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 …
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.
“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?
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.
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.
European Urology, December 2015, Volume 68, Issue 6, Pages 949–956
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.
Does your kid, or a kid who you know and care about smoke little cigars or some other kind of cheap, flavored tobacco? Are you frustrated because you can’t stop them? Do they have a major “don’t give a shit” attitude? Even if they are being little idiots, do you understand and still want to help?
I propose some evidence-based reality and an appeal to that little idiot’s well-concealed intelligence. Do you think you can you get this kid to sit with you for one hour and read this post together. In the post I will lay out hard evidence showing how their testicles and genetic materials (and those of their friends) are under stealth chemical attack from contaminated cheap products they are being suckered into smoking. Challenge yourselves to understand the science and read through the references together – they are linked to the original research. This isn’t obscure science – this is about clear evidence of specific chemicals known to attack male reproductive organs in the tobacco brand they smoke that are there because of a cheap, money-grubbing manufacturer’s carelessness and greed. See if your discussion doesn’t trigger an instinct for self-preservation in them and maybe even help them get a clue.
We all know that “please please don’t smoke” doesn’t work, and neither does “smoking is really really bad for you”. How many millions of dollars are still being wasted on endless repetition of some version of those two “nanny state” themes? Tell a kid that there are 4000 really really bad chemicals in that cigarette, or that he’s going to get lung cancer, and he will sneer to show you how tough he is. Tell him that the cheap-ass manufacturer of that crap he’s smoking is using trash tobacco that’s such shitty stuff that it’s contaminated with totally illegal chemicals that are attacking his balls every time he takes a hit. Tell him that the brands that are poisoned this way are pushed hard to people in poor neighborhoods who can only afford cheap poisoned shit, and to people who have enough money to afford less poisoned brands but are too stupid to know the difference. Show him the data tables below and ask him what he thinks – which brands are pushed to which people in which neighborhoods? Point out, in case he doesn’t get it, that when it comes to tobacco shit definitely rolls downhill.
BTW this post is for boys. I’m working on one for girls that will be titled “Girl – Those Swisher Things Are Frying Your Eggs!”
So young Dude, you smoke Swisher Sweets. Maybe some other brands too. Lots of people love to smoke Swisher Sweets, especially when they see hotties like Cardi B sucking on their favorite kind of Swisher. But those Swisher Sweets aren’t anything like what the Man behind Cardi B wants you to think they are. No indeed.
Dude, no joke – your balls are at serious risk smoking that shit. If you’re cool with that, no problem. It’s your life. But, for the sake of those who care about you, take a little time and think about a couple of things.
Let’s begin with a reality check on those sweet fruity little cigars. Do you think you’re going to get real tobacco at 2 sticks that weigh 3 grams each for $0.99? Really? Then you must have bought your share of baggies of Oregano thinking you were getting bargain dope, because the math doesn’t work. Even if they didn’t shrivel your nuts, little cigars are not real tobacco. They are worse trash than any toxic Mexican weed you ever smoked, even when you weren’t buying Oregano, and here’s why. Those little 3 gram sticks are made especially for poor kids and stupid kids and are loaded with chemicals that do all kinds of nasty shit, but only to the people who smoke the cheap stuff. Most of those chemicals aren’t even there in the pricier brands, and Swisher Sweet smokers and little cigar smokers in general get special treatment as you can see here. This data is from tests we just ran on off-the-shelf tobacco products popular with young smokers from all kinds of communities.
Community Tobacco Control Partners Test Results 12/18
Keep your eye on that Carbendazim under “Swisher Sweets” in the right-hand column because that’s the ball-shrinker we’re talking about. I’m going to explain the connection in a minute.
To be fair you have to ask why those friendly folks at Swisher Sweet would want to bother to shrink your balls? Well, they don’t actually. They don’t care about your balls, or the kids you may want to make someday with those balls. All they’re doing is spraying their tobacco fields with chemicals that kill off the bugs more effectively by shrinking adult bug balls so they can’t have baby bugs. It’s a new way of controlling bugs, and they will tell you they have to do it. You just can’t kill bugs with pure poisons anymore – they’ve gotten resistant. But their little balls are vulnerable as hell, and that’s what these chemicals are designed to attack and destroy, so you add chemicals like Carbendazim to your chemical cocktail and wham – no bugs, and a lot more valuable tobacco per acre.
OK, bugs don’t have balls, not little ones hanging on the outside anyway, but they do have male reproductive organs and those bug equivalents of your precious balls are what Carbendazim is designed to attack and destroy.
