This post is about a crime being committed right now, today and every day, against hundreds of thousands of Black and Brown living and unborn babies. Their lives are in grave danger from nerve gas and genetic toxins in those fruity little Sweets. Many babies and children have already been irreparably damaged. But those young Black and Brown lives don’t matter, not to Swisher Sweets. This is a WAY profitable product, made with the worst, most contaminated tobacco waste. They market directly to Black and Brown young people, especially girls and women, using every evil little “targeted marketing” trick in the tobacco industry’s book. The facts prove that they knowingly and without regard to human life produce an unreasonably dangerous, life-threatening product that has especially toxic impact on babies with Black or Brown genetics.
Pretty stark, I know, but check this table that shows you the concentration of DDT found in Swisher Sweets when I had them tested by a highly competent lab. There are many more neurotoxic fungicides and insecticides in good old fruity minty fun and funky Swishers, as you can see, but let’s just focus on the DDT.
That DDT concentration you can see in the table – 0.816 ppm – is 700+ times greater than the concentration of DDT in any 2019 food or other consumable product. That’s a HUGE problem for a fetus whose Mommy is inhaling that DDT 50-100 times a day or more. Many young Black and Latina women actually believe the street myth that smoking Swishers is safer than smoking cigarettes so they pass their entire pregnancy inhaling these fruity little sacks of nerve poison.
DDT has been banned for any use except extreme mosquito control for generations, and for plenty of good reasons. It’s still the best killer the chemical industry has ever come up with, bar none, and growers worldwide long to be able to use it again. But alas, they can’t. Unless they’re the tobacco industry, and then it’s OK. So – here it is, freshly applied to tobacco and being inhaled by 3 million+ young Swisher Sweets smokers, predominantly Black and Latinx, over half female.
How many Swisher smokers are pregnant today? We know that only 25% of them will stop smoking during pregnancy. There are communities full of damaged babies of Black & Brown smokers and nobody knows why so everybody just seems to accept it – that’s just the way it is if you smoke. Maybe you can see, after you’ve looked at this evidence, the real reason why so many babies of Black and Brown smokers are born damaged beyond belief. And why it doesn’t have to be that way.
The research evidence, quoted and linked in-depth below, is overwhelming that even the tiniest exposure to DDT at the right point in fetal development can be catastrophic. That’s true of other neurotoxins in Swishers, each with its own special kind of damage. After all, the whole purpose of these neurotoxins is to kill and destroy millions of tiny bugs in a field with just a few molecules of the neurochemical for each tiny life. These chemical companies are the direct descendants of Nazi nerve gas manufacturers and they have not changed their attitude toward “sub-humans” one little bit.
Babies in the womb are being drenched with these neurotoxins through their mother’s blood, across the placenta, straight to their emerging brain, glands and nervous system. Their effects at the molecular level are just being documented, but they are terrible and permanent.
The US and world governments have quite deliberately never tested for these neurochemicals although they spend hundreds of millions of taxpayers money trying to convince people that smoking is bad. Any high-paid government flunky care to really say why? They all know – Agriculture, Justice, the EPA, the FDA, the CDC. The industry has the system rigged at every level of government so it is exempt from regulation anywhere, anytime for this beyond-criminal behavior.
Aren’t these crimes against humanity? Against the unborn? Could they be genocide? Gassing babies ought to qualify, don’t you think maybe? See what the research says about gassing babies just below the data table showing you what they’re being gassed with.
If this table is too small check the one above – and I’ve also included full-size Swisher Sweet & Marlboro tables, without the little Sweetie, at the end of this post.
Current Opinion in Pediatrics
2008 Apr; 20(2):191-7.
Pesticides and child neurodevelopment
Recent studies on in-utero exposure to the organochlorine pesticide dichlorodiphenyltrichloroethane and its breakdown product, dichlorodiphenyldichloroethene, indicate that exposure is associated with impaired child neurodevelopment.
Basic Clinical Pharmacological Toxicology
Pesticide toxicity and the developing brain
We present the work of the CHAMACOS study, a longitudinal birth cohort study of Mexican-American children living in the Salinas Valley of California. In this study, we investigated the relationship of children’s neurodevelopment with maternal dichlorodiphenyltrichloroethane and dichlorodiphenyldichloroethylene serum levels, as well as prenatal and child organophosphate urinary metabolite levels. We observed a negative association of prenatal dichlorodiphenyltrichloroethane exposure and child mental development.
2016 Jan 15;145:255-64.
doi: 10.1016/j.lfs.2015.11.006. Epub 2015 Nov 5.
