Because of the heavy concentrations of DDT and other endocrine disrupting pesticide residues we recently detected contaminating popular tobacco brands, I’ve been thinking a lot about the fact that beginning with the 1950s every tobacco product being smoked, puffed, dipped or chewed in America had extremely heavy concentrations of organochlorine pesticides. Heavy use of xenobiotic “crop protection” agents for tobacco began in the 1950s with DDT and quickly included aldrin, endrin, dieldrin, chlordane and other byproducts of wartime toxic gas research.
With that in mind, please check this:
DDT Exposure in Utero and Breast Cancer The Journal of Clinical Endocrinology & Metabolism, Volume 100, Issue 8, 1 August 2015, Pages 2865–2872,
Maternal o,p′-DDT predicted daughters’ breast cancer (odds ratio fourth quartile vs first = 3.7, 95% confidence interval 1.5–9.0). Mothers’ lipids, weight, race, age, and breast cancer history did not explain the findings.
DDT and Breast Cancer: Prospective Study of Induction Time and Susceptibility Windows . Journal of the National Cancer Institute, 13 February 2019
“Considering the patterns we observed, working backward to determine when a woman first came into contact with the chemical could help inform early detection and treatment of DDT-associated breast cancer.”
Women who were born roughly between 1955-1980 to mothers who smoked (or dipped or chewed) any of the popular tobacco brands of the times were heavily exposed to DDT and other organochlorines in the womb and probably throughout early childhood as Mommy smoked to get rid of all that pregnancy weight and then kept on smoking, maybe in secret, just a little, because it calmed her nerves.
A confidential industry study done in 1972 that I located in the Tobacco Settlement files reported an average of almost 6 mg/kg total DDT over all the brands they tested anonymously. The report ended with a hope that DDT concentrations would be dropping in the future (it had just been banned worldwide for the first time in 1972), and a warning that the data must be kept secret.
But when you look at what we found in tobacco products in 2018 you can see how little progress has been made. While there is only one instance of DDT contamination here it is extreme, and as you can see there are several rather extreme concentrations of other hazardous endocrine disrupting pesticide residues here even in this small sample. There are also residues of pesticides for which no data exist – their effects are unknown. It’s a crap shoot with human lives rolling snake eyes.
Community Tobacco Control Partners Test Results 12/18
If my interpretation of how our new tobacco pesticide residue data applies to the breast cancer research on endocrine disrupting chemicals is right, and it seems pretty straightforward, women in 2019 with medical history that includes parental and especially maternal smoking during birth years 1955-1980 are at severely heightened risk that requires close attention. I am NOT saying that the threat ended in 1980 – it changed, and it got worse. As you can see from the data above, female babies born today to young mothers who smoke Swisher Sweets, or who live in a household where they are smoked, are continually exposed to heavy doses of DDT. What does that say about their risk for breast cancer in 2050?
But in this post I am talking only about DDT and organochlorine exposure of women who were born to smoking mothers 1955-1980.
Know thy unknowns: why we need to widen our view on endocrine disruptors, Journal of Epidemiology and Community Health, 71:3, 2016 (209-212)
These compounds ‘interfere with any aspect of hormone action’, and by doing so can adversely affect physiology and development and thus increase the risk of metabolic and reproductive disorders as well as hormone-sensitive carcinogenesis and impaired neurodevelopment
So keeping with the theme, here are a few more things you may want to review.
Environmental chemicals and breast cancer: An updated review of epidemiological literature informed by biological mechanisms, Environmental Research, 160, (152-182)
Organochlorine concentrations in adipose tissue and survival in postmenopausal, Danish breast cancer patients, Environmental Research, 163,(237-248)
Receptor activities of persistent pollutant serum mixtures and breast cancer risk, Endocrine-Related Cancer, 10.1530/ERC-17-0366, 25:3, (201-215),
Evidence of the Possible Harm of Endocrine-Disrupting Chemicals in Humans: Ongoing Debates and Key Issues, Endocrinology and Metabolism, 10.3803/EnM.2018.33.1.44, 33:1, (44),
Changes in the total effective xenoestrogen burden (TEXB) of breast cancer patients during an 18-month post-surgical follow-up, Reproductive Toxicology, 10.1016/j.reprotox.2017.03.007, 69, (212-220),
Finally, as you look at this last reference, note the “higher girl’s BMI” factor, and consider the role of EDC in obesity. What if the EDC’s in the mother’s tobacco products contribute in utero and during childhood to the child’s obesity which in turn adds to her potential for breast cancer development? If so, we know for sure harmful pre-natal EDC exposure is going on today and is not just something that happened 1955-1980.
Prenatal smoking and age at menarche: influence of the prenatal environment on the timing of puberty Human Reproduction, Volume 30, Issue 4, 1 April 2015, Pages 957–962
We find that older maternal AAM (hazards ratio (HR): 0.75, confidence interval (CI) (95%): 0.71–0.79) and higher birthweight (HR: 0.86, CI (95%): 0.75–0.97) lower the chance of earlier menarche; while higher girls’ BMI at 8–9 years (HR: 1.12, CI (95%): 1.10–1.15), and maternal cigarette smoking on ‘most days’ during gestation (HR: 1.40, CI (95%): 1.10–1.79 with ‘no smoking’ as the reference level) increased the chance of earlier menarche. All factors were statistically significant at P = 0.05.