Quote from eliza1275 on December 17, 2019, 1:33 pm

Thanks again for responding @lil-chick. My cat allergy leads to me not breathing within 15 minutes - it's been that way since I was a little girl, so I know I can never become a "cat lady". Even being in a room with someone who has cat hair on their clothes has made me wheezy and sneezy - and I didn't even know the person had cats until after I started having the reaction and asked. And lately certain foods are causing me breathing difficulty, so I cannot eat variety. I am seeing an allergist and possibly other specialists as soon as possible. For now, I have no choice but to eat limited foods (unless I feel like making several trips to the ER).

Quote from lil chick on December 17, 2019, 1:48 pm

I hope things look up very soon.

You know one of my fave people was a horrible asthmatic and his asthma seems to have been cured by his moving to a sunny clime.  Perhaps some of this is about vit D, (and VA blocking the action of D) as Tim and others were discussing yesterday.

Other people here have had an uptick in their asthma with detox.

You should see the crap I'm exposed to keeping chickens and all, and sometimes it is too much, but I can't help but wonder if my body has just deemed some of it "new normal".    I read a book called "the secret language of plants" (buhner) (I think that is where I'm getting this) and one of the plant lessons is: "dig in zee dirt".  🙂

Quote from eliza1275 on December 17, 2019, 1:58 pm

Actually, I live in TX now - so already in a warmer climate! Helps with the Raynauds, at least.

Quote from lil chick on December 17, 2019, 2:42 pm

Wowzer!  that's a big change.  I wonder if I will eventually tire of freezing too.

Quote from hillcountry on December 18, 2019, 2:14 pm

Quote from eliza1275 on December 17, 2019, 1:58 pm

Actually, I live in TX now - so already in a warmer climate! Helps with the Raynauds, at least.

howdy eliza1275 - don't blink if you ever get out Driftwood way, soon to be annexed by San Antonio, ha! Kyle and Buda are coming in on the left-flank (facing south), stealing their water with pipes and pumps, and a big Morgan Kinder gas-line is just about ready to plow on through. My old neighbors are feeling the pinch. I might buy the post-office if it comes up for sale and set up a lemonade stand. The only other reasonable option imho is heading west towards Marfa/Ft. Davis.  We lived the Galveston/Houston life a few incarnations before we hung out hats for 10 years in Driftwood - sure glad we did it in our 30's.  Miss the heck out of Texas. Best regards!

this one's kind of long, but you never know, synchronicity can happen at any time!! 

A friend of ours is a corporate research diva on health-products and food-ingredients. She is very concerned about these molecules called PFOS, PFAS, and a few others in the family of fluorosurfactants. She's really deep into it lately, after about a year of following the papers and connecting the dots. In light of her reaction, I've been looking into them off-and-on. When I read your recent posts, one word jumped out - eosinophil. I located a stashed paper referencing "eosinophil-count". It seemed odd that there were only four markers and that was one of them. The other papers excerpted below it, cover a wide-range of things, some include gut dysbiosis and asthma as a result of these molecules. Maybe there’s some bit of info here that can help you get better. I was in the middle of the binder-stuff and the enterohepatic-recirculation-stuff when I found the paper that said – “The enterohepatic circulation of PFHxS and PFOS likely contributes to their extended elimination half-lives”. Hopefully, they can be successfully eliminated via interrupting that pathway, as can retinyl palmitate. (pardon all the highlights, just a thing I do when reading.)

A critical review of perfluorooctanoate and perfluorooctanesulfonate exposure and immunological health conditions in humans       PMID: 26761418

One other study reported associations of PFAS (including PFOA and PFOS) levels with gene expression patterns, which were in turn related to immune-related outcomes (Pennings et al. 2015); this study is discussed in this section because, like biomarkers, gene expression patterns are nonspecific indicators that do not necessarily correspond to a clinically recognizable condition. Only four specific biomarkers were evaluated in more than one study: white blood cell count, total IgE, eosinophil count, and C-reactive protein. 

Environ Sci Pollut Res Int.    2017

Estrogen receptor beta mediates hepatotoxicity induced by perfluorooctane sulfonate in mouse.

