PART TWO ..CONTINUED FROM PART 1

Tarbuck said he isn’t sure how the wells at Riverside Station in Maine became contaminated. “Because these numbers are so incredibly small, it’s hard to pinpoint,” he said. “It’s a head-scratcher.” The site is located far from any industrial sources, but sampling has shown slightly elevated PFAS in the Kennebec, possibly originating from contaminated sludge used as fertilizer by upstream farms. “We believe that the PFAS is coming from the river,” Tarbuck said.

IN 2003, the U.S. Centers for Disease Control and Prevention published sampling results suggesting that nearly all Americans had measurable amounts of PFAS in their blood. Published studies had by that time associated PFOA and PFOS with liver disease, reproductive problems, and cancer in laboratory animals, and one study suggested a link between PFOS and human bladder cancer, but only among workers who were exposed to high levels on the job for at least five years. More recent evidence associates PFOA and PFOS with testicular and kidney cancers, and based on these results, the EPA now classifies both compounds as likely human carcinogens.

Internal industry documents show that 3M, DuPont, and other manufacturers secretly knew decades ago that PFAS are toxic. But it wasn’t until the 2000s that these companies voluntarily started pulling PFOA, PFOS, and other long-chain compounds off the market. By 2018, according to the CDC’s most recent data, blood levels of PFOA and PFOS in the U.S. population had plummeted by 70 and 85 percent, respectively.

But that’s not to say PFAS production ended. Companies merely substituted with different molecules, such as PFBS and GenX, called short-chain PFAS in part because they contain no more than six carbon atoms each. The thinking was that short-chain PFAS — still widely used in food wrappers, floor wax, paints, coatings, and many other products — were safer because they’re more rapidly excreted from the body. Yet mounting evidence shows that they too are environmentally persistent and have toxic effects. Short-chain PFAS have been shown to cause thyroid and liver problems in animal studies, and recent evidence links them to metabolic changes in isolated lab-grown human cells. Significant human exposures, Cousins said, come from short-chain PFAS contaminating the air and dust in homes. The chemicals are abundant in indoor environments, research shows, and the levels in human blood rise with increasing exposure to household dust as well as drinking water.

Evidence of PFAS toxicity prompted growing efforts to reduce human exposure in water and other sources. But the regulatory landscape evolved without any consistency, so now drinking water standards in the U.S. and elsewhere vary widely according to the “interpretations of different agencies and how they view the same data and what concentrations they think are appropriately protective,” said Tom Lee, a partner and leader of the PFAS team at Bryan Cave Leighton Paisner, LLP, an international law firm. MCLs in the U.S., for instance, currently range from a low of 6 ppt in Michigan for PFNA all the way to 400,000 ppt in Michigan for a compound called PFHxA.

The EPA’s pending standard could level the playing field for PFAS exposures in water. But the agency’s path to deriving the regulatory thresholds has proven divisive. In 2016, the EPA issued a health advisory of 70 ppt for PFOA and PFOS combined that EPA scientists said would be safe over a lifetime of exposure. According to the agency, the level had been derived using “the best available peer-reviewed studies” and would aid health officials confronting PFAS in their own local water systems. But health advisories such as this one are non-enforceable, and utilities were not actually bound to it.

Then, in 2022, the EPA pivoted to another, much lower non-enforceable target. This time, the agency called for limiting PFOS to 0.02 ppt and PFOA to just 0.004 ppt drinking water — levels even lower than what was being detected in rainwater at various sites around the world. Moving from these interim updated health advisory levels, as the EPA called them (they are also referred to as maximum contaminant level goals, or MCLGs), to the currently proposed standard could create concern among consumers who might feel that “no matter what’s in my water, it’s still dangerous,” said Andrew Cohen, a hydrogeologist based in Westfield, New Jersey, who specializes in PFAS and consults for DuPont.

Internal industry documents show that 3M, DuPont, and other manufacturers secretly knew decades ago that PFAS are toxic. But it wasn’t until the 2000s that these companies voluntarily started pulling long-chain PFAS off the market.

The EPA had set the 2022 values on the basis of evidence suggesting that PFOS and PFOA prevent diphtheria and tetanus vaccines from raising adequate immune responses in children. In the agency’s view, this immune system toxicity was the so-called critical effect — the first adverse effect that could be observed at the lowest tested dose — resulting from PFOA and PFOS exposure, explained Michael Dourson, a former EPA official who is also president and director of science at Toxicology Excellence for Risk Assessment, a nonprofit consulting firm that evaluates chemical hazards on behalf of industrial and government clients.

But the degree to which trace PFAS levels in the part per trillion range harm human immune systems is heavily debated, and some outside the EPA “have been very hesitant to use these data,” said Boobis, the emeritus professor at Imperial College London. Indeed, health agencies in different countries — and even within the U.S. — have based drinking water regulations on different critical effects seen at higher PFAS doses in animal studies. The Australian PFOA guideline, at 560 ppt, is the least stringent value cited in a 2023 paper on international safe doses, and is based on developmental and reproductive problems observed in exposed mice.

