Hidden DDT contamination of tobacco products may be a missing link in the equation connecting the Korean Genome, Tobacco product smoking, and the emerging Type 2 Diabetes epidemic in Korea.
Background
First, we have data-based hard evidence from lab tests just completed (12/18) that the American tobacco supply appears to be heavily contaminated (see data below), and we are certain based on this and other data that this reflects the global tobacco supply situation.
There is also this:
1. Solid research (cited below) that shows that exposure during fetal development to specific organochlorine pesticides including DDT leads by now-known genetic pathways to increased risk, and increased rates of Type 2 Diabetes in people with the Korean genome.
2. The connection between smoking tobacco products and Type 2 Diabetes among Koreans (cited below) is also well established, but there is no cross-over understanding of the role of pesticides in smoking-related disease.
Without taking the hidden pesticides in tobacco products into account, the relationship between smoking and Diabetes cannot be fully understood, and the specific genetic vulnerabilities of Korean people cannot be accounted for in making health care decisions. With such knowledge, doctors would be better able to treat patients, and reluctant patients would have new evidence-based smoking quitting motivation showing them the specific pesticides in their specific tobacco product brand choice and what those pesticides are doing to their treatment outcome.
3. Other research (cited below) shows that the damaging effects of DDT exposure persist across multiple generations, and that people of Asian ancestry are disproportionately vulnerable to certain specific genetic damage from DDT exposure in previous generations.
Unfortunately the problem of DDT and Diabetes doesn’t stop with the person who is smoking contaminated tobacco today. It appears that even if a person today is not a smoker, and not being exposed to DDT that way, if their mother or maternal grandmother smoked she was undoubtedly exposed to DDT with every puff, and that effect is now known to reach across generations and put exposed people at higher risk of multiple diseases.
This strongly implies that Koreans with Type 2 Diabetes today whose mother’s mother smoked may have inherited the damaged genes that led to their diabetes from a grandmother whose DNA was attacked by the pesticides in her cigarettes 50 years ago.
4. It’s an open secret that Asian tobacco products are heavily contaminated with pesticide residues including DDT and other organochlorine pesticides. Asian health authorities have been struggling for yearstrying to find a way to stop the tobacco pesticide contamination but the industry has the fix in at every important political and regulatory level in every country including, I’m very sure, in Korea.
5. In this post I will offer links to peer-reviewed research and hard data to demonstrate that this is a possibility worth examining. These pesticides are known contaminants of tobacco productsworldwide.
The Most Compelling Evidence
First, here’s new hard data showing the extent of pesticide contamination of American tobacco products. (Notice the multiple endocrine-disruptors.)
Community Tobacco Control Partners Test Results 12/18
Here’s a startling study linking DDT to obesity and diabetes across generations of people, which given the history of smoking in Korea suggests a link to today’s Korean Diabetes epidemic among others.
Ancestral environmental exposures to a variety of environmental factors and toxicants have been shown to promote the epigenetic transgenerational inheritance of adult onset disease. The present work examined the potential transgenerational actions of the insecticide dichlorodiphenyltrichloroethane (DDT) on obesity and associated disease.
Conclusions
Observations indicate ancestral exposure to DDT can promote obesity and associated disease transgenerationally. The etiology of disease such as obesity may be in part due to environmentally induced epigenetic transgenerational inheritance.
At least some portion of the Type 2 Diabetes epidemic among Korean smokers must be due to their genetic vulnerability to organochlorine pesticides like the DDT hidden in the tobacco products they are smoking.
In our recent tests of off-the-shelf American tobacco products for pesticide contamination, 20% of the samples tested revealed a high concentration of DDT. The following study looked at Koreans only but if this pattern is repeated or amplified among tobacco brands smoked by Asian populations, then smoking OC-contaminated tobacco products represents a hidden danger of increased risk for Type 2 Diabetes. This is due to the unreasonably dangerous exposure of smokers and their immediate households to OC pesticides in tobacco product smoke.
This research also has strong implications for Korean-American and in fact all Asian-American youth who disproportionately smoke thehighly contaminated brandsof tobacco products that are often the only choice available in marginalized Asian-American communities. Obviously Asian youth in America have Asian genomes, which means that they are at heightened risk of transgenerational pesticide-induced disease from smoking contaminated tobacco products.
Another Piece Of The Puzzle
We see that DDT damage crosses generations. Now let’s see what it specifically does to Koreans.