Perfluorooctane sulfonate (PFOS), an artificial fluorosurfactant and global contaminant, is used widely in various consumer products. In this study, we investigated the function of estrogen receptor β (ERβ) in PFOS-induced bile acid and cholesterol metabolism disorders and gut microbiome using ERβ knockout mice that were exposed to PFOS by gavage. Our results showed that a daily dose of 5 mg PFOS/kg   [comment: that is a huge amount]

significantly induced hydropic degeneration and vacuolation in hepatic cells, reduced bile acid, and cholesterol levels in liver tissue, and influenced the abundance and composition of gut microbiota.

Notably, ERβ deficiency not only ameliorated morphological alterations of hepatocytes but also relieved disorders in bile acids and cholesterol metabolism caused by PFOS. 

Furthermore, the changes in the gut microbiome by PFOS were also modulated.

The relative transcript abundance of key genes involved in bile acid and cholesterol metabolism exhibited similar changes. In HepG2 cells, PFOS increased ERβ expression, which could be blocked by adding PHTPP (a selective antagonist of ERβ).

[comment: I assume that means PHTPP occupies the ligand-pocket, and thereby the “expression” of the estrogen receptor is stopped, which means it doesn’t transcribe what it normally would, creating a "deficiency" I suppose.]

Our study thus provides new evidence that ERβ mediates PFOS-induced hepatotoxicity.

PMID:28386898

ERβ is a member of the family of estrogen receptors and the superfamily of nuclear receptor transcription factors. The gene product contains an N-terminal DNA binding domain and C-terminal ligand binding domain and is localized to the nucleus, cytoplasm, and mitochondria. Upon binding to 17-β-estradiol, estriol or related ligands, the encoded protein forms homo-dimers or hetero-dimers with estrogen receptor α that interact with specific DNA sequences to activate transcription. Some isoforms dominantly inhibit the activity of other estrogen receptor family members. Several alternatively spliced transcript variants of this gene have been described, but the full-length nature of some of these variants has not been fully characterized.^[7] ERβ may have anti-proliferative effects and therefore oppose the actions of ERα in reproductive tissue.^[8] ERβ may also have an important role in adaptive function of the lung during pregnancy.^[9] ERβ is a potent tumor suppressor and plays a crucial role in many cancer types such as prostate cancer.^[10][11]

 

Environ Health. 2019; 18: 79.  Published online 2019 Aug 30  

PMID: 31470871

Making the invisible visible: results of a community-led health survey following PFAS contamination of drinking water in Merrimack, New Hampshire

Rubenstein School of the Environment and Natural Resources, University of Vermont, Burlington Merrimack Citizens for Clean Water, Merrimack, NH Toxics Action Center,  Montpelier, VT 

Toxicol Rep. 2016

Hypercholesterolemia with consumption of PFOA-laced Western diets is dependent on strain and sex of mice.

Department of Pathology and Laboratory Medicine, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, GA. Department of Environmental Health, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, GA. University of Cincinnati College of Medicine, Cincinnati, OH and Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention

Perfluorooctanoic acid (PFOA) is a man-made surfactant with a number of industrial applications. It has a long half-life environmentally and biologically. Past studies suggest a direct relationship between plasma cholesterol and PFOA serum concentrations in humans and an inverse one in rodents fed standard rodent chow, making it difficult to examine mechanisms responsible for the potential PFOA-induced hypercholesterolemia and altered sterol metabolism. To examine dietary modification of PFOA-induced effects, C57BL/6 and BALB/c mice were fed PFOA in a fat- and cholesterol-containing diet. When fed these high fat diets, PFOA ingestion resulted in marked hypercholesterolemia in male and female C57BL/6 mice and less robust hypercholesterolemia in male BALB/c mice.

The PFOA-induced hypercholesterolemia appeared to be the result of increased liver masses and altered expression of genes associated with hepatic sterol output, specifically bile acid production.

mRNA levels of genes associated with sterol input were reduced only in C57BL/6 females, the mice with the greatest increase in plasma cholesterol levels. Strain-specific PFOA-induced changes in cholesterol concentrations in mammary tissues and ovaries paralleled changes in plasma cholesterol levels.

mRNA levels of sterol-related genes were reduced in ovaries of C57BL/6 but not in BALB/c mice and not in mammary tissues. Our data suggest that PFOA ingestion leads to hypercholesterolemia in mice fed fat and cholesterol and effects are dependent upon the genetic background and gender of the mice with C57BL/6 female mice being most responsive to PFOA.

PMID:26942110       Free PMC Article

 

Toxicol Sci. 2017

Organic Anion Transporting Polypeptides Contribute to the Disposition of Perfluoroalkyl Acids in Humans and Rats.

