panaceachronicles

Thoughts On Coca, Cannabis, Opium & Tobacco – Gifts Of The Great Spirit


Leave a comment

Did Mom Give You Testicular Cancer?

             Stu Kraft – Brother, Friend, Artist, Beloved Fisher

I dedicate this post to our brother Stu Kraft, a mountain man full of joy, talent, energy and life whose mother was a heavy smoker from the 1950’s until her death of lung cancer. Stu was born with reproductive system issues, and turned even that into art. He loved to make his friends uncomfortable by joking about his “monoball”, and once serenaded a large party with an impromptu and delightfully bawdy song about a sailor with one ball and the feats he manfully managed to perform. It turned out that Stu’s monoball must have been attacked in the womb by the hidden DDT in his Mom’s cigarettes, because when he was in his early 50’s monoball turned on him and killed him.

Researchers have long known there is a connection between smoking and testicular cancer. They just couldn’t explain what it is.

But when you examine a secret tobacco industry study from 1972 (see more below) then we can see that it’s more than just possible that a lot of 2019’s testicular cancer will arise from a genetic hit in the womb from the DDT in a mother’s (or grandmother’s) cigarettes in the 1960’s or 70’s. That genetic hit occurred because with every puff she was inhaling massive doses of hidden organochlorine pesticides.

Mothers weren’t being irresponsible by smoking in those days – many doctors even advised it. Mothers smoked because they believed it would help to keep their weight from getting out of control and to deal with the stress of Motherhood. Everybody did it.

Here’s How Mothers & Fetuses Were Exposed To DDT in the 1970’s

The problem with looking at DDT in Tobacco products is that all the DDT exposure studies ever done deal only with the health consequences of environmental exposure to DDT and ingestion in food or water. Nobody has ever studied the health effects of smoking pesticide contaminated tobacco products because the Tobacco industry knew about the problem and actively and completely suppressed that kind of research. It just hasn’t been done.  But DDT and other organochlorines have been there in heavy concentrations since 1955, and we now know that genetic damage caused by organochlorine pesticides is transgenerational, and targets specific parts of the genome in order to accomplish this stealth transmission of genetic disease.

Bottom line – if that mother or grandmother we referred to above was pregnant and smoking cigarettes between 1955-1980 she was without any question micro-dosing herself and her unborn child with DDT.

I referred to a confidential RJR report above. It’s from 1972, with all the original signatures, and reports on tests of DDT contamination of three RJR brands. All three brands show heavy contamination, and other research I’ve done shows that the entire tobacco product supply in the US in those days was loaded with enough chemicals to explain nearly all the smoking-related disease we see today.

If the anti-tobacco forces weren’t barely disguised Victorian moralists moralists, under the weight of factual evidence of pesticide contamination they would have to recognize that there is a legitimate question about whether it is actually tobacco that is responsible for all smoking-related disease and if not, what else is responsible and in what proportion? The fact is that there was DDT in every US cigarette in 1972, and that the sons of mothers born to mothers who smoked in those days are now known to be at high risk of testicular (and other) cancer in 2019. I’ll link you to peer-reviewed journal research on this below but first here’s a table summarizing the data on DDT in those three RJR brands in 1972. This is what millions of grandmothers of today’s middle-age men were inhaling. (BTW – this report only covered DDT – there were many other heavy organochlorine residues in 1972 cigarettes.)

RJR Confidential June 21, 1972

Project 2358 – Cigarette Development; Notebook Pages: 250701-250719

In The Cigarette

DDT – Range PPM (20 samples)

DDT – Avg PPM (20 Samples)

4841 – Regular Unfiltered

4.14 – 7.96

6.06 +/- 0.99

4842 – Filter King

3.38 – 6.65

4.95 +/- 0.90

4843 – Filter King

4.86 – 6.82

5.89 +/- 0.61

In The Cigarette Smoke

4841 – Regular Unfiltered

0.35 – 0.57

0.42 +/- 0.06

4842 – Filter King

0.16 – 0.35

0.025 +/- 0.05

4843 – Filter King

0.24 – 0.46

0.35 +/- 0.05

Here’s What’s Happening To Male Children Today

J Natl Cancer Inst. 2008 May 7;100(9):663-71.

