We’ve just finished testing off-the-shelf tobacco products from local mini-marts in Portland, Oregon and among the 20+ hidden, unregulated xenobiotic contaminants that we were able to identify (see below) we found extremely high concentrations of Carbendazim. This contamination occurred in a little cigar brand that is #1 in Latino communities and high in popularity in African-American, Native American and other marginalized & low-income communities where tobacco product choices are restricted to the cheapest, and now we know the most contaminated brands.
Carbendazim has been banned in the EU since 2014. It attacks and destroys the reproductive and immune systems of young people, particularly young Latinos, African-Americans, and Native Americans whose genetic materials are known to be more vulnerable to Carbendazim than youth of European ancestry. As you can see in the data, Carbendazim is only one many previously hidden, unregulated contaminants we found, each with it’s own health impact. But for the moment let’s focus just on the Carbendazim 0.843 mg/kg that’s being inhaled 20-40-60 times a day by @ 850,000 young people in the US right now today.
Carbendazim contamination disproportionately impacts marginalized young people who fall victim to tobacco products and who, because of poverty and carefully targeted marketing, have few choices available to them other than the cheapest and most contaminated brands. Please notice the relationship between price and contamination in the data below.
Community Tobacco Control Partners Test Results 12/18
As you can see, Carbendazim shows up in our first-ever data on pesticide contaminants of tobacco products (right hand column third row). This brand, Swisher Sweets, is #1 in popularity among young smokers, who are also right in the middle of their reproductive years. It is heavily marketed to youth, and is designed with sweet flavors and heavy social media advertising to be part of a cool lifestyle.
This means that these young people, in the middle of their reproductive years, are at the highest possible risk for suffering the known consequences of Carbendazim exposure. (And all the other pesticides you see there, each of which deserves it’s own discussion.) This is made more serious by the route of exposure, because inhalation exposure is far more toxic than eating or skin exposure, and the frequency, because smokers (and fetus and child) are exposed to the pesticides with every puff.
The bottom line is that 0.843 mg/kg is an extraordinary level of Carbendazim to find in any consumer product, but especially in an off-the-shelf tobacco product being marketed heavily to kids, considering that it has been totally banned in much of the world since 2014, is strictly regulated in the US, and is totally illegal on tobacco. Imagine the response of health authorities if this were found on school lunches, slurpees at the 7/11, beer at the mini-mart or granola at Whole Foods?
The problem isn’t just that the Carbendazim is present. For there to be that much Carbendazim residue, it had to have been sprayed on the tobacco deliberately, heavily and recently. There is full knowledge of the EU ban, and the reasons for it. All tobacco manufacturers have notified by their own scientific authority CORESTA. The manufacturers know, or have every reason to know, that they are committing serious race-based crimes against humanity. I can only assume that they have been at this for so long that they actually don’t realize what they are doing to so many people.
Here are just a few of the peer-reviewed research data links that throw light on this hidden relationship
“The literature review indicates that CBZ induces reproductive and developmental toxicity through alteration of many key events which are important to spermatogenesis. It seems that this fungicide may influence the hypothalamus-pituitary-gonad axis in addition to being a testicular toxicant.”
“2,5-Hexanedione (2,5-HD), a taxol-like promoter of microtubule assembly, and carbendazim (CBZ), a colchicine-like inhibitor of microtubule assembly, are two environmental testicular toxicants that target and disrupt microtubule function in Sertoli cells.”
“Administration of carbendazim induced significant decrease in testis weight, diameter, and germinal epithelial height of the seminiferous tubules. Histological results revealed degeneration of seminiferous tubules, loss of spermatogenic cells, and apoptosis. Moreover, carbendazim caused elevation of testicular malondialdehyde (MDA), marker of lipid peroxidation, and reduced the activity of the antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT).”
“Sertoli cells are the primary cellular target for a number of pharmaceutical and environmental testicular toxicants, including 2,5-hexanedione, carbendazim, and mono-(2-ethylhexyl) phthalate. Exposure to these individual compounds can result in impaired Sertoli cell function and subsequent germ cell loss. The loss of testicular function is marked by histopathological changes in seminiferous tubule diameter, seminiferous epithelial sloughing, vacuolization, spermatid head retention, germ cell apoptosis, and altered microtubule assembly.”
“We found that carbendazim causes embryotoxicity, apoptosis, teratogenicity, infertility, hepatocellular dysfunction, endocrine-disrupting effects, disruption of haematological functions, mitotic spindle abnormalities, mutagenic and aneugenic effect.”
And the issue isn’t just Carbendazim as you can see looking back in the data. Most of the individual contaminants are concerning by themselves, but they are additive and synergistic in effect and their impact on human health in that regard is absolutely unknown. What is known now, and IMO it ought to be enough, is that young smokers are inhaling a toxic cocktail of chemicals each designed to operate in different ways at the nano-level to disrupt basic life processes. The dosage of the most advanced pesticides doesn’t matter – they don’t need a “critical mass” to work. A couple of molecules, well below the level of detection, is enough for them to do what they were designed to do to the reproductive systems and genetic materials of bugs, and human teens are simply unfortunate collateral damage in the tobacco industry’s search for increased profits through chemistry.
There doesn’t seem to be any question about the connection between pesticide exposure of agricultural workers and prostate cancer. We know that this kind of exposure leads to prostate cancer, and we know which pesticides are the causal agents.
Through new research that we have just completed, we can also now identify specific pesticides that are known to cause prostate cancer that contaminate specific tobacco products. This means that a whole new connection between smoking and prostate cancer starts to emerge.