Department of Pharmacology, Toxicology and Therapeutics, The University of Kansas Medical Center, Kansas City. Pace Analytical Services, Minneapolis, Minnesota. Medical Department, 3M Company, St Paul, Minnesota. SaluTox, LLC, Lake Elmo, Minnesota.

Perfluoroalkyl sulfonates (PFSAs) such as perfluorohexane sulfonate (PFHxS) and perfluorooctane sulfonate (PFOS) have very long serum elimination half-lives in humans, and preferentially distribute to serum and liver.

The enterohepatic circulation of PFHxS and PFOS likely contributes to their extended elimination half-lives. We previously demonstrated that perfluorobutane sulfonate (PFBS), PFHxS, and PFOS are transported into hepatocytes both in a sodium-dependent and a sodium-independent manner.

We identified Na+/taurocholate cotransporting polypeptide (NTCP) as the responsible sodium-dependent transporter. Furthermore, we demonstrated that the human apical sodium-dependent bile salt transporter (ASBT) contributes to the intestinal reabsorption of PFOS.

However, so far no sodium-independent uptake transporters for PFSAs have been identified in human hepatocytes or enterocytes. In addition, perfluoroalkyl carboxylates (PFCAs) with 8 and 9 carbons were shown to preferentially distribute to the liver of rodents; however, no rat or human liver uptake transporters are known to transport these PFCAs. Therefore, we tested whether PFBS, PFHxS, PFOS, and PFCAs with 7-10 carbons are substrates of organic anion transporting polypeptides (OATPs). We used CHO and HEK293 cells to demonstrate that human OATP1B1, OATP1B3, and OATP2B1 can transport PFBS, PFHxS, PFOS, and the 2 PFCAs (C8 and C9).

In addition, we show that rat OATP1A1, OATP1A5, OATP1B2, and OATP2B1 transport all 3 PFSAs. In conclusion, our results suggest that besides NTCP and ASBT, OATPs also are capable of contributing to the enterohepatic circulation and extended human serum elimination half-lives of the tested perfluoroalkyl acids.   PMID:28013215     Free PMC Article

© The Author 2016. Published by Oxford University Press on behalf of the Society of Toxicology. 

 

Serum Polyfluoroalkyl Concentrations, Asthma Outcomes, and Immunological Markers in a Case–Control Study of Taiwanese Children   PMID: 23309686

This combination of extreme resistance to degradation and environmental ubiquity has raised concerns in recent years (Giesy and Kannan 2001; Lau et al. 2007). Furthermore, studies have shown that PFCs accumulate among the higher trophic level of the food chain, such as predators and human beings (Conder et al. 2008; Houde et al. 2006; Noorlander et al. 2011). Although data from the National Health and Nutrition Examination Survey have indicated a decrease in serum PFC concentrations in the general U.S. population since the production of some PFCs has been phased out [for example, the average concentration of perfluorooctane sulfonate (PFOS) decreased from 30.4 ng/mL in 1999 to 13.2 ng/mL in 2008] (Kato et al. 2011), PFCs are still manufactured abroad (Paul et al. 2009). PFCs bioaccumulate by binding to proteins in the liver and serum, in contrast with many other persistent organic pollutants that persist primarily in adipose tissue (Conder et al. 2008), and they are slowly eliminated without biotransformation (Lau et al. 2007). Serum half-life estimates in an occupationally exposed cohort ranged from 5.4 years for PFOS to 8.5 years for perfluorohexane sulfonic acid (PFHxS) (Olsen et al. 2007).

 

Potential Health Effects Associated with Dermal Exposure to Occupational Chemicals

PMID: 25574139

Emerging evidence suggests that dermal exposure to some chemicals, initially thought to be safe, may result in immune, reproductive, and/or developmental effects as well as cancer, diabetes, and obesity because of their endocrine disrupting properties.²⁷ Endocrine disrupting compounds (EDCs) are synthetic chemicals that can mimic or block hormones and disrupt the body’s normal function, resulting in the potential for numerous health effects. They can act through nuclear hormone receptors, non-steroid receptors, transcriptional coactivators, and other enzymatic pathways involved in steroid biosynthesis and metabolism. Similar to hormones, EDC can function at very low doses in a tissue-specific manner and may exert non-traditional dose–response because of the complicated dynamics of hormone receptor occupancy and saturation. Therefore, exposure to low doses of an EDC may produce a greater impact than exposure to high doses. 