Persistent organochlorine pesticides and risk of testicular germ cell tumors

https://www.ncbi.nlm.nih.gov/pubmed/18445826

CONCLUSIONS:

Increased exposure to p,p’-DDE may be associated with the risk of both seminomatous and nonseminomatous TGCTs, whereas exposure to chlordane compounds and metabolites may be associated with the risk of seminoma. Because evidence suggests that TGCT is initiated in very early life, it is possible that exposure to these persistent organic pesticides during fetal life or via breast feeding may increase the risk of TGCT in young men.

Here’s Why Even Tiny, Steady Doses Of DDT Matter

Male Reproductive Health and Environmental Xenoestrogens

https://ehp.niehs.nih.gov/doi/pdf/10.1289/ehp.96104s4741

Long-term exposure to small amounts of organochlorine contaminants leads to the accumulation of considerable burdens in animal and human tissues. It is therefore not the amount of DDT to which a mother is exposed during pregnancy that is critical but rather her lifetime exposure that will determine the level of exposure of the fetus and the breast-fed infant.

Here’s Evidence That This Is Happening Worldwide

Human Reproduction, Volume 16, Issue 5, 1 May 2001, Pages 972–978

Testicular dysgenesis syndrome: an increasingly common developmental disorder with environmental aspects: Opinion

https://academic.oup.com/humrep/article/16/5/972/2913494

This article summarizes existing evidence supporting a new concept that poor semen quality, testis cancer, undescended testis and hypospadias are symptoms of one underlying entity, the testicular dysgenesis syndrome (TDS), which may be increasingly common due to adverse environmental influences.

Experimental biological investigations and epidemiological studies leave little doubt that the TDS can be a result of disruption of embryonal programming and gonadal development during fetal life. As the rise in the incidence of the various symptoms of TDS occurred rapidly over few generations, the aetiological impact of adverse environmental factors such as hormone disrupters, probably acting upon a susceptible genetic background, must be considered.

While the focus of this post is on DDT and TDS, take a look at the pesticide contaminants that we just found in a sample of tobacco brands purchased off-the-shelf at out Portland-area minimarts, The first thing that stands out is the number of contaminants and – look at that – the cheaper the brand the higher the contamination and the worse the contaminants. In fact, the cheaper the brand the more Testicular disrupting/damaging chemicals there are – look at the Carbendazim in the Swisher Sweets. Combined with the action of DDT on Testicular tissues and hormones Carbendazim is equally well-documented as a male reproductive system poison and carcinogen.

Carbendazim is a broad-spectrum benzimidazole antifungal with potential antimitotic and antineoplastic activities. Although the exact mechanism of action is unclear, carbendazim appears to binds to an unspecified site on tubulin and suppresses microtubule assembly dynamic. This results in cell cycle arrest at the G2/M phase and an induction of apoptosis.

The point of this is to say that the brand of tobacco product your mother smoked matters more than just about any other factor in determining your risk of Testicular cancer as an adult. This means staying alert and getting checked often – which Stu did not do. I would end this with RIP, but there’s no way that “Tiny Ball” is laying around resting, wherever he is.

CURATED BLOG POSTS ON RELATED TOPICS

Hidden Causes Of HIV/AIDS Treatment Failure

https://wp.me/p48Z9A-nOD

The Korean Genome + Smoking + (DDT) = Diabetes Epidemic

https://wp.me/p48Z9A-nO6

Ancestral DDT Exposure & Trans-generational Obesity

https://wp.me/p48Z9A-nNO

Smoking & Breast Cancer – A New Link?

https://wp.me/p48Z9A-nNl

Little Cigars And High Liver Cancer Rates In Marginalized Communities

https://wp.me/p48Z9A-nMy

Sweet Cheap Poison At The Bodega

https://wp.me/p48Z9A-nLj

Prostate Cancer & Tobacco Pesticides: Hidden Links

https://wp.me/p48Z9A-nKy

Obesity & Obesogens: The Tobacco Connection

https://wp.me/p48Z9A-nJ4

Tobacco Pesticides & Childhood Leukemia

https://wp.me/p48Z9A-nIL


Leave a comment

Smoking & Breast Cancer – A New Link?

