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 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 Carly B sucking on their favorite kind of Swisher. But those Swisher Sweets aren’t anything like what the Man behind Carly 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 are what Carbendazim targets.
But, unfortunately, those chemicals the manufacturers use in their tobacco fields don’t only bust bug balls, they twist and shrink the balls of every critter they touch, like human Swisher Sweet smokers. That would be you, young Dude, wouldn’t it? Well hey, as long as you keep buying that shit and smoking it what do they care about you and your precious little balls? Nobody says it’s illegal for them to have ball-busting chemicals in their little cigars so why worry about it – they keep the bugs from eating all those valuable tobacco leaves that the companies sell in premium brands while poor folks and kids stupid enough to think they’re getting a sweet deal get to smoke the trash the bugs leave behind.
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
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 be a major factor in childhood cancer, once their presence and nature is recognized. Simply controlling pesticide residues in tobacco products by imposing reasonable standards on manufacturers would lower the incidence of childhood cancer, perhaps dramatically, in certain groups of people.
The reason this hasn’t been realized is that:
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 heavy consumers of the cheapest tobacco products, driven by price and attracted by fruity sweet flavors and targeted social media marketing, nevertheless;
None of the researchers knew that tobacco products, and particularly those smoked and preferred by young Hispanics and Native Americans, are heavily contaminated with the kinds of 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.
Here is what they do know (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 pesticide exposure at specific points in fetal development. There are other causes, but the wrong kind of pesticide exposure at the wrong time 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 think is going on.
We believe that our new data on pesticide contamination of tobacco products offers a novel and powerful 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.
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.
(Ed. Note: the authors of the study mean “parental”, not “paternal”.)
OBJECTIVE:
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).