But, unfortunately, those chemicals in the tobacco fields don’t only bust bug balls, they retain the chemical potency to twist and shrink the balls of every creature they touch, like human Swisher Sweet smokers. That would be you, young Dude, wouldn’t it?
Well hey, as long as you keep buying their shit why should they worry about a few chemicals you don’t seem to mind even if they are attacking your balls? Nobody says it’s illegal for them to have ball-busting chemicals in their little cigars, so why worry about it. Nobody inspects tobacco products for pesticides anyway because they think that anyone who smokes deserves anything that happens to them and this means that everyone from doctors to FDA to inspectors to anti-tobacco crusaders all totally ignore the presence of pesticides in tobacco products and what they would have to admit that means.
OK, this has all been trash talk. Now I’m going to assume that you understand regular English and basic science. I’m also going to assume that if you’ve read this far maybe you’re ready for some straight talk, and that you may, secretly even, be starting to give a shit. So here’s just a taste of the straight science behind your shrinking balls in regular English, with links for you to follow and make up your own mind what you’re going to do about it.
This first reference just about says it all for any young man who smokes little cigars and expects to have children:
Then there are all these peer-reviewed scientific findings:
“Although the exact mechanism of action is unclear, carbendazim appears to bind 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.” (translation: it shrinks your balls.)
“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).” (translation: it shrinks them and totally fucks them up.)
“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.” (translation: testicle toxins work together.)
“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.”(translation: prolonged exposure destroys the genetic materials in your balls.)
If you want to read more on other linkages between pesticide contamination of tobacco products and disease please follow these links to other recent posts:
Obesity & Obesogens: The Toxic Chemical Connection
The Tobacco companies aren’t deliberately mass murderers. They do maim and kill genocidal levels of people every single year, but that’s just as a byproduct of their business decisions. They don’t actually intend to have their customers sicken and die- it’s just so damned profitable to use stuff like DDT instead of labor to grow tobacco.
They do know that it’s the DDT and other xenobiotic chemicals they use in the fields, invisible to everyone, that are actually killing most of the people dying of “smoking-related disease.” They’ve spent huge amounts of money to keep that particular little piece of information top secret even though it’s been in plain view for fifty years. That has been quite a trick, but they have managed to pull it off pretty well so far. However, bad news is coming for the so-called “Tobacco” industry. All it’s going to take is one well-informed class-action lawsuit based solidly on injury by preventable pesticide contamination and this whole nasty conspiracy will finally come crashing down.
The thing is, these murderous companies don’t actually want to kill off their customers, although because they know that they do, they spend lots of money creating large numbers of what they call “replacement smokers” every year. They spend vast sums advertising heavily to kids worldwide, making cheap fruity sweet tobacco products readily available and now packaging straight nicotine in glycerin for vaping just to give kids a taste of the real thing. And those cute little replacement smokers just keep lining up.
Oh, and those small farmers in remote areas that work like slaves for the Tobacco companies and apply all those chemicals that should be labeled “severe hazard – inhalation”, but aren’t? There aren’t any labels on the 55 gallon drums of pesticide that the tobacco company agent drives up and hands to the farmers and says – “spray this tonight”. They aren’t complaining because if they do they won’t get their tobacco allotment next time and their families will starve, plain and simple. Yes everybody is always sick, and they have lost a few babies to disease, but they have to eat. So it’s really just business all up and down the line. Except that a lot of people seem to be dying at every step.
Even fifty years after global governments first banned DDT, and with every health agency in the world classifying it as an extreme hazard, the Tobacco companies are still forcing illiterate farmers in remote Tobacco-growing regions to drench the Tobacco crops with it. Why do this? Because if you use enough DDT all you need is one peasant with a tank on his back walking through the field killing all the bugs and worms with chemicals rather than twenty men, women and children working that same field, taking care of the tobacco using the old ways, and earning at least something of a wage, and not being drenched with DDT drift day and night.
Oh sure, the global tobacco industry could pay people to work the tobacco fields by hand and maybe even pay them a decent wage. Then tobacco products would be more expensive, which of course is exactly what American health authorities think is the only way to get people to cut down, quit or never start. You would think that everyone would get behind organic tobacco because it would be much more expensive, but that would mean more profits for the tobacco industry and not more taxes for the bureaucrats so of course that isn’t an appealing tobacco control strategy.