Low-dose organochlorine (OC) pesticides have recently been associated with type 2 diabetes in several non-Asian general populations. As there is currently epidemic type 2 diabetes in Asia, we investigated the associations between OC pesticides and type 2 diabetes in Koreans.
Most OC pesticides showed strong associations with type 2 diabetes after adjusting for age, sex, BMI, alcohol consumption, and cigarette smoking.
In this exploratory study with small sample, low-dose background exposure to OC pesticides was strongly associated with prevalent type 2 diabetes in Koreans even though absolute concentrations of OC pesticides were no higher than in other populations. Asians may be more susceptible to adverse effects of OC pesticides than other races.
Notice that this study found the effects of OC pesticides even AFTER smoking was controlled as a factor, which means that the effects of the pesticide contaminants in the tobacco products were masked in the data, but would have spiked the results even more if shown.
Unfortunately multiple research studies show that older Koreans strongly tend to continue smoking after being diagnosed with Diabetes, which means that those smokers are continuing to reinforce the cause of their disease while being treated. I have to also wonder about the cross-interactions between all of the pesticides in what they are smoking and the medications that they are taking to treat the disease.
In other words, unknown to them or their doctors, smoking is continuing to expose them to the OC pesticides that caused their diabetes in the first place, which probably effectively cancels out any positive impact treatment may be having.
Younger age, lower economic status, heavier smoking habit, lower Charlson Comorbidity Index and comorbid hypertension were identified as factors associated with continued smoking after the diagnosis of type 2 diabetes.
Older patients and patients with longer diabetic duration were more likely to quit smoking.
Contrastingly, smokers in the lower economic status and heavier smoking habit categories were more likely to continue smoking after the diagnosis.
Conclusion
The economic, social and personal cost burden that the 100% preventable OC pesticide contamination of tobacco products imposes on Asian countries may represent the difference between a viable healthy economy and society and a sickened, low-productivity, low energy society in Asia.
Given the rapidly advancing chemistry of pesticide agents and their increasing impact on the human endocrine system, Asian societies must control this devastating hidden and unregulated poisoning of their people by the international tobacco cartels.
As you can see in these related posts, this issue is by no means confined to people with Asian genomes, not to DDT, nor to Diabetes.
We’ve shown through lab analysis that there are high concentrations of DDT and other endocrine-disrupting pesticides present in tobacco products.
Community Tobacco Control Partners Test Results 12/18
These pesticides are proven to cause severe developmental and cognitive deficiencies. Since many dropout teen smokers were also born to smoking mothers, we have to ask if there could be a birth to death connection between tobacco product pesticide contamination and lifelong failure for some, or even many of the 1.2 million children who drop out every year? Are these the “replacement smokers” the industry talks about?
What if DDT-contaminated tobacco products, and perhaps especially little cigars like Swisher Sweets, are directly responsible for at least some of America’s high school dropouts? Could the extreme levels of DDT and other endocrine-disruptors recently (2018) detected in little cigars be contributing to the unusually high rates of ADHD and poor cognitive performance metrics among high school dropouts who smoke them?
Our research strongly suggests that many dropouts may actually be victims of the tobacco product choices that they are being driven to make by poverty, social class, race, and by terribly wrong-headed public policy. Anyone who truly understands the tobacco industry knows that the cheaper the tobacco product, the more contaminated with pesticide residues.
Could high school dropout rates be reduced simply by restricting or banning community-wide sales of tobacco products that are proven to be contaminated with illegal pesticides that are known to present extreme hazards to critical human developmental processes that affect learning and cognition?
We know that 1.2 million children dropped out of High School in the US in 2016.
We know that poor non-white children are disproportionately represented in the dropout population and suffer the lifelong consequences disproportionately.
We know that poor non-white children who are regular smokers disproportionately smoke “little cigars” and that economics is a major factor in this behavior.
We know that “little cigars” are disproportionately marketed by the manufacturers to poor, non-white and young neighborhoods and communities that, coincidentally or not, have the highest dropout rates.
Our recent lab results show that Swisher Sweets, the most popular brand by far among child smokers 11-17, has extremely hazardous levels of DDT and other endocrine-disrupting pesticides. We are certain that these contamination levels will prove to be representative of little cigars as a product category.
Endocrine-disrupting pesticides are known to present multiple severe hazards to human fetal and child development including high risk of cognitive deficit disorders.