Because of the heavy concentrations of DDT and other endocrine disrupting pesticide residues we recently detected contaminating popular tobacco brands, I’ve been thinking a lot about the fact that beginning with the 1950s every tobacco product being smoked, puffed, dipped or chewed in America had extremely heavy concentrations of organochlorine pesticides. Heavy use of xenobiotic “crop protection” agents for tobacco began in the 1950s with DDT and quickly included aldrin, endrin, dieldrin, chlordane and other byproducts of wartime toxic gas research.

With that in mind, please check this:

DDT Exposure in Utero and Breast Cancer  The Journal of Clinical Endocrinology & Metabolism, Volume 100, Issue 8, 1 August 2015, Pages 2865–2872,

Maternal o,p′-DDT predicted daughters’ breast cancer (odds ratio fourth quartile vs first = 3.7, 95% confidence interval 1.5–9.0). Mothers’ lipids, weight, race, age, and breast cancer history did not explain the findings.

DDT and Breast Cancer: Prospective Study of Induction Time and Susceptibility Windows . Journal of the National Cancer Institute, 13 February 2019

“Considering the patterns we observed, working backward to determine when a woman first came into contact with the chemical could help inform early detection and treatment of DDT-associated breast cancer.”

Women who were born roughly between 1955-1980 to mothers who smoked (or dipped or chewed) any of the popular tobacco brands of the times were heavily exposed to DDT and other organochlorines in the womb and probably throughout early childhood as Mommy smoked to get rid of all that pregnancy weight and then kept on smoking, maybe in secret, just a little, because it calmed her nerves.

A confidential industry study done in 1972 that I located in the Tobacco Settlement files reported an average of almost 6 mg/kg total DDT over all the brands they tested anonymously. The report ended with a hope that DDT concentrations would be dropping in the future (it had just been banned worldwide for the first time in 1972), and a warning that the data must be kept secret.

But when you look at what we found in tobacco products in 2018 you can see how little progress has been made. While there is only one instance of DDT contamination here it is extreme, and as you can see there are several rather extreme concentrations of other hazardous endocrine disrupting pesticide residues here even in this small sample. There are also residues of pesticides for which no data exist – their effects are unknown. It’s a crap shoot with human lives rolling snake eyes.

Community Tobacco Control Partners Test Results 12/18

If my interpretation of how our new tobacco pesticide residue data applies to the breast cancer research on endocrine disrupting chemicals is right, and it seems pretty straightforward, women in 2019 with medical history that includes parental and especially maternal smoking during birth years 1955-1980 are at severely heightened risk that requires close attention. I am NOT saying that the threat ended in 1980 – it changed, and it got worse. As you can see from the data above, female babies born today to young mothers who smoke Swisher Sweets, or who live in a household where they are smoked, are continually exposed to heavy doses of DDT. What does that say about their risk for breast cancer in 2050?

But in this post I am talking only about DDT and organochlorine exposure of women who were born to smoking mothers 1955-1980.

Know thy unknowns: why we need to widen our view on endocrine disruptors, Journal of Epidemiology and Community Health, 71:3, 2016 (209-212)

These compounds ‘interfere with any aspect of hormone action’, and by doing so can adversely affect physiology and development and thus increase the risk of metabolic and reproductive disorders as well as hormone-sensitive carcinogenesis and impaired neurodevelopment

So keeping with the theme, here are a few more things you may want to review.