“We believe that making tobacco products more expensive reduces smoking, and it is a primary strategy for control and prevention. But, we don’t want to make tobacco more expensive by requiring that it be organic or at least meet reasonable pesticide residue standards, we want to leave outrageously dangerous pesticide contaminated tobacco alone and just make it more expensive using taxation. Our job isn’t to protect people – it’s to preach at them and take away their money so they can’t do bad things with it.”
Tobacco has always been an extremely profitable crop, but a very tough crop to farm. The problem is that bugs love tobacco more than just about any other plant. Tobacco is so high in both sugars and very rich protein that every kind of bug, animal and worm in nature loves to eat those incredibly valuable tobacco leaves. So, for centuries growing tobacco meant prodigious hand labor in the tobacco fields day and night (by guess who), along with great wealth (owned by guess who) that built the American society. But that tobacco wealth wasn’t an industry until agricultural chemicals came along, and then tobacco was one of the earliest and strongest adopters of pesticides.
With the chemical revolution came highly effective Organochlorine pesticides that sprang directly from WWII Nazi poison gas experiments, and virtually overnight the tobacco companies switched from human labor in America to ever-diversifying chemical “crop protection agents” in the Third World that let them grow tobacco at a fraction of the cost of human labor, increasing their already insane profits even more. The difference in profit between growing tobacco using hand labor and using chemicals is what has made the tobacco industry rich beyond imagination since 1950, and they’ve used that wealth to make sure that no government gets in the way of their use of those extremely profitable chemicals.
As a result, chemical contaminants that are totally banned on any other consumable product are not regulated at all on tobacco, and the tobacco industry is continually coming up with new exotic chemicals to use on their fields of GM tobacco and all those chemicals are winding up in the lungs of poor smokers and vapers.
The anti-tobacco crusaders have been raising taxes for years, showing studies that prove when tobacco products get more expensive, people smoke less. We’ve got a winner folks – increase prices. That finances a huge bureaucracy that can then run around and invent a lot of ways to justify its existence by “educating” people. They can all have comfy salaries and a “sense of mission”, spending all that easy-come tax money on themselves so that they can “educate” and “persuade” people. They can’t actually”protect” people of course, because the tobacco industry has tied these well-meaning but also self-satisfied and very comfortable health bureaucrats up in very subtle legislative knots to where they actually say that they can’t regulate pesticides in tobacco products and then in the next breath play CYA by saying, with complete sincerity, “We believe that tobacco is so bad that there is no need to focus on pesticide residues.”
Of course, if you DID focus on the pesticide residues, then you would HAVE to do something about tobacco products – like regulate them for example.
Community Tobacco Control Partners Test Results 12/18
The pesticide residues that contaminate tobacco products are simply the incidental result of crop management decisions the industry makes every day. Since these giant international companies grow most of their tobacco in remote parts of the world, out of sight of any regulators who can’t be easily managed with a few dollars they are free to use the most effective crop chemicals available on their Tobacco crops, which means using chemicals that are so toxic to living things (xenobiotics) that they are banned in every place where regulations matter. There is plenty of DDT and other banned pesticides available anywhere in the world outside of the tightly regulated countries, where almost all of the tobacco is grown for US consumption.
The problem with pesticide contamination of Tobacco products is that the Tobacco companies have arranged legislation in the US so that all that health departments can do is “encourage” people to stop smoking and ‘discourage’ them from starting, but they can’t actually touch the tobacco products themselves because they are protected by a core assumption that has cost the Tobacco companies billions to put in place. That core assumption is that Tobacco itself is so bad that nothing else matters. All I have to say is – who benefits from that assumption? Only the Tobacco industry.
Community Tobacco Control Partners Test Results 12/18
Toxicologists have just designated a new class of chemicals, aptly naming them Obesogens. With chronic exposure, or with exposure before birth at a critical development point, these chemicals initiate body processes that lead directly to childhood, teen and adult obesity and the range of related diseases.
Tobacco products are full of Obesogens, far more of them in far greater concentrations than in any other environmental or consumer product source. Yes Obesogenic chemicals are everywhere, and yes they are in every diet, but their presence as heavy contaminants of tobacco products is a unique kind of hidden health threat whose proportions are unseen.
The data above displays some of the pesticides we just identified in our tests of tobacco brands popular with kids. Our tests were the first ever of off-the-shelf tobacco brands for pesticide Obesogens. We’re especially concerned about the concentrations of some of the azole fungicides we found, in addition to the DDT.
