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Topics: Five Questions, Funding, Health, Pilot Funding, Public Health
Five Questions with Qi Sun
‘Forever chemicals’ and heart disease: Pilot funding awardee tackles PFAS.
In a world where chemicals have become household staples, where just by living we are exposed to toxins in innumerable forms, Qi Sun, DSc, MD, dares imagine a future free of the toxic soup of everyday pollutants. More realist than utopian, he recognizes it’s an aspirational and long-term goal. So he plugs away at the minutiae of science to document the collective health effects of so-called “forever chemicals,” even as industry pumps out new versions to skirt the few regulations in place. With an 11-year-old daughter, an organic garden, and a commitment to reducing his family’s exposure to these ubiquitous pollutants, the battle is both personal and professional.
Sun is an associate professor in nutrition and epidemiology at Harvard T. H. Chan School of Public Health, where he is a principal investigator or co-PI on four current RO1s focused primarily on diabetes. One of his interests is how environmental pollutants such as per- and polyfluoroalkyl substances (PFAS) may factor into rising rates of obesity and type 2 diabetes. In 2021, he received pilot funding through our Everyday Exposures – Toxins & Health program to tackle a key unresolved question around this huge and growing class of pollutants: Do they raise heart disease risk? If so, how? Sun tapped into data from three large, long-term epidemiological studies – the Nurses’ Health Study I and II and the Health Professionals Follow-Up Study – to prospectively examine how PFAS exposure interacts with cholesterol levels and heart disease incidence.
We caught up with him as he was just starting to crunch the data.
Why are you interested in PFAS?
PFAS are known as forever chemicals, which precisely describes them. Molecularly, PFAS are unique chemicals structured with a carbon backbone bound to fluorine. This carbon-fluorine bond is very hard to break; it’s probably the most stable in chemistry. It’s this feature that makes PFAS both dangerous for the environment and useful for consumer products because it imparts water-, oil- and stain-repellency. PFAS are in the coating on nonstick cookware and the stain repellent on carpets. They’re used to make paper and cardboard oil-repellent for food products like French fries and microwave popcorn. They’re applied on skis to make them more slippery. They are everywhere. We are surrounded by these chemicals.
When we dispose of these products, the chemicals enter the environment. The fluorine and carbon bonds are so strong that they last essentially forever in the environment, contaminating soil and water, which is why we call them “forever chemicals”. They don’t degrade. Research has shown how they are already penetrating food chains and water systems in the United States. At the same time, we’re learning more about the significant threats they pose to human health, including cancer, obesity, and metabolic disorders. The strongest association we have is between PFAS exposure and type 2 diabetes.
“They are everywhere. We are surrounded by these chemicals.”
Other evidence suggests PFAS may increase heart disease risk, and this is the basis for my study. Occupational studies where participants are heavily exposed to PFAS and other studies among more general populations show changes in cholesterol levels that have been difficult to sort out. We want to understand whether PFAS promote coronary heart disease risk and how they might do that.
Your previous research linked PFAS exposure to higher levels of both the “good” (HDL) and “bad” (LDL) cholesterol levels, seemingly confounding its role in heart disease. How are you addressing that paradox?
That’s a critical question. For some reason that we don’t understand, PFAS exposure is linked to both higher LDL and higher HDL. The net result may be neutral, may be good, or may be bad. It’s just hard to tell, but we have some clues.
In the past decade, research has revealed that HDL is actually a heterogeneous group of particles, some of which are beneficial while others are detrimental. Proteins called apolipoproteins, which are embedded on the surface of HDL particles, seem to drive these differences – in particular the subtype apolipoprotein C3 (Apo-C3). In fact, HDL particles lacking Apo-C3 are the only ones associated with greater coronary heart disease risk, so if PFAS only increase the HDL particles that carry Apo-C3, that would call into question a role in heart disease via this mechanism. There might be other ways PFAS damage the heart, possibly by increasing LDL or promoting other HDL particles that are detrimental. These are open questions.
The goal is to have a complete picture about these associations. What’s going on between PFAS and coronary heart disease? What’s going on between PFAS and different apolipoprotein species that predict heart disease risk? How do the different apolipoprotein species mediate the association between PFAS and coronary heart disease?
What was the benefit of the pilot funding in helping clarify these questions?
The Harvard Catalyst grant allowed us to generate preliminary evidence to help us judge whether our hypothesis is likely to be true. This will be really important for deciding the next step, whether we try to substantiate those associations in a much larger population or we stop here and move on to look at other adverse effects of PFAS. So far, I think this is still a viable and promising hypothesis that is worth our time and energy to examine.
What do you do when you’re not working?
(Laughing) Usually driving somewhere to pick up my 11-year-old daughter.
Before the pandemic I loved to ride my bicycle to the T station and take the subway to school. That was interrupted by Covid and I really hope to resume, because I truly believe that having a world unpolluted by chemicals is a better world. I also practice organic farming in our backyard and in a community garden where I have a small plot to grow vegetables. It’s a little bit of work, a lot of planning, and a fun way to spend some time gardening and promote healthy eating.
As a parent, knowing what you do about the risk of these chemicals and how ubiquitous they are, what do you do to protect your family?
It’s very hard, very hard. There’s a silver lining in this because people nowadays are very aware of these chemicals, and they can try to avoid products that contain them. That puts pressure on industry to switch their product lines and stop using PFAS.
“The Harvard Catalyst grant allowed us to generate preliminary evidence to help us judge whether our hypothesis is likely to be true.”
I think it’s essentially impossible to entirely avoid PFAS contamination, but there are ways that you can potentially reduce your exposure. You can switch to alternative products. For example you could only buy popcorn packaged without PFAS. That’s absolutely doable. By foregoing food that uses coated paper containers, you’ll reduce your PFAS exposure and also, most likely, decrease empty calories.
I think people should also start monitoring their drinking water for PFAS and avoid drinking contaminated water. I understand that buying water can be expensive and out of reach for many people, often the very communities whose water is contaminated. Research is needed to understand how scientists or government can clean up contaminated water.
Another concern is that the industry has not stopped producing chemicals that fall in the category of PFAS. Production continues. Only two of the most notorious PFAS — PFOA and PFOS – are phased out and banned from production. Thousands of others are still in production. I don’t think industry knows half the effects of those new chemicals they are introducing into our environment, and the science really lags behind because we don’t even know what they’re producing. It’s an ongoing issue between scientists and industry. But they could help us. Working together, we could hopefully build an environment that is less impacted by these forever chemicals.