Forever chemicals ~ a saving breakthrough in the making

[Bo Atkinson]

Cleanup reagent discovered the as a possible beginning stage, to break down the toxic pollution! Two Articles:

https://scienceblog.com/533029/forev...UQ2tzMFdHjLVdg


https://www.livescience.com/pfas-for...6-cfbbb45a367f

[ExomatrixTV]

• PFAS: The Secret Toxins In Your Body

Source: https://youtube.com/watch?v=lVcOxZZGrBc

• Forever Chemicals PFAS, PFOA, PFOS, BPA, Explained Clearly:

Source: https://youtube.com/watch?v=8QuvTjLZaXs

• PFAS and How to Remove the Silent Threat in Our Water:

Source: https://youtube.com/watch?v=43ZbkT3lw0w

• Scientists Found the ‘Achilles’ Heel’ That Could Destroy ‘Forever Chemicals’ for Good

Chemists discovered a simple way to get rid of some types of PFAS, the toxic chemicals left over from plastics

• On Wisconsin’s French Island, residents live with lingering ‘Forever Chemicals’
• Scientists Have Discovered How to Break Down Some ‘Forever Chemicals’

Source: https://youtube.com/watch?v=HQWHj_gx-t8

[ExomatrixTV]

• Study: No Rainwater Anywhere Safe To Drink Due To ‘Forever Chemicals’:

Source: https://youtube.com/watch?v=c1uVyeBPNoI

• PFAS: Last Week Tonight with John Oliver (HBO):

Source: https://youtube.com/watch?v=9W74aeuqsiU

• 5,216,242+ views

• PFAS: Treatment: How We "Clean Up" The Contamination:

Source: https://youtube.com/watch?v=MmSDCNiXrcQ

• Characterization And Engineering Of A Plastic-degrading Aromatic Polyesterase

• Synthetic polymers are ubiquitous in the modern world but pose a global environmental problem. While plastics such as poly(ethylene terephthalate) (PET) are highly versatile, their resistance to natural degradation presents a serious, growing risk to fauna and flora, particularly in marine environments. Here, we have characterized the 3D structure of a newly discovered enzyme that can digest highly crystalline PET, the primary material used in the manufacture of single-use plastic beverage bottles, in some clothing, and in carpets. We engineer this enzyme for improved PET degradation capacity and further demonstrate that it can also degrade an important PET replacement, polyethylene-2,5-furandicarboxylate, providing new opportunities for biobased plastics recycling.

• Abstract
  
  Poly(ethylene terephthalate) (PET) is one of the most abundantly produced synthetic polymers and is accumulating in the environment at a staggering rate as discarded packaging and textiles. The properties that make PET so useful also endow it with an alarming resistance to biodegradation, likely lasting centuries in the environment. Our collective reliance on PET and other plastics means that this buildup will continue unless solutions are found. Recently, a newly discovered bacterium, Ideonella sakaiensis 201-F6, was shown to exhibit the rare ability to grow on PET as a major carbon and energy source. Central to its PET biodegradation capability is a secreted PETase (PET-digesting enzyme). Here, we present a 0.92 Å resolution X-ray crystal structure of PETase, which reveals features common to both cutinases and lipases. PETase retains the ancestral α/β-hydrolase fold but exhibits a more open active-site cleft than homologous cutinases. By narrowing the binding cleft via mutation of two active-site residues to conserved amino acids in cutinases, we surprisingly observe improved PET degradation, suggesting that PETase is not fully optimized for crystalline PET degradation, despite presumably evolving in a PET-rich environment. Additionally, we show that PETase degrades another semiaromatic polyester, polyethylene-2,5-furandicarboxylate (PEF), which is an emerging, bioderived PET replacement with improved barrier properties. In contrast, PETase does not degrade aliphatic polyesters, suggesting that it is generally an aromatic polyesterase. These findings suggest that additional protein engineering to increase PETase performance is realistic and highlight the need for further developments of structure/activity relationships for biodegradation of synthetic polyesters.

• source

While this study successfully degraded ten perfluoroalkyl carboxylic acids (PFCAs) and perfluoroalkyl ether carboxylic acids (PFECAs), there’s a long way to go. The EPA estimates that 11,990 PFAS types are still out there.
source

[ExomatrixTV]

• Human Health Concerns Associated With PFASS

On their introduction in the 1940s, per- and polyfluoroalkyl substances (PFASs) were considered inert.[15][16] In fact, early occupational studies revealed elevated levels of fluorochemicals, including perfluorooctanesulfonic acid (PFOS) and perfluorooctanoic acid (PFOA, C8), in the blood of exposed industrial workers, but cited no ill health effects.[17][18] These results were consistent with the measured serum concentrations of PFOS and PFOA in 3M plant workers ranging from 0.04 to 10.06 ppm and 0.01–12.70 ppm respectively, well below toxic and carcinogenic levels cited in animal studies.[18] Given, however, the "forever chemical" property of PFASs (serum elimination half-life 4–5 years) and widespread environmental contamination, molecules have been shown to accumulate in humans to such a degree that adverse health outcomes have resulted.[15]


Hormone-disrupting chemicals, including PFASs, are linked with rapid declines in human fertility.[25] In a metanalysis for associations between PFASs and human clinical biomarkers for liver injury, authors considered both PFAS effects on liver biomarkers and histological data from rodent experimental studies and concluded that evidence exists showing that PFOA, perfluorohexanesulfonic acid (PFHxS), and perfluorononanoic acid (PFNA) are hepatotoxic to humans.[26]