Kids who smoke these tobacco products are being exposed to a pesticide cocktail with each inhalation, 50-100 times a day. This is a level that is unmatched by any other type of exposure to Obesogens or to any class of pesticides. None of the studies of obesogenic chemicals look at what happens to young people who are dosing themselves with a cocktail of these endocrine-disrupting chemicals every waking hour, but it’s pretty easy to see what researchers will find when they do the science.
Here’s some of what is already known.
“Obesogens disrupt the molecular mechanisms controlling the development and maintenance of adipose tissue. This disruption has the potential to produce larger and more numerous fat cells, which could in turn lead to obesity and related complications. Obesogens can also alter programing of metabolic set points, appetite, and satiety.” https://ehp.niehs.nih.gov/doi/full/10.1289/EHP2545
Consider the extreme concentration of DDT we found in the Swisher Sweets (in the data above). This brand is #1 in popularity among child and teen little cigar smokers in marginalized communities. Keeping the Swisher Sweet DDT concentration of 0.816 mg/kg in mind, check this out:
Obesogenic chemicals trigger complex responses by human endocrine and immune systems. Pesticides that persist in body tissues like DDT and Carbendazim are particularly powerful Obesogens that operate 24/7, so even when a child is sleeping these Obesogens are at work deep in their tissues.
Pesticide researchers are hard-pressed to study the effects of a single pesticide thoroughly, and when it comes to the multiplying effects of combined pesticides they pretty much throw up their hands – although they do it sounding very scientific and technical. But whatever brand a child or teen is smoking, when you look at the dozens of Obesogenic pesticides that are being inhaled puff after puff as a toxic cocktail we can be sure that the potential for inflammatory obesity is multiplied.
The cheaper the tobacco product the more Obesogens it has. Notice the progression from American Spirit Blue cigarettes to Swisher Sweet little cigars in the data table above. In a new variation on an old story, the very communities where the cheapest tobacco products are marketed are communities of children and adults who are most genetically vulnerable to inhaled pesticides and their Obesogenic effects. Hispanic, African-American and Native American children and teens seem to be particularly susceptible to Obesogenic chemicals. These communities also have the highest rates of both smoking and obesity. I think we have the connection in Obesogenic pesticides.
Unfortunately all the research on inhaled pesticide exposure so far is either on exposure through diet or through environmental causes – accidental releases, agricultural drift, etc. Nobody has ever studied the health impact of inhaling a pesticide cocktail 50-100 times a day, but when it comes to dosing yourself with Obesogens that sounds like a pretty dramatic way to do it.
Heindel J J, Newbold R, Schug T T.2015. Endocrine disruptors and obesity. Nat Rev Endocrinol 11(11):653–661, PMID: 26391979, https://doi.org/10.1038/nrendo. 2015.163
My concern is that those fruity, sweet, cheap and heavily marketed “Little Cigars” that are especially appealing to Hispanic and African-American children and teens who smoke are the most heavily contaminated with obesogenic pesticides of any tobacco product category we’ve tested so far. Obesogenic pesticides in these cheap tobacco products being marketed to dietarily and genetically vulnerable youth may account for some of the increased incidence of obesity among children and young people in these communities.
Of course, it isn’t just pesticides in cheap tobacco products making poor marginalized people obese – there are obesogenic chemicals in everything that people incarcerated in marginalized communities have available to eat and drink, and in virtually everything in their toxic environment. It’s just that tobacco products are the most concentrated source of the worst possible kinds of pesticides all blended together into a toxic cocktail that you inhale rather than drink, and that as one of its main side-effects makes smokers obese.
Eskenazi B, Chevrier J, Rosas L G, Anderson H A, Bornman M S, Bouwman H, et al. 2009. The Pine River statement: human health consequences of DDT use. Environ Health Perspect 117(9):1359–1367, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737010/
The big difference between tobacco products as an Obesogenic chemical source and all other sources is that illegal obesogenic pesticides in cheap tobacco products are 100% preventable as a contributing factor to childhood obesity.
Kids are being subjected to these hidden, unregulated obesogenic chemicals for just one reason – they mean higher profits for the tobacco manufacturer. Tobacco companies take the cheapest possible tobacco trash swept up off the dirt floors of their factories in Third-World countries and ship it to the US by the freighter-load to make into those sweet, fruity little treats that teens love to smoke. (What happens to the actual tobacco leaf is another long story.)
More importantly, the obesogens in tobacco products are inhaled, not eaten. This is absolutely critical. All the research on the toxicity of pesticides shows much higher toxicity for the most hazardous chemicals when inhalation is the route of exposure, even though there is no research on what happens when pesticides are inhaled regularly every day, every waking hour.