Environmental chemicals and breast cancer: An updated review of epidemiological literature informed by biological mechanisms, Environmental Research, 160, (152-182)

Organochlorine concentrations in adipose tissue and survival in postmenopausal, Danish breast cancer patients, Environmental Research, 163,(237-248)

Receptor activities of persistent pollutant serum mixtures and breast cancer riskEndocrine-Related Cancer, 10.1530/ERC-17-036625:3, (201-215),

 Evidence of the Possible Harm of Endocrine-Disrupting Chemicals in Humans: Ongoing Debates and Key IssuesEndocrinology and Metabolism10.3803/EnM.2018.33.1.4433:1, (44), 

 Changes in the total effective xenoestrogen burden (TEXB) of breast cancer patients during an 18-month post-surgical follow-upReproductive Toxicology10.1016/j.reprotox.2017.03.007, 69, (212-220),

A Ternary Mixture of Common Chemicals Perturbs Benign Human Breast Epithelial Cells More Than the Same Chemicals Do IndividuallyToxicological Sciences10.1093/toxsci/kfy126

Finally, as you look at this last reference, note the “higher girl’s BMI” factor, and consider the role of EDC in obesity. What if the EDC’s in the mother’s tobacco products contribute in utero and during childhood to the child’s obesity which in turn adds to her potential for breast cancer development? If so, we know for sure harmful pre-natal EDC exposure is going on today and is not just something that happened 1955-1980. 

Prenatal smoking and age at menarche: influence of the prenatal environment on the timing of puberty  Human Reproduction, Volume 30, Issue 4, 1 April 2015, Pages 957–962

We find that older maternal AAM (hazards ratio (HR): 0.75, confidence interval (CI) (95%): 0.71–0.79) and higher birthweight (HR: 0.86, CI (95%): 0.75–0.97) lower the chance of earlier menarche; while higher girls’ BMI at 8–9 years (HR: 1.12, CI (95%): 1.10–1.15), and maternal cigarette smoking on ‘most days’ during gestation (HR: 1.40, CI (95%): 1.10–1.79 with ‘no smoking’ as the reference level) increased the chance of earlier menarche. All factors were statistically significant at P = 0.05.


Leave a comment

Little Cigars And High Liver Cancer Rates In Marginalized Communities

As I continue to mine the data from our December 2018 tests of off-the-shelf tobacco products for pesticide residues I keep running across small surprises that have big implications. Here’s a good example – the data has just shown me a likely connection between little cigar use and the puzzling high rates of liver cancer in Hispanic, Black and Native American communities.

The connection may lie in two of the pesticide contaminants just found in Swisher Sweets – check the carbendazim and cypermethrin in the right-hand data column below. Exposure to either of these chemicals is strongly linked to liver disease; exposure to the two chemicals together appears to have much greater impact than just the simple sum of their effects. They are more than merely additive and they are synergistic. (many additional citations below)

Basic Clin Pharmacol Toxicol. 2012 May;110(5):433-40

“Carbendazim impends hepatic necrosis when combined with imazalil or cypermethrin.”

“Low doses of carbendazim in combination with low doses of imazalil or cypermethrin caused very pronounced hepatic necrosis, more than any of the three individually applied pesticides or combination of imazalil and cypermethrin.”

Community Tobacco Control Partners Test Results 12/18

This study, like the others cited below, is an experiment to see what happens when you combine these two liver toxins. They use mice and rats. They aren’t saying that in the real world you would ever find people exposed to levels of carbendazim and cypermethrin like this at the same time. That would never happen. Except …

If you’re a super-cool young Latino dude smoking Swisher Sweets and fantasizing Carly B, or maybe a young Black mother smoking them because she’s heard they’re less harmful than cigarettes. They’re going to get the full load of carbendazim and cypermethrin together, over and over with every puff. 

Hum Exp Toxicol. 2012 May;31(5):492-505

“Carbendazim combined with imazalil or cypermethrin potentiate DNA damage in hepatocytes of mice.”

“In combination with carbendazim clastogen, properties of imazalils and cypermethrins were potentiated compared to all other treatments and control.

Higher long tail nuclei (LTN) in females indicate that certain cells in females were especially prone to total nucleus disintegration. ‘

Due to synergistic effects, low environmentally present concentrations of imazalil and cypermethrin in food, and especially their mixtures with carbendazim have genotoxic potential that could be particularly dangerous over prolonged exposure in mammalian organism.”

There’s not a single study anywhere that looks at individual pesticides in tobacco products and their impact on human health as inhaled toxins, much less when they are inhaled together day after day in a supertoxic cocktail. I suppose you could call this a simple oversight on the part of thousands of highly trained, highly paid scientists, doctors and regulators. I suppose you could say that.