We can see that specific pesticide contaminants of tobacco products are the same pesticides that have been shown to cause prostate cancer in exposed farm workers. (I discuss farm worker exposure vs smoker exposure below.)
Check out this data from lab tests we’ve just finished running on off-the-shelf tobacco products. Notice the totally illegal and banned worldwide DDT. Notice all the Azole fungicides like Penconazole. Check that amazing concentration of Cypermethrin. But really, with 0.816 mg/kg of DDT in every puff, all day every day, what other direct linkages to prostate cancer would you need? How about that 0.843 mg/kg of Carbenzadim, banned in the EU since 2014.
We are sadly confident that the entire tobacco product supply in the US will prove to be similarly heavily contaminated. We plan to test as many brands as possible as soon as funding becomes available. But here’s what we’ve found so far.
Community Tobacco Control Partners Test Results 12/18
Farm workers are exposed heavily to known prostate carcinogens regularly during certain parts of the year, whereas smokers of the brands shown above are inhaling known prostate carcinogens 50-100 times a day and more, year-round. So we are looking at two kinds of exposure – heavy during the season for farm workers, and low-level 7/365 for smokers. Intermittent mid-level exposure vs chronic low-level exposure. Also the farm workers are being exposed to one chemical at a time where the smoker is getting a toxic cocktail. Then of course there are farm workers who smoke the cheap tobacco brands like little cigars because that’s all they can afford. Double or triple whammy there.
One thing that needs special attention with this new connection is the clear evidence that a smoker with prostate cancer risks that cancer turning very aggressive if it feeds on DDT and other endocrine-disrupting pesticides, which we can now show are just what that aggressive cancer is getting with every puff. Doctors see this happen in relapsing patients and know that it’s connected with their smoking but can’t explain why it’s happening.
Here’s the message: If you stop feeding that thing in your prostate the chemicals that turn it aggressive maybe it will calm down and maybe you and the docs can get it under control.
So, here are a few key references. There are plenty more – it just depends on how much convincing anyone needs.
Results: The review included 49 studies published between 1993 and 2015. All studies were in English and analyzed exposure to pesticides and/or agricultural activities. Most studies (32 articles) found a positive association between prostate cancer and pesticides or agricultural occupations, with estimates ranging from 1.01 to 14.10.
So, what if tobacco products were loaded with pesticides but nobody knew about that contamination, so even though they knew there was a link between smoking and prostate cancer they didn’t know why? Would that show up in smoking & prostate cancer studies? Well, it seems that it might.
Data from the peer-reviewed literature suggested an association of smoking and aggressive PCa. Although the pathophysiology underlying this association remains unclear, smokers presented higher PCa mortality and worse outcome after treatment. Smoking-cessation counseling should be implemented for patients with PCa, although its effect on PCa progression should be investigated.
OK, but how do we know that the pesticides in tobacco products have anything to do with prostate cancer? Well, first, pesticides used in tobacco are heavily used throughout agriculture. Second, we know that at least two of the contaminants of the little cigar we tested are potent human carcinogens and one acts specifically on human testicles. Now your testicles aren’t your prostate, but that’s getting close enough to merit a second glance if you’re a smoker, don’t you think?
“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.”
Oh, and that other carcinogen – the one that directly impacts your prostate?
p,p′-Dichlorodiphenyltrichloroethane (p,p′-DDT) and p,p′-dichlorodiphenyldichloroethylene (p,p′-DDE) repress prostate specific antigen levels in human prostate cancer cell lines
“Thus, we conclude that men who have been exposed to either DDT or DDE may produce a false-negative PSA test when screening for prostate cancer, resulting in an inaccurate clinical diagnosis. More importantly, prolonged exposure to these anti-androgens may mimic androgen ablation therapy in individuals with prostate cancer, thus exacerbating the condition by inadvertently forcing adaptation to this stress early in the disease.”
These are farmers, not smokers, but their prostate didn’t like the DDT exposure and neither will the prostate of anyone who inhales pesticide-contaminated tobacco product smoke (or vapor).
Prostate cancer risk and exposure to pesticides in British Columbia farmers.
“The significant association between prostate cancer risk and exposure to DDT (OR = 1.68; 95% CI: 1.04-2.70 for high exposure), simazine (OR = 1.89; 95% CI: 1.08-3.33 for high exposure), and lindane (OR = 2.02; 95% CI: 1.15-3.55 for high exposure) is in keeping with those previously reported in the literature.
If you keep smoking things just get worse; if you quit after 10 years the risk disappears. But if you are going to keep smoking at least pay attention to the pesticides that you’re inhaling and choose the least contaminated brand possible.
Association of Cigarette Smoking and Smoking Cessation with Biochemical Recurrence of Prostate Cancer in Patients Treated with Radical Prostatectomy
We investigated the effect of smoking on the risk of prostate cancer recurrence in patients with treated with surgery. We found that former smokers and current smokers were at higher risk of cancer recurrence compared to patients who never smoked; the detrimental effect of smoking was mitigated after 10 yr or more of smoking cessation.
I’m not writing this post as a science paper – I’m writing it to point out a connection that is as obvious as it is hidden, and hoping that the message will reach people who can benefit. The message to smokers is that if you are going to smoke, pay close attention to the contaminants in your brand and stop feeding your cancer with banned pesticides. I know this is heresy but – if you’re going to keep smoking than at least smoke American Spirit organic tobacco. Fair disclosure – I invented American Spirit but lost the company to the tobacco industry not long after we started and I have absolutely no connection of any kind to the company. I don’t benefit in any way from anyone choosing American Spirit. Well, actually, the benefit I get is the only one I want, which is knowing that I may have made a contribution to the health and happiness of another person.