Perfluorinated compounds (PFCs)

Another class of compounds suspected to function as EDC includes PFCs, which are synthetic, highly stable chemicals used in manufacturing of protective coatings for carpets, stain- and grease-resistant clothing, paper coatings, and non-stick pans.¹¹⁷ PFC includes chemicals such as perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluorohexane sulfonate (PFHxS), and perfluoroundecanoic acid (PFUnA).

Their high stabilities and extremely low surface tensions, which lend them to be useful in consumer and industrial applications, have also led to their environmental persistence. Increased concerns have focused specifically on occupationally exposed individuals as their serum PFC concentrations have been found to be up to 1,000 times higher than that of the general population.¹¹⁸ PFCs have been associated with a number of health effects related to reproductive function and thyroid dysfunction in the general public^119,120 and cancer in a contaminated community.¹²¹ While inhalation and oral are common exposure routes, studies support the potential for skin absorption of these compounds.¹²² Occupational exposure has been linked to health effects such as prostate cancer and non-hepatitis liver diseases, malignant and nonmalignant renal diseases, diabetes mellitus, chronic renal disease, and female hypothyroidism.^123,124

Perfluorooctane sulfonate (PFOS) is an environmental contaminant that has been manufactured to be used as surfactants and repellents in industry. Due to long half-life for clearance and degradation, PFOS is accumulative in human body and has potential threat to human health. Previous studies have shown the development and function of immune cells can be affected by PFOS. Although PFOS has a high chance of being absorbed through the oral route, whether and how PFOS affects immune cells in the gut is unknown. Using mouse model of Citrobacter rodentium infection, we investigated the role of PFOS on intestinal immunity. We found at early phase of the infection, PFOS inhibited the expansion of the pathogen by promoting IL-22 production from the group 3 innate lymphoid cell (ILC3) in an aryl hydrocarbon receptor dependent manner. Nevertheless, persistent PFOS treatment in mice finally led to a failure to clear the pathogen completely. At late phase of infection, enhanced bacterial counts in PFOS treated mice were accompanied by increased inflammatory cytokines, reduced mucin production and dysbiosis, featured by decreased level of Lactobacillus casei, Lactobacillus johnsonii and increased E. coli. Our study reveals a deleterious consequence in intestinal bacterial infection caused by PFOS accumulation.

Perfluorooctane sulfonate (PFOS) is widely used as surface treatment chemical, polymerization acid and surfactant in industry, due to its chemical stability, high surface activity and water and oil repellence property.

The 3 M Company, main manufacturer of PFOS, phased out the product in 2002 because of toxic effects of PFOS to the human endocrine, reproductive and immune systems¹–⁴.

In 2009, the 4^th meeting of the Conference of the Parties to the Stockholm Convention listed PFOS to the Annex B to limit the use of PFOS⁵. Though the application of PFOS has been abandoned by its main manufacturer, emission of PFOS still persists in many countries due to a lack of cost-efficient alternatives⁶, ⁷. Besides, the half-life for clearance of PFOS in the serum is as long as 4.8 years on average⁸. Thus, PFOS is bio-accumulative in water and ground and remains to be a potential threat to human health worldwide.

PFOS has been reported to affect the immune cells in the central and peripheral lymphoid organs by various mechanisms⁹–¹⁶. Animal studies have shown high dose of PFOS treatment causes atrophy of the thymus and spleen¹⁰, ¹⁵. And in vivo PFOS treatment inhibits Th1 responses while Th2 responses are promoted⁹, ¹³, ¹⁴. Being a paper-packaging material and a contaminant in the water, PFOS can frequently be absorbed through the oral route and accumulate in the intestine, thus modulate intestinal immunity under physiological and pathological conditions. However, it is not known whether and how PFOS affects the intestinal immune cells, especially during pathological conditions such as intestinal bacterial infections.

PFOS exposure caused persistent inflammation in the intestine accompanied by decreased mucin production from goblet cells and dysbiosis, which finally led to a failure to clear C. rodentium at late phase of infection. Our finding reveals that PFOS exposure leads to a detrimental consequence in intestinal bacterial infection.