But that’s exactly what millions of Latino, Black and Native people throughout the Americas are doing – inhaling that carbendazim/cypermethrin cocktail 20-40-60 times a day every day. That’s their only option too, because their only choices are the cheapest most contaminated brands of tobacco products, not the relatively cleaner high-end cigarettes smoked in economically privileged White communities. 

Young Latino, Black and Native American little cigar smokers are also inhaling at least 16 other pesticides in combination with the carbendazim/cypermethrin. No studies exist on what that incredible level of toxic synergy may be doing, but the studies on just the carbenzadim/cypermethrin combination are certainly suggestive. How about if you just add a little DDT to the mix? Done.

Both carbendazim and cypermethrin (and DDT) are potent high-tech Endocrine Disruptors, and they are present here in very significant concentrations, not traces, although endocrine disruptors have been conclusively shown to operate independently of concentration. This characteristic is known as a non-monotonic dose response, and is a much-needed refinement of the standard approach to determining a pesticide’s hazardous levels of exposure. This is especially true with the ED pesticides like Carbendazim and Cypermethrin that appear to have no safe level of exposure at all.

Extraordinarily important work by Dr. Laura Vandenberg of Massachusetts Public Health has shown that the classic way of looking at pesticide toxicity is not only wrong but dangerous in an age of designer pesticides that no longer rely on the brute force of chemical poison. http://dose-response.org/wp-content/uploads/2014/06/Vandenberg-2013-dose-response.pdf

According to Dr. Vandenberg, and these are my words, there is a strong belief among regulators, and way too many scientists, that once you establish a level at which a pesticide does measurable damage you can simply project backwards in a straight line to lower doses and estimate a level where it can’t possibly do any harm.

That makes regulators happy – they have a number. That means they have a full-time job monitoring that number. Above that number – we have a problem and we get to enforce our rules. Below that number – you’re good to go and we’ve done our job protecting the public. Next!

That approach worked great with the first pesticides, which were all heavy-duty poisons. The more poison you use, the more bugs you kill. When bugs develop resistance, use more. If the first spray doesn’t get them all, spray again. But regulators keep people “safe” by limiting the amount that can be used per acre. If you’re a farmer and you reach that amount and the bugs keep eating your crop you yell at the chemical companies and they come up with a newer, stronger, different kind of poison using the same process.

What dose of this new shit kills all the rats? OK, that’s too much. How about a lower dose? Hmmm – still kills a bunch and now it seems to cause tumors. How about this teeny weeny dose? Hey, that seems to work. Look – no bugs, and the rats are alive. Well, most of them. We’re good to go! Off to the tobacco fields! Better living through chemistry.

But then all the poisons stopped working. Well, not entirely, but you had to keep piling them on and it got to the point where all those organochlorine pesticides were causing some alarm. Some may remember Rachel Carson’s “Silent Spring”. The tobacco industry, from the very beginning the world’s heaviest users of these poisons because bugs love tobacco leaves more than any other plant, realized that they needed something better. Not safer, just better. They already owned all the regulators and were in the process of owning the scientific community so nobody was looking at pesticides in tobacco products, even though cancer was beginning to explode and everybody knew it was “smoking-related”. Nobody ever asked “smoking what?” because “everybody knew” it was tobacco. The fact that the tobacco pesticides were beginning to be identified as super-toxic environmental carcinogens somehow escaped attention, and gave the chemical industry time to develop other kinds of “Crop Protection Agents”.

Endocrine disruptors break out of the old poison/dose relationship completely, but regulators haven’t even thought of keeping up. Endocrine disruptors are the ag industry’s answer to poison fatigue. You don’t have to keep using more and more, and the numbers don’t set off any regulatory alarms because you’re using stuff that nobody understands. All we know is that it takes care of our bug problem.

ED’s are designed to work at any level – in the latest ones all it takes is a couple of molecules at the right place at the right time and – voila – no baby insects or, more commonly, “non-viable offspring”. The bugs have babies but they don’t survive to eat those valuable cops like tobacco – their fave in the whole world.

