In this post, Tyler Hoskins, a research assistant professor in the College of Agriculture and member of the Purdue Institute for a Sustainable Future, discusses his recently published research “Toxicities of Legacy and Current-Use PFAS in an Anuran: Do Larval Exposures Influence Responses to a Terrestrial Pathogen Challenge?,” which appears in Environmental Science & Technology with the support of the Department of Defense, Strategic Environmental Research and Development Program.
What did you want to know?
Per- and polyfluorinated alkyl substances (PFAS), sometimes called “Forever Chemicals,” are a large group that have become a concern for human and environmental health, because they are persistent, they accumulate in organisms (including humans), and because they can be toxic. Studies in human populations show that some PFAS can depress immune responses, especially by reducing effectiveness of vaccines in children. Exposure during fetal development can also increase risk of certain infections later in life. These human health effects raise the question of whether wildlife might be affected in similar ways. Because disease is a major cause of biodiversity loss, we wanted to know whether exposure to PFAS might worsen effects of a wildlife disease that has led to extinctions for some species of amphibians (frogs, toads, and salamanders). Further, some PFAS have been taken out of production because they are toxic, but they have been replaced by other PFAS that have been branded as “safer alternatives.” Whether these newer PFAS are actually less toxic than the PFAS they replace is not well-understood, so we also wanted to understand how toxicity of a current-use replacement compared to better-established toxicity of the PFAS it replaced.
What did you achieve?
We exposed grey treefrogs (Hyla versicolor), an Indiana-native frog, to three different PFAS: perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) are no longer produced in the United States, but are still common in the environment and in the blood of Americans. The third PFAS, hexafluoropropylene dimer acid (sometimes called “GenX”), has replaced PFOA and is in current use. We exposed tadpoles to these PFAS (analogous to a uterine exposure for humans), then raised frogs for 50 days after metamorphosis, monitoring their growth and survival. Half of these frogs were also exposed to the amphibian chytrid fungus, Batrochocytrium dendrobatidis, and monitored in the same way.
We found that GenX, the current-use chemical, was more toxic than the chemical it replaced in some cases. At concentrations as low as 1 microgram/Liter (Ug/L) GenX reduced growth more than PFOA, the chemical it replaced; for context, 1 Ug/L is the equivalent of the width of a human hair compared to 68 miles. Not only did PFAS reduce growth after aquatic exposure ended, but PFAS exposure sometimes made effects of the pathogen on body size more dramatic. These results demonstrate that early-life PFAS exposure can reduce growth later in life and can exacerbate effects of disease in wildlife. Given that GenX often caused stronger effects than PFOA, the chemical it replaced, GenX was not a safer alternative in the scenarios we tested.
What is the impact of this research?
First and foremost, concerns about PFAS occurrence in blood of most Americans and evidence demonstrating PFAS toxicity have led industry to transition from “legacy PFAS,” like PFOS and PFOA, to alternative PFAS, like GenX. Chemical properties of these replacement PFAS suggest that they should be less toxic, but studies like this one clearly demonstrate the need to rigorously test this. More tests, across a range of taxa and diseases are needed, as replacement PFAS are being released and wildlife and humans are being exposed. This highlights the urgency of understanding toxicity of current-use PFAS. Our study is part of emerging evidence that GenX and other current use PFAS are not always less toxic than PFAS they replaced.
Effects of PFAS on growth of frogs after tadpole exposures ended suggest that early life exposure can elicit effects later in life. This is consistent with the “Developmental Origins of Adult Disease” hypothesis, which posits that early life exposure leads to delayed health effects that only emerge later in life. This paper demonstrates the importance of developmental exposures and to need to follow outcomes into later life.
PFOS, PFOA, and GenX altered responses to a pathogen often encountered by wild frogs. This shows that wildlife may suffer similar immunotoxic effects as those observed in people. Wildlife diseases are causing biodiversity loss, so understanding how PFAS might make this problem worse is a pressing need. Ultimately, we need to understand how
PFAS can make wildlife diseases worse and how to mitigate this phenomenon.