Perfluorooctane sulfonate (PFOS) exhibits differential roles at different stages of intestinal bacterial infection

Interestingly, E. coli was found to increase in PFOS treated group compared to control group at late but not early phase of infection, suggesting the presence of dysbiosis specifically at late phase of infection

Mucins produced by goblet cells in the intestinal epithelium are crucial for maintaining a healthy community of microbiota in the gut⁵⁰, ⁵¹. Pro-inflammatory cytokines including IL-17 and IFN-γ have been indicated to cause tissue damage or result in loss of goblet cells during intestinal inflammation⁵², ⁵³. We suspect the enhanced inflammation induced by PFOS at late stage of C. Rodenium infection may cause a defective mucin production by goblet cells. We then analyzed the mRNA expression of mucins in colon tissues by real-time RT-PCR. We observed significant reduction of mRNA expression of mucin 1 and mucin 2 at late stage but not early stage of C. rodentium infection in PFOS treated mice compared to control (Fig. 7A and B), while expression of mucin 3 was comparable between two groups (Fig. 7A and B). Interestingly, we found the mRNA expression of RELM-β, a resistin-like molecule specifically expressed by goblet cells, decreased in PFOS treated mice at late but not early phase of C. rodentium infection (Fig. 7C and D). The combinatorial downregulation of mucins and RELM-β may result in dysbiosis featured by increased E. coli and decreased Lactobacillus species⁵¹.

The above data suggest long-term treatment of PFOS suppresses the expression of mucin 2 independent of infection.

Since anti-microbial peptides are well-known as targets of IL-22²⁵, the failed induction of anti-microbial peptides in response to higher IL-22 in PFOS treated mice at late phase of infection may due to a damage of epithelial cells caused by overt inflammation. Previous studies have revealed the pathogenic role of IL-17 and IFN-γ in tissue damage and loss of goblet cells⁵², ⁵³

The effect of PFOS on ILC3 is organ-specific because ILC3s and Th17 cells are specifically abundant in the intestine but rare in other organs under the steady state in mice⁵⁷–⁵⁹. PFOS has been reported to affect the immune cells in the central and peripheral lymphoid organs by various mechanisms⁹–¹², ¹⁴–¹⁶. High dose of PFOS exposure has been shown to cause atrophy of the thymus and spleen, as well as the percentages of T cell subsets in the spleen¹⁰, ¹⁵. In this study, we used a previously reported low dose of PFOS to avoid direct toxicity to the thymus and spleen¹⁰. Except for the role of PFOS in promoting Th17 cell responses in the gut, similar effect is likely to occur in different autoimmune disorders where Th17 cells are pathogenic, such as multiple sclerosis and rheumatoid arthritis⁶⁰, ⁶¹. Thus, it brings out an alert that PFOS accumulation may be detrimental for autoimmune diseases. Epidemiologic and experimental studies are called for further evaluation for the correlation of PFOS accumulation and autoimmune diseases.

 

Quote from eliza1275 on December 18, 2019, 3:11 pm

@hillcountry I had to look up Driftwood and Marfa/Ft. Davis - I'm still very new to the state. I live in Allen, just north of Plano (Dallas area). Love it here so far! 

Anyway, thank you so much for your response and all of the information on PFAS, PFOA, etc.  I do believe we are inundated with chemicals, and it's difficult to know from where and how great the exposure is. I do have non-stick cookware, which I will be promptly replacing with cast iron. Other than that, I eat bagged potato chips, but I didn't much before this all happened to me. In fact, I was a "healthy" eater, preparing most of my food at home. It all happened after I had a baby. I've read about immune system changes after pregnancy, so perhaps that tipped the scale as well. 

I'm drinking FIJI water currently, but previously drank tap water. I wonder about that, with regards to PFAS. Any tips you have would be much appreciated.

Quote from lil chick on December 18, 2019, 4:18 pm

I use basic stainless steel and worry about using my cast iron pan (which I love) because it does appear that storing iron (as well) might be a part of being a va-toxic person.

There are tricks to using plain stainless, it doesn't have to be a nightmare of scrubbing if you manage it!  🙂 

Quote from lil chick on December 18, 2019, 4:21 pm

Did you have any vaccines around the time when you had the baby?  I did, and I really do think they sped up my problems, but I think they were going to come at some point.  Eventually, after long and hard thinking I became an anti-vaxer.  It certainly wasn't overnight, it took me years to begin to doubt vaccines.  I had an extremely bad reaction to a vax in my child-bearing years.

Quote from lil chick on December 18, 2019, 4:23 pm

Your attraction to chips is quite opposite from what I'm feeling about them lately!