While many of the pesticides identified in Swisher Sweets are unregulated and have very little human toxicological history, DDT has an unequivocal status as an “extreme hazard” to humans and in itself may be sufficient to account for an undetermined portion of observed ADHD and cognitive deficits among child smokers.
We know that DDT specifically crosses the placental barrier and that this puts the unborn children of pregnant teens who smoke little cigars at severe risk of life-long DDT-related developmental learning disabilities.
We know that 27% of girls who drop out are pregnant.
We know that inhaled DDT is incrementally more toxic than dietary DDT.
We know that poor human diet/nutrition exacerbates the impact of DDT
So, girls who smoke DDT-contaminated little cigars, who are pregnant, who have poor diets, and who drop out of school are themselves severely compromised by the impact of pesticides and are also at heightened risk of giving birth to a baby who is developmentally compromised due to DDT exposure in utero.
We talk about the cycle of poverty. Could tobacco product pesticide poisoning be a 100% preventable driver of a major part of that cycle, failure at school?
Multiple studies show that children who initiate smoking with little cigars are predominantly from low-income families and choose contaminated little cigars over less contaminated cigarettes because of price, convenience and marketing. In other words, their decisions are price-sensitive but otherwise mindless.
We know that a primary tobacco prevention and control strategy is to raise taxes on the theory (that they are scrambling to prove) that higher prices discourage starting and promote quitting. The claim is that this strategy reduces overall harm from smoking. This is demonstrably counter-factual when actual price-sensitive behavior is accounted for, which consists of simply switching to or starting with cheaper brands with greater pesticide contamination. Therefore greater not less harm is done especially to young smokers by increasing taxes as a control and prevention strategy.
We must ask public health authorities and legislators whether tax-based tobacco control and prevention strategies are unintentionally reinforcing dropout rates by driving young smokers to cheaper, more contaminated brands of tobacco products?
“We conclude that prenatal DDT levels may be associated with delayed Processing Speed in children at age 7 years and the relationship between prenatal DDE levels and children’s cognitive development may be modified by sex, with girls being more adversely affected.”
“A critical window of exposure to DDE in utero may be the first trimester of the pregnancy, and psychomotor development is a target of this compound. Residues of DDT metabolites may present a risk of developmental delay for years after termination of DDT use.”
“Prenatal exposure to DDT, and to a lesser extent DDE, was associated with neurodevelopmental delays during early childhood, although breastfeeding was found to be beneficial even among women with high levels of exposure. Countries considering the use of DDT should weigh its benefit in eradicating malaria against the negative associations found in this first report on DDT and human neurodevelopment.”
“The authors found higher risk for ADHD-like behaviors assessed with the CRS-T at higher levels of PCBs and p,p’-DDE. These results support an association between low-level prenatal organochlorine exposure and ADHD-like behaviors in childhood.”
“Children with higher urinary DMP concentrations may have a twofold to threefold increased risk of being diagnosed with ADHD. We report a dose-response relationship between child DMP levels and ADHD. Organophosphate pesticide exposure may have deleterious effects on children’s neurodevelopment, particularly the development of ADHD.”
“Results found an association between increasing pyrethroid pesticide exposure and ADHD which may be stronger for hyperactive-impulsive symptoms compared to inattention and in boys compared to girls.”
“The results indicate that both pesticides may induce altered levels of neuroproteins, important for normal brain development, and neurobehavioral abnormalities manifested as altered adult spontaneous behavior and ability to habituate to a novel home environment. The neurotoxic behavioral effects were also present several months after the initial testing, indicating long-lasting or even persistent irreversible effects.”
“Epidemiologic data reveal that children aged 6-15 with detectable levels of pyrethroid metabolites in their urine were more than twice as likely to be diagnosed with ADHD.”
“Results support an association of prenatal OP exposure with deficits in social functioning among blacks and among boys, although this may be in part reflective of differences in exposure patterns.”
“Among the findings associated with increased pesticide levels are poorer mental development by using the Bayley index and increased scores on measures assessing pervasive developmental disorder, inattention, and attention-deficit/hyperactivity disorder. Related animal toxicology studies provide supportive biological plausibility for these findings.
Additional data suggest that there may also be an association between parental pesticide use and adverse birth outcomes including physical birth defects, low birth weight, and fetal death, although the data are less robust than for cancer and neurodevelopmental effects.
Children’s exposures to pesticides should be limited as much as possible.”
Summary