A Swisher Sweets smoker, whether they are smoking the little cigar intact or just using the wrapper as a blunt, is inhaling a blend of carbendazim and cypermethrin with every puff. Since smoking patterns vary, let’s just say that little cigar smokers are exposed through inhalation multiple times a day every day. Since these chemicals operate independently of dose, their concentration matters for other reasons but not to explain what they so to the smoker’s liver. What they are likely to do to smokers when they are inhaled together seems pretty clear, even though these studies are only on rats and the rats are eating the cancerous combo, not smoking it.

Here are a few of the studies that seem to make the connection – what do you think? There are lots of related refs – but how many do we need to begin asking questions about the safety of some of these tobacco products?

Int J Exp Pathol. 2012 Oct;93(5):361-9

“Effect of cypermethrin, carbendazim and their combination on male albino rat serum”

Alpha-cypermethrin and carbendazim are synthetic; α-cypermethrin belongs to a class of synthetic pyrethroids and carbendazim belongs to the class of carbamate fungicides. The current study was carried out to evaluate the low-dose exposure of individual and mixed forms of cypermethrin and carbendazim.

The experimental results indicate that even low-dose use of the synthetic pyrethroid carbamate and their combined form results in consequential negative effects on cell function.

Toxicol Sci. 2015 Sep;147(1):116-26.

“Oral Exposure of Mice to Carbendazim Induces Hepatic Lipid Metabolism Disorder and Gut Microbiota Dysbiosis”

Carbendazim (CBZ) has been considered as an endocrine disruptor that caused mammalian toxicity in different endpoints. Here, we revealed that oral administrations with CBZ at 100 and 500 mg/kg body weight for 28 days induced hepatic lipid metabolism disorder which was characterized by significant increases of hepatic lipid accumulation and triglyceride (TG) levels in mice.

The serum cholesterol (TC), high-density lipoprotein, and low-density lipoprotein levels also increased after CBZ exposure.

Correspondingly, the relative mRNA levels of some key genes related to lipogenesis and TG synthesis increased significantly both in the liver and fat.

Moreover, the increase in serum IL-1β and IL-6 levels by the treatment of CBZ indicated the occurring of inflammation.

Furthermore, the levels of bioaccumulation of CBZ in the liver and gut were very low as compared in the feces, indicating that most of CBZ stayed in gastrointestinal tract and interacted with gut microbiota until excreted.

At phylum level, the amounts of the Bacteroidetes decreased significantly in the feces after 5 days CBZ exposure. High throughput sequencing of the 16S rRNA gene V3-V4 region revealed a significant reduction in richness and diversity of gut microbiota in the cecum of CBZ-treated mice. UniFrac principal coordinates analysis observed a marked shift of the gut microbiota structure in CBZ-treated mice away from that of the controls.

More deeply, operational taxonomic units’ analysis identified that a total of 361 gut microbes were significant changed. In CBZ-treated groups, the relative abundance of Firmicutes, Proteobacteria, and Actinobacteria increased and that of Bacteroidetes decreased.

Our findings suggested that CBZ could lead to hepatic lipid metabolism disorder and gut microbiota dysbiosis in mice

Toxicol In Vitro. 2014 Dec;28(8):1507-20. 

“Potential involvement of chemicals in liver cancer progression: an alternative toxicological approach combining biomarkers and innovative technologies.”

Pesticides as well as many other environmental pollutants are considered as risk factors for the initiation and the progression of cancer. In order to evaluate the in vitro effects of chemicals present in the diet, we began by combining viability, real-time cellular impedance and high throughput screening data to identify a concentration “zone of interest” for the six xenobiotics selected: endosulfan, dioxin, carbaryl, carbendazim, p’p’DDE and hydroquinone.

Endosulfan, was able to strongly modulate all the studied cellular processes in HepG2 cells, followed by dioxin, then carbendazim.

Our in vitro data indicate that these xenobiotics may contribute to the evolution and worsening of hepatocarcinoma, whether via the induction of the EMT process and/or via the deregulation of liver key processes such as cell cycle and resistance to apoptosis.