Plastic made its name by doing nothing. A bag does not react with the bread inside it, and a cup does not react with the coffee. Chemists call this inertness, and it is the reason the material is everywhere. Because plastic is everywhere, its crumbs are too. Microplastics have turned up in drinking water, in human blood, in arteries, in brains. Nobody can yet say what they do once they get there.

As Jacek Krywko reported for Ars Technica, a team led by Wei Min, a chemist at Columbia University, now has evidence that the doing-nothing stops where plastic meets water. The paper, “Intrinsic physicochemical activity at microplastic–water interfaces”, appeared in Nature on October 14, according to Columbia’s announcement. The first author is the postdoctoral researcher Naixin Qian, and Teresa Head-Gordon’s group at UC Berkeley ran the theoretical calculations. Min starts from what is not known. “Whether microplastics can directly cause human disease is still being researched,” he said.

A suspicion borrowed from droplets

Min’s laboratory has spent years on microdroplet chemistry, the study of what water does at its boundary with air once it is broken into tiny droplets. Such droplets have been reported to produce reactive oxygen species, or ROS, a family of harmful molecules that contain oxygen. “ROS will essentially bump into proteins, lipids, DNA, and cause damage,” Min said. “You could break a DNA strand into segments. You could mutate DNA; you could misfold proteins.”

Many animal studies had already linked the toxicity of microplastics to oxidative stress, which ROS cause. So the team asked whether the boundary between water and plastic might behave like the boundary between water and air. “We got inspired by that field,” Min said.

Ten days of a fading dye

The first test was simple. The researchers stirred polystyrene powder into water containing methyl orange, a yellow dye that ROS break apart. Over 10 days the solution lost nearly 90 percent of its dye and became almost colourless. In ethanol and other solvents the dye stayed intact, so whatever the polystyrene was doing needed water. Columbia says the reaction ran in total darkness, with no ultraviolet light and no chemical additives.

Next came electron spin resonance, which detects radicals directly: atoms or molecules with an unpaired electron that makes them highly reactive. The mixture contained hydroxyl radicals, one of the most reactive kinds of ROS. A fluorescent sensor that lights up only when it meets hydroxyl radicals told the same story. Under the microscope the glow gathered on the surfaces of the plastic particles and grew stronger over time. “You don’t see it, but once it reacts with local ROS, it turns into a bright color,” Min said.

Polystyrene was not alone. All six common plastics the team tested produced radicals: polyethylene, polypropylene, polystyrene, PVC, PET and acrylic. The most water-repellent, polyethylene and polypropylene, were the most active. PET and acrylic, whose chemical groups attract water, were the least. In bulk water, each molecule sits in a network of hydrogen bonds with its neighbours. The few layers pressed against a water-repellent surface lose some of those partners. “Their structure is no longer the regular water structure. They are perturbed, and their energy is also significantly increased,” Min said.

Turning one of water’s few hydroxide ions into a hydroxyl radical means removing an electron, which normally takes a lot of energy. In the group’s simulations, hydroxide ions at a polyethylene surface, short of hydrogen bonds, needed far less. The plastic also builds up a negative charge in water, and that lowered the cost further.

Old quarrels

Min’s earlier microdroplet work has drawn heavy criticism. Some researchers argue that the reactive chemicals he reported came from contamination or measurement artifacts. This time the team used several independent detection methods. They also added a detergent-like surfactant that coats the plastic and disrupts the layer of water at its surface. The more surfactant they added, the weaker the plastic’s charge and the fewer radicals it produced. “We only change one parameter while keeping all the rest [the same],” Min said. Impurities, he explained, tend to be stable molecules with no reason to produce radicals on their own. Then he set his own limit:

“To be absolutely clear, we cannot 100 percent rule out the involvement of impurities. But our controls and our theoretical computation studies highly suggest that this is intrinsic to the microplastic-water interface.”

Proteins and blood

The team then turned to living matter. Proteins and DNA can collect on plastic surfaces, and lysozyme, a standard test protein, began to clump there. Adding caffeine, which mops up radicals, largely stopped the clumping, which points to the radicals as the cause. Mouse red blood cells that touched polystyrene particles broke apart. Across the plastics, the damage tracked how many radicals each one produced, and the effect held in blood serum.

Min did not jump from mouse cells to human illness. Animal studies often name ROS as possible roots of oxidative stress and chronic inflammation, but the body makes ROS in many ways, including ordinary metabolism. He admitted that comparing this effect with the ROS our own cells produce is difficult.

A few microns

“If you are really at the interface, you could be significantly affected by this effect, whereas if you are just a few microns away, you don’t feel it anymore,” Min said. Exposure is another blank. Nobody can yet say how many microplastics an average person takes in each year from food, water and air.

The plastics in the study were mostly fresh powders bought for the lab, not the weathered particles found in the world. Older particles with more oxidised surfaces gave somewhat weaker signals. “This aging process is very heterogeneous,” Min said. “Some microplastic particles were made 50 years ago, some were made five days ago.”

Then there is size. Microplastics are usually defined as particles smaller than five millimetres, with a lower cutoff that varies between 100 and 1,000 nanometres. The team did not test how size changes the chemistry. The researchers suspect it matters, because the same mass of plastic ground into nanoparticles has far more surface. “This may be another reason for nanoplastics to be more dangerous,” Min said.

If water-repellent surfaces drive the effect, the researchers argue, plastics could be made less water-repellent by changing their molecular structure or adding additives. Min wants to answer the open question first. “We definitely want to see how much this effect is directly contributing to disease or biological problems in animals and humans,” he said.