Many comprehensive epidemiological studies linking adverse human health effects to PFASs, particularly PFOA, come from the C8 Science Panel,[27] formed as part of a contingency to a class action lawsuit brought by communities in the Ohio River Valley against DuPont in response to landfill and wastewater dumping of PFAS-laden material from DuPont's West Virginia Washington Works Plant.[27] The panel measured PFOA (also known as C8) serum concentrations in 69,000 individuals from around DuPont's Washington Works Plant and found a mean concentration of 83.0 ng/mL, compared to 4 ng/mL in a standard population of Americans.[28] This panel reported probable links[vague] between elevated PFOA blood concentration and hypercholesterolemia, ulcerative colitis, thyroid disease, testicular cancer, kidney cancer as well as pregnancy-induced hypertension and preeclampsia.[29][30][31][32][33]

In a report by the Nordic Council of Ministers the total annual health-related costs associated with human exposure to PFASs were estimated to be at least €52-€84 billion in the European Economic Area (EEA) countries.[34] Aggregated annual costs covering environmental screening, monitoring where contamination is found, water treatment, soil remediation and health assessment total €821 million-€170 billion in the EEA plus Switzerland.[34]

Proposed Mechanisms Of PFAS-related Adverse Health Outcomes

• Hypercholesterolemia

Animal studies in the 1990s and early 2000s primarily aimed to investigate the effect of two widely used long-chain PFASs, perfluorooctanoic acid (PFOA, C8) and perfluorooctane sulphonic acid (PFOS, C8), on peroxisome proliferation in rat livers.[35] These studies determined that PFOA and PFOS acted as Peroxisome proliferator-activated receptor (PPAR) agonists, increasing lipid metabolism.[35] A paradoxical response is observed in humans where elevated PFOS levels were significantly associated with[vague] elevated total cholesterol and LDL cholesterol, highlighting significantly reduced PPAR expression and alluding to PPAR independent pathways predominating over lipid metabolism in humans compared to rodents.[36]

• Ulcerative colitis

PFOA and PFOS have been shown to significantly alter immune and inflammatory responses in human and animal species. In particular, IgA, IgE (in females only) and C-reactive protein have been shown to decrease whereas antinuclear antibodies increase as PFOA serum concentrations increase.[37] These cytokine variations allude to immune response aberrations resulting in autoimmunity. One proposed mechanism is a shift towards anti-inflammatory M2 macrophages and/or T-helper (TH2) response in intestinal epithelial tissue which allows sulfate-reducing bacteria to flourish. Elevated levels of hydrogen sulfide result which reduce beta-oxidation and thus nutrient production leading to a breakdown of the colonic epithelial barrier.[38]

• Thyroid Disease

Hypothyroidism is the most common thyroid abnormality associated with[vague] PFAS exposure.[39] PFASs have been shown to decrease thyroid peroxidase, resulting in decreased production and activation of thyroid hormones in vivo.[40] Other proposed mechanisms include alterations in thyroid hormone signaling, metabolism and excretion as well as function of nuclear hormone receptor.[39]

• Cancer

Rat studies investigating the carcinogenicity of PFASs reported significant correlation with liver adenomas, Leydig cell tumors of the testis and pancreatic acinar cell tumors and dietary PFOA consumption.[40] The C8 Science Panel investigated the potential relationship between PFAS exposure and these three cancer types as well as 18 other cancer types in their epidemiological studies. Contrary to the animal studies, the C8 studies did not find a probable link[vague] between elevated C8 exposure and liver adenomas or pancreatic acinar cell tumors; however, a probable link[vague] was found with regards to testis and kidney cancer.[41] Two mechanisms have been proposed by which PFOA could cause Leydig cell tumors. Both mechanisms start by proposing that PROA exposure results in increased PPAR alpha activation in the liver which increases hepatic aromatase concentration and subsequent serum estrogen levels. The mechanisms now diverge, with one pathway suggesting elevated estradiol levels increase Tissue Growth Factor alpha (TGF alpha) which prompts Leydig cell proliferation. The other pathway suggests that aromatization of testosterone to estradiol reduces serum testosterone levels resulting in increased release of luteinizing hormone (LH) from the pituitary gland which directly results in Leydig Cell tumorgenesis.[42] A mechanism has not yet been proposed to explain how kidney cancer could be caused by C8 exposure as no in vivo animal studies have been able to model this epidemiological outcome.[43]

• Pregnancy-induced hypertension and pre-eclampsia

Pregnancy-induced hypertension is diagnosed when maternal systolic blood pressure exceeds 140 mmHg or diastolic blood pressure exceeds 90mmHg after 20 weeks gestation.[44] Diagnostic criteria are the same for pre-eclampsia as pregnancy-induced hypertension; however, it also confers proteinuria. Mechanisms by which pregnancy-induced hypertension and preeclampsia could be caused by PFAS exposure have remained elusive and are largely speculative to date. One proposed mechanism highlights alterations in immune function leading to disruption of placentation, specifically as it pertains to natural killer (NK) cell infiltration of the placenta to facilitate trophoblastic integration with placental blood supply.[45] Another mechanism refers to agonism of PPARs contributing to alterations in cholesterol, triglyceride and uric acid levels which may lead to vascular inflammation and elevated blood pressure.[45]

Other adverse health outcomes that have been attributed to elevated PFAS exposure but were not found to be probable links[vague] in the C8 studies are decreased antibody response to vaccines, asthma, decreased mammary gland development, low birth weight (-0.7oz per 1 ng/mL increase in blood PFOA or PFOS level), decreased bone mineral density and neurodevelopmental abnormalities.[46][47][48]

• source

[ian33]

https://www.slu.se/en/research/knowl.../pfas-ozon-en/

[ExomatrixTV]

• The PFAS Cover-Up ... 2 Dutch-English Special 2023 Reports