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)
“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 …
“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.
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?
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.
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
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.