Roots Of The Atrocity
Tobacco has always been an extremely profitable crop, but a very tough crop to farm. The problem is that bugs love tobacco more than just about any other plant. Tobacco is so high in every kind of sugar and high-quality protein that every bug, animal and worm in nature is irresistibly drawn to munch on those extremely tasty, extremely valuable tobacco leaves. So, for centuries growing tobacco meant prodigious hand labor in the tobacco fields day and night by black and brown people, with great wealth accruing of course to White people who used that wealth as the basis for early American economic development, and for hundreds of years Tobacco steadily built the foundation of American wealth along with cotton, sugar and alcohol of course.
But all that tobacco wealth, with all the power that it conveyed, wasn’t a real industry until agricultural chemicals came along, and then when they did tobacco was one of the earliest and strongest adopters of pesticides. That was because they saw immediately that $100 worth of chemicals could increase profits $500 an acre because of the extra tobacco not eaten by bugs, and $10,000+ for the manufactured products from that extra tobacco. So really, from the tobacco companies’ point of view, using those chemicals was and still is largely a business decision. If smokers die early well, that’s why they advertise so heavily to kids. The industry actually uses the term “Replacement Smokers”.
With the chemical revolution came highly effective Organochlorine pesticides that sprang directly from WWII Nazi poison gas experiments, and virtually overnight the tobacco companies switched from human labor in America to ever-diversifying chemical “crop protection agents” in the Third World that let them grow tobacco at a fraction of the cost of human labor, increasing their already insane profits even more. The difference in profit between growing tobacco using hand labor and using chemicals is what has made the tobacco industry rich beyond imagination since 1950, and they’ve used that wealth to make sure that no government gets in the way of their use of those extremely profitable chemicals.
As a result, chemical contaminants that are totally banned on any other consumable product are not regulated at all on tobacco, and the tobacco industry is continually coming up with new exotic chemicals to use on their fields of GM tobacco and all those chemicals are winding up in the lungs of poor smokers and vapers.
Those little cigars that are being marketed so successfully to young Latino and Black kids are loaded with the residues of the chemicals used to control bugs on the tobacco because they are made with the waste from higher quality tobacco products made for sale in wealthier communities. Tobacco leaf, which is relatively less contaminated then the trashy parts of the plant, goes into the expensive cigarettes. Again, check the data at the top of the post and ask yourself – which gets sold at the suburban mini-mart and which gets sold at the bodega?
White smokers get to choose the cleaner, higher quality tobacco leaf if they’re informed enough to do so while Black and Latino smokers get little cigars made with the trash swept up off the tobacco factory floor and don’t have any choice except other equally contaminated cheap shit.
Here’s why the trashy parts are the most contaminated parts of the plant. The tobacco industry pays huge bucks to its scientists to design chemicals that will kill the bugs on the tobacco leaves and then trans-locate into the stems, stalks and roots of the plant so that they don’t affect the flavor of that precious tobacco leaf that’s going into the premium smokes. The contaminated trash parts of the tobacco plant – after the leaf is removed – is what goes into making all those cheap, fruity smokes that poor Black & Latino kids are being trained to love.
So that’s it. Poor young Black and Latino people who fall for the tobacco companies’ propaganda are being sickened, poisoned and made morbidly obese all simply because the tobacco companies can make more money using chemicals that happen to be Obesogenic, and carcinogenic, and teratogenic, and just plain xenobiotic on their crops that they don’t have to account for when they are selling their trash to kids in poor communities around the world.
It doesn’t really matter to the tobacco companies if their smokers get sick and obese and diabetic and have cancer and die young as long as they (1) keep smoking and (2) create at least a couple of replacement smokers before they die. It’s all just a numbers game to them.
But as for us? All it will take to answer this arrogance with finality is for one communities to act to investigate their local tobacco product supply. Then if they find it contaminated, and especially if some of that contamination is from banned substance like DDT, they can then pass local ordinances that impose reasonable pesticide residue standards on tobacco products being sold in their community.
If a child struggling with obesity has a smoking mother, both mother and child should be tested for Obesogenic pesticide poisoning which if found could lead to treatment. Anyone struggling with obesity who smokes, especially little cigars, should get their blood tested for Obesogenic pesticides. As long as the body is carrying a burden of Obesogenic chemicals, especially if they’re being constantly replenished by smoking or breathing second-hand smoke, no amount of dieting, pharmaceuticals or surgery will help.
