I dedicate this post to our brother Stu Kraft, a mountain man full of joy, talent, energy and life whose mother was a heavy smoker from the 1950’s until her death of lung cancer. Stu was born with reproductive system issues, and turned even that into art. He loved to make his friends uncomfortable by joking about his “monoball”, and once serenaded a large party with an impromptu and delightfully bawdy song about a sailor with one ball and the feats he manfully managed to perform. It turned out that Stu’s monoball must have been attacked in the womb by the hidden DDT in his Mom’s cigarettes, because when he was in his early 50’s monoball turned on him and killed him.
Researchers have long known there is a connection between smoking and testicular cancer. They just couldn’t explain what it is.
But when you examine a secret tobacco industry study from 1972 (see more below) then we can see that it’s more than just possible that a lot of 2019’s testicular cancer will arise from a genetic hit in the womb from the DDT in a mother’s (or grandmother’s) cigarettes in the 1960’s or 70’s. That genetic hit occurred because with every puff she was inhaling massive doses of hidden organochlorine pesticides.
Mothers weren’t being irresponsible by smoking in those days – many doctors even advised it. Mothers smoked because they believed it would help to keep their weight from getting out of control and to deal with the stress of Motherhood. Everybody did it.
Here’s How Mothers & Fetuses Were Exposed To DDT in the 1970’s
The problem with looking at DDT in Tobacco products is that all the DDT exposure studies ever done deal only with the health consequences of environmental exposure to DDT and ingestion in food or water. Nobody has ever studied the health effects of smoking pesticide contaminated tobacco products because the Tobacco industry knew about the problem and actively and completely suppressed that kind of research. It just hasn’t been done. But DDT and other organochlorines have been there in heavy concentrations since 1955, and we now know that genetic damage caused by organochlorine pesticides is transgenerational, and targets specific parts of the genome in order to accomplish this stealth transmission of genetic disease.
Bottom line – if that mother or grandmother we referred to above was pregnant and smoking cigarettes between 1955-1980 she was without any question micro-dosing herself and her unborn child with DDT.
I referred to a confidential RJR report above. It’s from 1972, with all the original signatures, and reports on tests of DDT contamination of three RJR brands. All three brands show heavy contamination, and other research I’ve done shows that the entire tobacco product supply in the US in those days was loaded with enough chemicals to explain nearly all the smoking-related disease we see today.
If the anti-tobacco forces weren’t barely disguised Victorian moralists moralists, under the weight of factual evidence of pesticide contamination they would have to recognize that there is a legitimate question about whether it is actually tobacco that is responsible for all smoking-related disease and if not, what else is responsible and in what proportion? The fact is that there was DDT in every US cigarette in 1972, and that the sons of mothers born to mothers who smoked in those days are now known to be at high risk of testicular (and other) cancer in 2019. I’ll link you to peer-reviewed journal research on this below but first here’s a table summarizing the data on DDT in those three RJR brands in 1972. This is what millions of grandmothers of today’s middle-age men were inhaling. (BTW – this report only covered DDT – there were many other heavy organochlorine residues in 1972 cigarettes.)
RJR Confidential June 21, 1972
Project 2358 – Cigarette Development; Notebook Pages: 250701-250719
|In The Cigarette||DDT – Range PPM (20 samples)||DDT – Avg PPM (20 Samples)|
|4841 – Regular Unfiltered||4.14 – 7.96||6.06 +/- 0.99|
|4842 – Filter King||3.38 – 6.65||4.95 +/- 0.90|
|4843 – Filter King||4.86 – 6.82||5.89 +/- 0.61|
|In The Cigarette Smoke|
|4841 – Regular Unfiltered||0.35 – 0.57||0.42 +/- 0.06|
|4842 – Filter King||0.16 – 0.35||0.025 +/- 0.05|
|4843 – Filter King||0.24 – 0.46||0.35 +/- 0.05|
Here’s What’s Happening To Male Children Today
J Natl Cancer Inst. 2008 May 7;100(9):663-71.
Persistent organochlorine pesticides and risk of testicular germ cell tumors
Increased exposure to p,p’-DDE may be associated with the risk of both seminomatous and nonseminomatous TGCTs, whereas exposure to chlordane compounds and metabolites may be associated with the risk of seminoma. Because evidence suggests that TGCT is initiated in very early life, it is possible that exposure to these persistent organic pesticides during fetal life or via breast feeding may increase the risk of TGCT in young men.
Here’s Why Even Tiny, Steady Doses Of DDT Matter
Male Reproductive Health and Environmental Xenoestrogens
Long-term exposure to small amounts of organochlorine contaminants leads to the accumulation of considerable burdens in animal and human tissues. It is therefore not the amount of DDT to which a mother is exposed during pregnancy that is critical but rather her lifetime exposure that will determine the level of exposure of the fetus and the breast-fed infant.
Here’s Evidence That This Is Happening Worldwide
Human Reproduction, Volume 16, Issue 5, 1 May 2001, Pages 972–978
Testicular dysgenesis syndrome: an increasingly common developmental disorder with environmental aspects: Opinion
This article summarizes existing evidence supporting a new concept that poor semen quality, testis cancer, undescended testis and hypospadias are symptoms of one underlying entity, the testicular dysgenesis syndrome (TDS), which may be increasingly common due to adverse environmental influences.
Experimental biological investigations and epidemiological studies leave little doubt that the TDS can be a result of disruption of embryonal programming and gonadal development during fetal life. As the rise in the incidence of the various symptoms of TDS occurred rapidly over few generations, the aetiological impact of adverse environmental factors such as hormone disrupters, probably acting upon a susceptible genetic background, must be considered.
While the focus of this post is on DDT and TDS, take a look at the pesticide contaminants that we just found in a sample of tobacco brands purchased off-the-shelf at out Portland-area minimarts, The first thing that stands out is the number of contaminants and – look at that – the cheaper the brand the higher the contamination and the worse the contaminants. In fact, the cheaper the brand the more Testicular disrupting/damaging chemicals there are – look at the Carbendazim in the Swisher Sweets. Combined with the action of DDT on Testicular tissues and hormones Carbendazim is equally well-documented as a male reproductive system poison and carcinogen.
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.
The point of this is to say that the brand of tobacco product your mother smoked matters more than just about any other factor in determining your risk of Testicular cancer as an adult. This means staying alert and getting checked often – which Stu did not do. I would end this with RIP, but there’s no way that “Tiny Ball” is laying around resting, wherever he is.
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