Assessments of obesity risk may need to include the white-glove test. If your gloved hand picks up any dust when it is run across a surface in your home, you may have bigger worries than your lack of cleanliness. You may be exposing yourself to environmental contaminants that could act as metabolic disruptors—chemicals such as flame retardants, phthalates, and bisphenol-A. Such chemicals, which are common in consumer goods, can mimic or interfere with the body’s hormones. They can even act as “obesogens,” according to animal studies that have linked early-life chemical exposures to subsequent weight gains. And now, these chemicals have been found—and their obesogenic potential confirmed—in dust.
The new findings were presented by Duke University scientists who evaluated the adipogenic activity of indoor house dust extracts and a suite of semivolatile organic chemicals (SVOCs) that are often ubiquitously detected in indoor environments. The researchers collected samples of indoor dust from 11 homes in North Carolina and tested extracts from the samples in a mouse preadipocyte cell model, 3T3-L1 cells, often used to test compounds for potential effects on the accumulation of triglycerides, a type of fat.
Detailed results appeared July 12 in the journal Environmental Science & Technology, in an article entitled “Characterization of Adipogenic Activity of House Dust Extracts and Semi-Volatile Indoor Contaminants in 3T3-L1 Cells.” This article indicates that small amounts of household dust containing endocrine-disrupting chemicals, or EDCs, can spur fat cells to accumulate more triglycerides in a lab dish.
“Ten of 11 house dust extracts exhibited significant triglyceride accumulation and/or proliferation at environmentally relevant levels (<20 μg of dust/well), and significant adipogenic activity was also exhibited by 28 of the SVOCs,” wrote the article’s authors. “Notably, pyraclostrobin, dibutyl phthalate, tert-butyl-phenyl diphenyl phosphate, and the isopropylated triaryl phosphates (ITPs) exhibited near maximal or supra-maximal triglyceride accumulation relative to the rosiglitazone-induced maximum.”
The scientists, who evaluated 44 household dust contaminants, emphasized that the strongest fat-producing effects were due to pyraclostrobin, a pesticide; tert-butyl-phenyl diphenyl phosphate (TBPDP), a flame-retardant; and dibutyl phthalate (DBP), a plasticizer. Amounts of dust as low as 3 μg—well below the mass of dust that children are exposed to daily—caused measurable effects.
According to the U.S. Environmental Protection Agency (EPA), children consume 50 mg of house dust each day. And indoor dust, which can be inhaled, ingested, or absorbed through the skin, has been suspected to contain EDCs. Now the presence of EDCs in household dust has been confirmed by the Duke University team, which was led by Heather Stapleton, Ph.D., a professor of environmental ethics and sustainable environmental management. In addition, Dr. Stapleton’s team has shown that household dust is a likely exposure source of chemicals that may be able to disrupt metabolic health.
“The adipogenic activity in house dust occurred at concentrations below EPA estimated child exposure levels, and raises concerns for human health impacts, particularly in children,” the authors of the current study concluded. “Our results delineate a novel potential health threat and identify putative causative SVOCs that are likely contributing to this activity.”
The relationship between environmental metabolic disrupting chemicals, obesity, and related metabolic disorders was discussed a few years ago at a workshop hosted by the University of Parma. The workshop issued the “Parma consensus statement,” which described how future work might detail the effects of metabolic disruptors.
“There are no known classical genetic mechanisms that could explain the remarkable changes in body composition that have occurred over recent decades,” the workshop statement indicated. “Therefore, there has been a significant focus on identifying changes in gene expression and epigenetic marks caused by environmental factors, such as stress, drugs (for example nicotine), and a number of endocrine disrupting chemicals during development (in utero and early childhood) in relation to the risk of metabolic diseases later in life.”
Key recommendations from the workshop included the following:
- Characterizing adverse outcome pathways through which metabolic disruptors lead to different manifestations of metabolic syndrome.
- Assessing epigenomic and other markers underlying altered developmental programming of metabolic functions and endpoints in human studies and in animal models.
- Improving exposure assessments in human studies: integrate genetics, genomics, proteomics, and metabolomics with environmental exposures to better understand the role of metabolic disruptors in disease onset and severity.