I believe that those states where Cannabis is legal and where pesticide residue standards have already been put in place with lots of careful consideration will be the first where communities will insist on these reasonable standards. Our federal and state agencies and legislators have largely been compromised by tobacco industry stealth tactics over the past 50 years of carefully tended regulatory loopholes, exemptions and curious omissions. Local community officials have not been so compromised because the tobacco industry likes to work from the top down – they think of themselves as too wealthy and powerful to be accountable.
They just haven’t met the right Justice of The Peace or Magistrate yet who has a dear niece who can’t stop smoking Swisher Sweets and who is obese, diabetic, and has one child with leukemia and another with ADHD. Show the judge that list of Obesogenic and Xenobiotic pesticides in what his niece has been smoking and ask him if he’s OK with that.
Community Tobacco Control Partners Test Results 12/18
Heavy concentrations of pesticide residues in cheap tobacco products being smoked by mothers, fathers or others in the household are likely to be a factor in the high rates of childhood Leukemia (ALL) among Hispanic and Native American children.
I believe these hidden, unregulated pesticides will prove to be a major factor in childhood cancer, once their presence and nature is recognized. It will be seen that simply controlling the most hazardous pesticide residues in tobacco products by imposing reasonable standards on manufacturers could lower the incidence of childhood cancer and many other diseases, perhaps dramatically, especially in the most genetically vulnerable groups of people.
The reasons the link between tobacco pesticide contaminants and childhood leukemia remains obscure are:
While the link between pesticide exposure of the fetus and development of childhood Leukemia (ALL) is proven, and;
While parental smoking and childhood Leukemia are strongly associated, and;
While Hispanic and Native American children are proven to have higher rates of ALL and;
While marginalized young people are known to be the heaviest consumers of the most heavily contaminated brands, nevertheless;
Nobody seems to know that tobacco products, and particularly those smoked and preferred by young Hispanics and Native Americans, are heavily contaminated with some of precisely the pesticides that are known to cause ALL, and;
Although researchers say that they can see clearly that pesticides, smoking and ALL are linked, they can’t explain the connections because;
There has never been any reference research published showing pesticide contamination of tobacco products, until our little study, and;
Researchers almost never have any reality-based background knowledge of tobacco industry practices to guide their research objectives
Here is what researchers know about Childhood Leukemia that is relevant to tobacco pesticide contamination (journal citations are below the narrative).
In addition to Hispanic and Native American children having higher rates of childhood leukemia (ALL) than other groups, research shows that children with at least 10% Native American ancestry have 59% higher relapse rates after being “cured” of ALL the first time.
Childhood Leukemia is known to be initiated by specific pesticide exposure at specific points in fetal development. There are other causes, but the wrong kind of pesticide exposure at exactly the wrong fetal developmental point initiates genetic processes leading directly to childhood Leukemia.
The relationship between fetal pesticide exposure and increased likelihood of childhood Leukemia in Hispanic and Native American children is proven. The multiple causes of ALL are not clear to researchers, but the associations with pesticides are strong.
Here’s what we want to contribute to the discussion.
We believe that our new data on pesticide contamination of tobacco products offers a novel and powerful even if partial explanation for the association between parental smoking and childhood Leukemia in Hispanic, Native American and other vulnerable populations.
The pesticides that we identified contaminating tobacco products marketed to and smoked by poor, young non-white people included multiple heavy concentrations of specific pesticides that are known to initiate childhood leukemia disproportionately in Hispanic and Native American babies. We refer specifically to Carbendazim and DDT.
A significant proportion of young, low-income Hispanics and Native Americans smoke little cigars, and because this is a very heavily contaminated tobacco product category, their children are exposed beginning with conception to xenobiotics that are known pathways to childhood leukemia and that show particular virulence in Hispanic and Native American children. Little cigars are by no means the only pesticide-contaminated tobacco products – they are simply the most contaminated of any that we have been able to test so far.
Because childhood Leukemia is known to initiate its growth at specific developmental stages, chronic smoking of tobacco products containing high concentrations of pesticides by the pregnant mother, or by anyone in the household, guarantees that xenobiotics will be present at every critical point for the initiation of development of childhood Leukemia in the growing child.
Since pesticide exposure levels required for initiation of disease processes during fetal development can be very low, concentrations remaining in second-hand smoke might be sufficient to initiate these disease-inducing genetic changes in the fetus even when the pregnant woman does not smoke.
But it’s not just pregnant mothers and smoking family members who give babies Leukemia. A new relationship has just been established between smoking by Hispanic fathers and leukemia in their children.
