Pollutants From Household Furniture Linked to Aging-Related Effects on Body

Some environmental pollutants begin their lives as common household items. A metal used in household wires or a compound used to treat furniture may seem innocuous, but over time these pollutants find their way into human bodies where they can extract lasting effects on health, happiness, and according to research released Wednesday in Environmental Science & Technology, how our bodies age from the inside out.

This study, led by Michelle Plusquin, Ph.D., a professor at Hasselt University’s Centre for Environmental Sciences, shows that a handful of chemicals that humans encounter in the environment can cause well-established hallmarks of aging to appear in the body’s cells.

Plusquin found significant effects on human telomeres and mitochondrial DNA when humans had elevated levels of copper perfluorohexane sulfonic acid (PFHxS) and perfluorooctanesulfonic acid (PFOS) levels in their blood. These may sound foreign, but they’re actually more common than you might think.

“These are compounds that are present in our environment; they have been selected based on their relevance in Flanders. However, also in other countries, these pollutants are found in the environment,” Plusquin tells Inverse. “These compounds can mainly enter the human body via the air, food, or skin contact.”

Copper, says Plusquin, is commonly used in household wires and ends up in the environment when they’re thrown out and then incinerated. The other two chemicals, PFOS and PFHxS, belong to a class called perfluorinated chemicals, which is made up of a cast of notoriously dangerous characters. PFOS, the EPA notes, can contaminate groundwater and was once a major ingredient in Scotchguard. PFHxS, meanwhile, are usually “used for treatment of textile and furniture to obtain a higher resistance against dirt,” adds Plusquin, and have been traced to spray-based treatments for carpets.

"These are compounds that are present in our environment.”

Pluquin’s work shows that having elevated levels of these chemicals in the body — which she detected in the urine and blood samples of 175 individuals — can have a myriad of strange effects on cellular aging.

First, they found that some classes of chemicals shortened telomeres, the protective caps on the ends of chromosomes. For example, higher urinary concentrations of copper and PFOS were significantly correlated with shortened telomere length. “Negative associations are an indication of increased cellular aging,” she explains.

But, adding to the strangeness, she also found that these pollutants had differing effects on mitochondria — the energy-producing powerhouses in the cell. People who had high levels of urinary copper and PFHxS in their blood had less mitochondrial DNA (mtDNA). But strangely, those who had high levels of PFOS tended to have higher levels of mtDNA. In this case, she says, the increase in mtDNA is probably a sign of more serious cellular issues happening because of the exposure and are not necessarily a good thing.

“Mitochondrial DNA content is known to fluctuate, and a higher content might mean that there is a higher need for mitochondria. As mitochondria deliver energy to the cell, they might need more energy due to these exposures,” she says.

The good news is that agencies are already aware of the risks of some of these pollutants. The EPA, for its part, is now seeking comments for draft guidance on a proposed plan to help monitor and remove traces of PFOS and similar chemicals in groundwater.

Even if cellular aging isn’t on the forefront of the EPA’s agenda, Plusquin’s study adds a growing body of previous work showing that these chemicals can have lasting effects that may seem counterintuitive and strange effects on the human body:

“Based on previous studies I indeed think that these pollutants have lasting impact,” she adds. “Our study further clarifies how these effects happen and what can be a possible mechanism behind this effect.”

Abstract: Mitochondrial DNA (mtDNA) content and telomere length are putative aging biomarkers and are sensitive to environmental stressors, including pollutants. Our objective was to identify, from a set of environmental exposures, which exposure is associated with leukocyte mtDNA content and telomere length in adults. This study includes 175 adults from 50 to 65 years old from the cross-sectional Flemish Environment and Health study, of whom leukocyte telomere length and mtDNA content were determined using qPCR. The levels of exposure of seven metals, 11 organohalogens, and four perfluorinated compounds (PFHxS, PFNA, PFOA, PFOS) were measured. We performed sparse partial least-squares regression analyses followed by ordinary least-squares regression to assess the multipollutant associations. While accounting for possible confounders and coexposures, we identified that urinary cadmium (6.52%, 95% confidence interval, 1.06, 12.28), serum hexachlorobenzene (2.89%, 018, 5.68), and perfluorooctanesulfonic acid (11.38%, 5.97, 17.08) exposure were positively associated (p < 0.05) with mtDNA content, while urinary copper (−9.88%, −14.82, −4.66) and serum perfluorohexanesulfonic acid (−4.75%, −8.79, −0.54) exposure were inversely associated with mtDNA content. Urinary antimony (2.69%, 0.45, 4.99) and mercury (1.91%, 0.42, 3.43) exposure were positively associated with leukocyte telomere length, while urinary copper (−3.52%, −6.60, −0.34) and serum perfluorooctanesulfonic acid (−3.64%, −6.60, −0.60) showed an inverse association. Our findings support the hypothesis that environmental pollutants interact with molecular hallmarks of aging.