Potential role of organochlorine pesticides in the pathogenesis of neurodevelopmental, neurodegenerative, and neurobehavioral disorders: A review
The growing body of evidence has demonstrated that prenatal exposure to organochlorines (OCs) is associated with impairment of neuropsychological development. It has been suggested that maternal exposure to OCPs results in impaired motor and cognitive development in newborns and infants. Moreover, in utero exposure to these compounds contributes to the etiology of autism.
Indian J Med Res. 2016 Jun; 143(6): 685–687.
Organochlorine pesticides exposure & preterm birth
This study confirms the association between maternal serum concentration of OCPs and preterm labour, and also reports an increased mRNA expression of inflammatory pathway genes such as TNF-α and COX-2, which have not been correlated with OCPs levels in previous studies concerning preterm birth aetiology. Even if COX-2 and TNF-α cannot be considered as direct biomarkers for pesticide exposure, since these are involved in all inflammatory processes that contribute to the onset of PTB, a possible gene-environment interaction may occur. The association between OCPs with mRNA expression of TNF-α gene should be further investigated.
2013 May 10;307:136-45.
doi: 10.1016/j.tox.2012.06.009. Epub 2012 Jun 21.
Toxic effects of pesticide mixtures at a molecular level: their relevance to human health
The toxicological effects of low-dose pesticide mixtures on the human health are largely unknown, although there are growing concerns about their safety. The combined toxicological effects of two or more components of a pesticide mixture can take one of three forms: independent, dose addition or interaction.
Not all mixtures of pesticides with similar chemical structures produce additive effects; thus, if they act on multiple sites their mixtures may produce different toxic effects. The additive approach also fails when evaluating mixtures that involve a secondary chemical that changes the toxicokinetics of the pesticide as a result of its increased activation or decreased detoxification, which is followed by an enhanced or reduced toxicity, respectively.
This review addresses a number of toxicological interactions of pesticide mixtures at a molecular level.
Examples of such interactions include:
- the postulated mechanisms for the potentiation of pyrethroid, carbaryl and triazine herbicides toxicity by organophosphates;
- how the toxicity of some organophosphates can be potentiated by other organophosphates or by previous exposure to organochlorines;
- the synergism between pyrethroid and carbamate compounds and
- the antagonism between triazine herbicides and prochloraz.
Particular interactions are also addressed, such as:
- pesticides acting as endocrine disruptors,
- the cumulative toxicity of organophosphates and organochlorines resulting in estrogenic effects, and
- the promotion of organophosphate-induced delayed polyneuropathy.
Current Opinion jn Pediatrics
Prenatal tobacco smoke and postnatal secondhand smoke exposure and child neurodevelopment
Prenatal tobacco and postnatal secondhand smoke exposure is consistently associated with problems in multiple domains of children’s neurodevelopment and behavior.
The literature on both prenatal and postnatal exposure is remarkably consistent in showing associations with increased rates of behavior problems, including irritability, oppositional defiant behavior, conduct disorders and attention deficit hyperactivity disorder.
Environ Health Perspect
doi: 10.1289/ehp.1307044. Epub 2014 Jan 23.
Neurodevelopmental disorders and prenatal residential proximity to agricultural pesticides: the CHARGE study
Conclusions: This study of ASD strengthens the evidence linking neurodevelopmental disorders with gestational pesticide exposures, particularly organophosphates, and provides novel results of ASD and DD associations with, respectively, pyrethroids and carbamates
Environ Health Perspectives
2017 May 25;125(5):057002.
Prenatal Residential Proximity to Agricultural Pesticide Use and IQ in 7-Year-Old Children
This study identifies potential relationships between maternal residential proximity to agricultural use of neurotoxic pesticides and poorer neurodevelopment in children.
Proc Natl Acad Sci U S A
2019 Sep 10;116(37):18347-18356.
doi: 10.1073/pnas.1903940116. Epub 2019 Aug 26.
Prenatal exposure to organophosphate pesticides and functional neuroimaging in adolescents living in proximity to pesticide application
OP exposure was associated with altered brain activation during tasks of executive function.
Environ Health Perspect
2018 Apr 25;126(4):047012.
Prenatal Organophosphate Pesticide Exposure and Traits Related to Autism Spectrum Disorders in a Population Living in Proximity to Agriculture
Conclusions: These findings contribute mixed evidence linking OP pesticide exposures with traits related to developmental disorders like ASD. Subtle pesticide-related effects on ASD-related traits among a population with ubiquitous exposure could result in a rise in cases of clinically diagnosed disorders like ASD
doi: 10.1016/j.envres.2016.05.048. Epub 2016 Jun 6.
Residential proximity to organophosphate and carbamate pesticide use during pregnancy, poverty during childhood, and cognitive functioning in 10-year-old children
Conclusions: Residential proximity to OP and carbamate pesticide use during pregnancy and both household- and neighborhood-level poverty during childhood were independently associated with poorer cognitive functioning in children at 10 years of age.