Pesticide contamination of the products that young Hispanic fathers are smoking appears to be a novel, powerful and unrecognized connection between their smoking and childhood Leukemia in their children. These findings are further reinforced by recent findings of paternal smoking influence in childhood Leukemia in a non-Hispanic White Australian population. It is therefore highly likely that this link applies to Native American fathers as well.
See for yourself what the research says. Here are some of the core research articles that I believe support a clear link between contaminated tobacco products and childhood Leukemia.
“Linking Pesticide Exposure with Pediatric Leukemia: Potential Underlying Mechanisms”
Leukemia is the most common cancer in children, representing 30% of all childhood cancers. The disease arises from recurrent genetic insults that block differentiation of hematopoietic stem and/or progenitor cells (HSPCs) and drives uncontrolled proliferation and survival of the differentiation-blocked clone. Pediatric leukemia is phenotypically and genetically heterogeneous with an obscure etiology.
The interaction between genetic factors and environmental agents represents a potential etiological driver. Although information is limited, the principal toxic mechanisms of potential leukemogenic agents (e.g., etoposide, benzene metabolites, bioflavonoids and some pesticides) include topoisomerase II inhibition and/or excessive generation of free radicals, which may induce DNA single- and double-strand breaks (DNA-DSBs) in early HSPCs.
Chromosomal rearrangements (duplications, deletions and translocations) may occur if these lesions are not properly repaired.
The initiating hit usually occurs in utero and commonly leads to the expression of oncogenic fusion proteins. Subsequent cooperating hits define the disease latency and occur after birth and may be of a genetic, epigenetic or immune nature (i.e., delayed infection-mediated immune deregulation).
Here, we review the available experimental and epidemiological evidence linking pesticide exposure to infant and childhood leukemia and provide a mechanistic basis to support the association, focusing on early initiating molecular events.”
“Paternal smoking and risk of childhood acute lymphoblastic leukemia: systematic review and meta-analysis”
To investigate the association between paternal smoking and childhood acute lymphoblastic leukemia (ALL).
METHOD:
We identified 18 published epidemiologic studies that reported data on both paternal smoking and childhood ALL risk. We performed a meta-analysis and analyzed dose-response relationships on ALL risk for smoking during preconception, during pregnancy, after birth, and ever smoking.
RESULTS:
The summary odds ratio (OR) of childhood ALL associated with paternal smoking was 1.11 (95% Confidence Interval (CI): 1.05-1.18, I(2) = 18%) during any time period, 1.25 (95% CI: 1.08-1.46, I(2) = 53%) preconception; 1.24 (95% CI: 1.07-1.43, I(2) = 54%) during pregnancy, and 1.24 (95% CI: 0.96-1.60, I(2) = 64%) after birth, with a dose-response relationship between childhood ALL and paternal smoking preconception or after birth.
CONCLUSION:
The evidence supports a positive association between childhood ALL and paternal ever smoking and at each exposure time period examined. Future epidemiologic studies should assess paternal smoking during well-defined exposure windows and should include biomarkers to assess smoking exposure and toxicological mechanisms.
“Correlates of Prenatal and Early-Life Tobacco Smoke Exposure and Frequency of Common Gene Deletions in Childhood Acute Lymphoblastic Leukemia”
“In summary, we provide evidence that increased tobacco smoke exposure increases the generation of somatic ALL-associated driver deletions. To our knowledge, this is also the first reported application of an epigenetic biomarker to assess the effects of an environmental exposure on leukemogenic alterations.”
“Our findings should be added to an already compelling list of reasons for minimizing the prenatal and early life tobacco smoke exposure of children.”
“Childhood Leukemia Incidence in California: High and Rising in the Hispanic Population”
“Ethnic disparities in children’s exposure to chemicals at home, as well as ethnic disparities in their parents’ exposures to chemicals at work, may contribute to the higher burden of childhood leukemia in Hispanic children.
A more complete evaluation of the role of specific environmental factors that disproportionally affect the Hispanic community in the increased risk of leukemia in Hispanic children is warranted.”
“Native American ancestry linked to greater risk of relapse in young leukemia patients”
The study found that ALL cancer was 59 percent more likely to return in patients whose genetic makeup reflected at least 10 percent Native American ancestry.
Investigators also found ALL patients with greater Native American ancestry who received additional chemotherapy as part of a COG clinical trial benefited more from the extra treatment than other children.
