pickwick papers. Now we call this sleep apnea. One of the big questions about sleep apnea is how much is it due to being overweight and how much does it cause obesity. It seems to be a nasty feed-back loop.

But - we've always had fat people, and for a long time we traditionally told them to cut back on simple carbs.

We still have people who eat incredible amounts of food. Get some of these people to assume a normal diet, and ta-da!, they assume a normal appearance.

But why, across the entire world, do we now have an entire generation of obese children? We can't just assume they're all lazy gluttons. We need to find out why some people gain weight and others don't, why some people lose weight and others don't. We have a lot of fat people, but do we really know why they are fat?

A marker for an unsolved medical problem is a proliferation of quack cures. When medical science can't provide an answer, the con artists pile in. Just google "weight loss" and then try to tell me medical science knows what it's talking about in this area!

[BlueIris]

10. Thanks for this. Great article. nt

[OKIsItJustMe]

11. You’re welcome

I found it interesting.