Now the EPA is striking out in a different direction. Rather than basing the enforceable limits on immune effects, the agency instead derived the upcoming MCLs with an eye largely towards protecting people from cancer. But the agency took a highly precautionary stance — one that in this case amounts to a cautious policy choice, “not the state of the science,” wrote Lynne Haber, a toxicologist and a faculty member at the University of Cincinnati College of Medicine who specializes in the assessment of cancer risks, in an email to Undark.

The EPA’s default position when setting cancer-protective exposure levels is that, without evidence to the contrary, just one molecule of a carcinogen can spawn cancerous changes in a cell. This controversial — and some would say outdated — line of thinking is grounded in what toxicologists know as the linear no-threshold dose-response model. Dating back to the late 1920s, that model assumes that any exposure to ionizing radiation or a chemical carcinogen, no matter how small, can set off cancerous changes in a cell. Because no amount of exposure is safe, the EPA rationalizes, the MCLG for a carcinogen should be set at zero.

But a standard of zero is unmeasurable and therefore unenforceable, according to Detlef Knappe, a professor of civil, construction, and environmental engineering at North Carolina State University. So, the EPA instead is tying the MCL to the lowest concentration of a given carcinogen that analytical instruments can reliably detect. And in the case of PFOA and PFOS, that concentration happens to be 4 ppt.

The linear model is plausible, Dourson said, only in the hypothetical event that a single molecule enters the cell nucleus and changes DNA. Under that scenario, a genetically damaged cell could theoretically multiply into a tumor. Carcinogens that act on DNA are said to be mutagenic, in that their effects result from how they cause cancer-inducing mutations in the genome. But mounting research shows carcinogens can also work in ways other than interacting with DNA, Haber said. For instance, a chemical might cause cancer only after doses cross a threshold that results in organ injury. That’s the case with chloroform. A common contaminant in drinking water, it causes liver and kidney cancer in mice, but only at levels high enough to injure cells in those organs first. Tumors develop secondarily after cells start to regenerate during the healing process.

The EPA’s default position when setting cancer-protective exposure levels is that, without evidence to the contrary, just one molecule of a carcinogen can spawn cancerous changes in a cell.

Weihsueh Chiu, a quantitative risk scientist at Texas A&M University, chaired the EPA’s PFAS review panel. He said the agency will depart from the assumption that a chemical follows the linear model, but only if evidence reveals a key biological event upon which cancerous changes depend, such as cell toxicity and regenerative proliferation in the case of chloroform. Scientists face a burden to prove this sort of nonlinearity, Chiu explained in an email, and in the absence of that proof, “it is assumed that there is a linear relationship between dose and probability of tumors.” When it came to PFOA and PFOS, the EPA could not establish or identify a key event that would support a nonlinear response, Chiu added.

But squabbles have broken out over the underlying data, and evidence in support of either linear or nonlinear approaches is very much in question. Saying that “no one really believes that one molecule of any chemical is going to cause cancer,” Dourson, whose connections to industry have sometimes drawn scrutiny, insisted that PFAS do not cause gene mutations. “So how do you get a linear dose response curve from that?” he asked. “Well, you don’t.”

Boobis concurred, saying that most health authorities outside the U.S. would say that PFAS has a dose threshold, whereby cancer would be considered possible only at levels greater than a single molecule of exposure. Linear low dose extrapolation is a “uniquely American problem,” Boobis said, adding “nobody in Europe, for example, has used the cancer endpoint to drive the risk assessment” for PFAS.

https://undark.org/2024/01/15/drinking-water-pfas-cost/?utm_source=pocket-newtab-en-us#:~:text=In%20a%20recently,down%20over%20time.%E2%80%9D

Calonge, chair of the National Academies panel that produced the report, added that the members tried to distinguish between health effects for which there was sufficient as opposed to more limited evidence. But a key limitation in assessing the potential risks — one that also fuels Calonge’s skepticism towards the new MCL — is that scientists still haven’t resolved how PFAS levels in blood and drinking water relate to each other.

The chemicals are slowly excreted from the body in urine and during menstruation, so “how much would you have to drink before you reached the serum level that would put you into an area of concern?” Calonge, who is also the chief medical officer for the Colorado Department of Public Health and Environment, asked. No one knows that, and that’s “the problem with the EPA standard.” The EPA should base its MCL on a concentration that leads to harmful blood serum levels, Calonge said, instead of just analytical detection limits.

THE MAXIMUM PFAS concentration detected so far at GAUD’s Riverside well was PFOA at a level of 7.3 ppt, in November 2022. To drop below 4 ppt, GAUD plans to install a multimillion-dollar system that works by trapping PFAS molecules in granular activated carbon. Tarbuck said that system will be housed in a facility outfitted with heating, ventilation, and air conditioning, and will require permitting and additional labor to sustain operations. Disposal of the spent carbon filters is also an issue since they’re contaminated with PFAS and “that’s material that nobody wants to touch,” Tarbuck said.

CONTINUED IN PART 3 ...