“In utero pesticides exposure and generation of acute myeloid leukemia associated translocation (8;21)”
“The present study was set to detect t (8;21) translocation in umbilical cord blood samples from neonates as in utero primary molecular hit in the pathway of childhood leukemia in apparently healthy neonates and to delineate the relationship between generation of this translocation and prenatal pesticide exposure.
Four pesticides were studied including Malathion and Diazinon as organophosphates, and DDT and Lindane as organochlorines. The choice of these four pesticides was based on their popular use in the community under investigation and their well-established role in cancer pathology.”
“Of the studied pesticides, DDT was accompanied by highest risk for carrying the fusion Oncogene [OR 3.55 (95%CI 1.53-8.26), P=0.003].”
“Since pediatric leukemia involves both genetics and environmental interactions, pesticides provide a perfect link in such regard. In this relatively large study we report on a direct relation of prenatal Malathion and DDT exposure and the incidence of leukemia translocation in neonates.”
“To the best of our knowledge, the current study is the first study to evaluate the effect of pesticides on acquiring AML fusion Oncogene in Egypt, where the analyzed Xenobiotics are still used and not banned yet.” (Published November 28, 2016)
“In Utero Pesticide Exposure and Leukemia in Brazilian Children < 2 Years of Age”
“Our findings suggest that children whose mothers were exposed to pesticides 3 months before conception were at least twice as likely to be diagnosed with ALL in the first year of life compared with those whose mothers did not report such exposure.
Adjusted ORs for AML in the first year of life ranged from 2.75 (95% CI: 0.96, 7.92) for any pesticide exposure in the first trimester of pregnancy, to 7.04 (95% CI: 2.47, 20.10) for exposure during breastfeeding.
A systematic review and meta-analysis of 15 studies of the association between residential exposure to pesticides during selected time windows (preconception, pregnancy, and childhood) and childhood leukemia carried out during 1950–2009. (Turner et al. 2010) reported associations with pregnancy exposure to unspecified pesticides (OR = 1.54; 95% CI: 1.13, 2.11), insecticides (OR = 2.05; 95% CI: 1.80, 2.32), and herbicides (OR = 1.61; 95% CI: 1.20, 2.16).
Another meta-analysis of 31 studies of parental occupational exposure to pesticides and childhood leukemia (Wigle et al. 2009) reported associations with occupational exposure to insecticides (OR = 2.72; 95% CI: 1.47, 5.04) and herbicides (OR = 3.62; 95% CI: 1.28, 10.3) during pregnancy.
A French study also examined the association between pesticide exposure and infant leukemia (Rudant et al. 2007). According to use of any pesticide, the observed risk estimates (ORs) were 2.3 (95% CI: 1.9, 2.8) for ALL and 2.2 (95% CI: 1.4, 3.3) for AML. These authors also suggested that a domestic use of pesticides may play a role in the etiology of leukemia, and that prenatal exposure may be a window of fetal vulnerability.
Incidence rates of childhood leukemia in the United States have steadily increased over the last several decades, but only recently have disparities in the increase in incidence been recognized.
“Trends in Childhood Leukemia Incidence Over Two Decades from 1992–2013”
In the current analysis, Surveillance, Epidemiology and End Results (SEER) data were used to evaluate recent trends in the incidence of childhood leukemia diagnosed at age 0–19 years from 1992–2013, overall and by age, race/ethnicity, gender, and histologic subtype. Hispanic White children were more likely than non-Hispanic White, non-Hispanic Black or non-Hispanic Asian children to be diagnosed with acute lymphocytic leukemia (ALL) from 2009–2013.
From 1992–2013, a significant increase in ALL incidence was observed for Hispanic White children (annual percent change (APC)Hispanic=1.08, 95%CI:0.59, 1.58); no significant increase was observed for non-Hispanic White, Black or Asian children.
ALL incidence increased by about 3% per year from 1992–2013 for Hispanic White children diagnosed from 15–19 years (APC=2.67; 95%CI:0.88, 4.49), and by 2% for those 10–14 years (APC=2.09; 95%CI:0.57, 3.63), while no significant increases in incidence were observed in non-Hispanic White, Black, or Asian children of the same age.
Acute myeloid leukemia (AML) incidence increased among non-Hispanic White children under 1 year at diagnosis, and among Hispanic White children diagnosed at age 1–4. The increase in incidence rates of childhood ALL appears to be driven by rising rates in older Hispanic children (10–14, and 15–19 years).
More bad news. It looks like we should be concerned about pesticides in tobacco products and childhood brain cancer.
Environ Health Perspect. 2009 Jun; 117(6): 1002–1006.
