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.