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:
Cano-Sancho G, Salmon A G, LaMerrill M A. 2017. Association between exposure to p,p0-DDT and its metabolite p,p0-DDE with obesity: integrated systematic review and meta-analysis. Environ Health Perspect 125(9)
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.
Janesick A S,Blumberg B. 2016. Obesogens: an emerging threat to public health. Am J Obstet Gynecol 214(5):559–565, https://www.ncbi.nlm.nih.gov/pubmed/26829510
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.
Black and Brown kids are forced by economics and corporate marketing to choose only from among the lowest quality, most contaminated, most “Obesogenic” tobacco products. That’s all you find for sale in marginalized communities.
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.
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.
We have just completed our first tests of off-the-shelf tobacco products for pesticide residues (12/18). We randomly selected samples from a universe of tobacco products known to be popular with young smokers.
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).
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.
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.
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.
Studies conducted in other countries have also reported positive associations between pesticide exposure and hematopoietic neoplasms in children, especially leukemias and lymphomas (Ma et al. 2002; Meinert at al. 2000; Menegaux et al. 2006; Rudant et al. 2007; Zahm and Ward 1998).
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.
“Parental Exposure to Pesticides and Childhood Brain Cancer: U.S. Atlantic Coast Childhood Brain Cancer Study”
Cancer Causes Control. 2013 Jul;24(7):1269-78.