Two VERY interesting sentences are: Epidemiological studies show an association between testicular cancer and male reproductive toxicity (low Sperm count that we are plagued with) and exposure to PFOA and PFOS. And... For instance, PFOA and PFOS cause immunosuppression in humans and animals.
By Alexis Temkin, Ph.D.
The fluorinated chemicals called PFAS, for per- and polyfluoroalkyl substances, are a class of synthetic, toxic and persistent chemicals used in more than 1,000 consumer and industrial products and applications. After revelations of their health hazards surfaced, the two most notorious PFAS compounds – PFOA, formerly used to make DuPont’s Teflon, and PFOS, formerly an ingredient in 3M’s Scotchgard – were phased out under pressure from the Environmental Protection Agency.
They have been replaced by a new generation of structurally different PFAS compounds that the chemical industry claims are safer. But the more we learn about these replacements, the more the evidence mounts of their close similarity to the phased-out compounds, and of the concerns they share with first-generation PFAS about health hazards and contamination of our bodies and the environment.
This science review details what we know and what we are still learning.
Structurally, all PFAS are made of molecules containing carbon and fluorine atoms directly attached to one another, providing an extremely strong bond. Although these bonds enable PFAS to repel water and oil, they also make PFAS environmentally persistent, which means they are extremely resistant to degradation – the reason they are often described as “forever chemicals.”
In the early 2000s, PFAS were effectively split into two groups
– so-called long-chain compounds, like PFOA and PFOS, which were being phased out, and the new generation of short-chain compounds. The difference lay in the number of carbon atoms in their structure.
Long-chain PFAS were defined as substances having six or more carbons for the kind of chemicals called sulfonates, and eight or more carbons for chemicals called carboxylic acids. Short-chain PFAS were defined as substances with five or fewer carbons for sulfonates and seven or fewer carbons for carboxylic acids. The chemical industry said short-chain PFAS were safer, primarily because they tend to leave our bodies more quickly, and the structural differences were a way for companies to avoid the regulatory pressure directed at long-chain PFAS.
Toxicity and health effects
Well-studied PFAS, such PFOA and PFOS and other long-chain compounds, are known to pose a risk to the health of animals and people, including harm to the immune system, such as reduced effectiveness of vaccines; harm to development and the reproductive system, such as reduced birth weight and impacts on fertility; increased risk of certain cancers; and effects on metabolism, such as changes in cholesterol and weight gain.1
Several of these health harms have been observed in thorough, well-executed epidemiological studies that measure exposure to PFAS in humans, as well as controlled laboratory studies in animals. For example, the C8 Health Project
studied nearly 70,000 residents in the mid-Ohio River valley whose water was polluted for decades with high levels of PFOA from a DuPont manufacturing plant. (C8 was DuPont’s internal name for PFOA.) The study determined PFOA exposure was linked to six major health problems, including kidney and testicular cancer, ulcerative colitis, thyroid disease, high cholesterol and pregnancy-induced hypertension.
Multiple government agencies, including the EPA, the National Toxicology Program and the Agency for Toxicological Substances and Disease Registry, have noted that other long-chain PFAS similar to PFOA and PFOS, like PFNA and PFHxS, as well as short-chain PFAS used to replace them, such as GenX, PFBS and PFHxA, can cause similar health effects in animals, with some epidemiological studies reporting similar findings. EPA toxicity assessments of short-chain PFAS have found similar toxicity for both the replacement GenX and its predecessor PFOA, and for PFBS and phased-out PFOS.2
Short-chain PFAS – GenX, PFBA, PFBS, PFHpA, PFPeA, PFPeS, 6:2 FTSA and PFHxA – are commonly detected in drinking water and other environmental samples. EWG scientists reviewed government agency toxicological reports and searched the peer-reviewed literature for toxicity data available for these replacement compounds. In recent years, the number of studies on replacement chemicals
has increased. However, particularly for short-chain PFAS, there are limited data for the health harms associated with long-chain PFAS, such as immune system effects. Where data are available, multiple short-chain PFAS appear to behave much like their long-chain counterparts.
For instance, PFOA and PFOS cause immunosuppression in animal studies, as well as reducing the effectiveness of vaccines in humans.3 For PFBS, a short-chain replacement chemical, comparable animal studies do not exist, yet studies in human cells indicate PFBS decreases cytokine levels, suggesting PFBS may also alter immune function.4 Human studies indicate an association with other immune outcomes, including a connection between asthma and PFBS exposure.5 A recent study found that a higher level of PFBA in the blood is associated with more severe Covid-19 infection.6 PFBA is similar in chain length to PFBS. In animal studies, GenX, the PFOA replacement chemical, can cause immunosuppression similar to that of PFOA.7
Similarly, epidemiological studies show an association between testicular cancer and male reproductive toxicity
and exposure to PFOA and PFOS.8 A recent study investigated changes in the reproductive hormone levels of offspring of mothers’ exposure to short-chain PFAS, PFBS and PFHpA, and identified similar findings previously described for PFOA and PFOS.9 The National Toxicology Program performed 28-day toxicity studies in rats with long- and short-chain compounds, including PFBS, PFHxS, PFOS, PFHxA, PFOA, PFNA and PDFA, to compare their toxicity. They found that all PFAS affected the same target organs, including the thyroid and the liver, decreasing thyroid hormone levels and increasing liver weight and liver enzyme activity.10, 11