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Thoughts On Coca, Cannabis, Opium & Tobacco – Gifts Of The Great Spirit

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Smoking & Breast Cancer – A New Link?

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),

A Ternary Mixture of Common Chemicals Perturbs Benign Human Breast Epithelial Cells More Than the Same Chemicals Do Individually, Toxicological Sciences, 10.1093/toxsci/kfy126

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.


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Sweet Cheap Poison At The Bodega

We’ve just finished testing off-the-shelf tobacco products from local mini-marts in Portland, Oregon and among the 20+ hidden, unregulated xenobiotic contaminants that we were able to identify (see below) we found extremely high concentrations of Carbendazim. This contamination occurred in a little cigar brand that is #1 in Latino communities and high in popularity in African-American, Native American and other marginalized & low-income communities where tobacco product choices are restricted to the cheapest, and now we know the most contaminated brands.

Carbendazim has been banned in the EU since 2014. It attacks and destroys the reproductive and immune systems of young people, particularly young Latinos, African-Americans, and Native Americans whose genetic materials are known to be more vulnerable to Carbendazim than youth of European ancestry.  As you can see in the data, Carbendazim is only one many previously hidden, unregulated contaminants we found, each with it’s own health impact. But for the moment let’s focus just on the Carbendazim 0.843 mg/kg that’s being inhaled 20-40-60 times a day by @ 850,000 young people in the US right now today.

Carbendazim contamination disproportionately impacts marginalized young people who fall victim to tobacco products and who, because of poverty and carefully targeted marketing, have few choices available to them other than the cheapest and most contaminated brands. Please notice the relationship between price and contamination in the data below. 

(from): Summary of Science Behind 2014 EU Ban on Carbendazim “Independent literature shows that the pesticide Carbendazim is a very dangerous toxin, capable of causing malformations in the foetus at very low doses and it’s still uncertain if a safe level exists at all. Carbendazim is also capable of disrupting chromosome unfolding, can cause infertility of men and cancer.”   

Community Tobacco Control Partners Test Results 12/18

As you can see, Carbendazim shows up in our first-ever data on pesticide contaminants of tobacco products (right hand column third row). This brand, Swisher Sweets, is #1 in popularity among young smokers, who are also right in the middle of their reproductive years. It is heavily marketed to youth, and is designed with sweet flavors and heavy social media advertising to be part of a cool lifestyle.

Here is a detailed study of how the most toxic brands, with Swisher Sweets the “most toxic”, are marketed in low-income, Latino, Black, and Native American communiities.

This means that these young people, in the middle of their reproductive years, are at the highest possible risk for suffering the known consequences of Carbendazim exposure. (And all the other pesticides you see there, each of which deserves it’s own discussion.) This is made more serious by the route of exposure, because inhalation exposure is far more toxic than eating or skin exposure, and the frequency, because smokers (and fetus and child) are exposed to the pesticides with every puff.

The bottom line is that 0.843 mg/kg is an extraordinary level of Carbendazim to find in any consumer product, but especially in an off-the-shelf tobacco product being marketed heavily to kids, considering that it has been totally banned in much of the world since 2014, is strictly regulated in the US, and is totally illegal on tobacco. Imagine the response of health authorities if this were found on school lunches, slurpees at the 7/11, beer at the mini-mart or granola at Whole Foods?

The problem isn’t just that the Carbendazim is present. For there to be that much Carbendazim residue, it had to have been sprayed on the tobacco deliberately, heavily and recently. There is full knowledge of the EU ban, and the reasons for it. All tobacco manufacturers have notified by their own scientific authority CORESTA. The manufacturers know, or have every reason to know, that they are committing serious race-based crimes against humanity. I can only assume that they have been at this for so long that they actually don’t realize what they are doing to so many people.

Here are just a few of the peer-reviewed research data links that throw light on this hidden relationship

1. Regul Toxicol Pharmacol. 2014 Aug;69(3):476-86. Reproductive and possible hormonal effects of carbendazim.

“The literature review indicates that CBZ induces reproductive and developmental toxicity through alteration of many key events which are important to spermatogenesis. It seems that this fungicide may influence the hypothalamus-pituitary-gonad axis in addition to being a testicular toxicant.”

“2,5-Hexanedione (2,5-HD), a taxol-like promoter of microtubule assembly, and carbendazim (CBZ), a colchicine-like inhibitor of microtubule assembly, are two environmental testicular toxicants that target and disrupt microtubule function in Sertoli cells.”

3. Toxicol Ind Health. 2014 Apr;30(3):259-67. Carbendazim-induced testicular damage and oxidative stress in albino rats: ameliorative effect of licorice aqueous extract

“Administration of carbendazim induced significant decrease in testis weight, diameter, and germinal epithelial height of the seminiferous tubules. Histological results revealed degeneration of seminiferous tubules, loss of spermatogenic cells, and apoptosis. Moreover, carbendazim caused elevation of testicular malondialdehyde (MDA), marker of lipid peroxidation, and reduced the activity of the antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT).”

4. Toxicol Pathol. 2007 Aug;35(5):719-27. “Dose-dependent effects of sertoli cell toxicants 2,5-hexanedione, carbendazim, and mono-(2-ethylhexyl) phthalate in adult rat testicles.“

“Sertoli cells are the primary cellular target for a number of pharmaceutical and environmental testicular toxicants, including 2,5-hexanedione, carbendazim, and mono-(2-ethylhexyl) phthalate. Exposure to these individual compounds can result in impaired Sertoli cell function and subsequent germ cell loss. The loss of testicular function is marked by histopathological changes in seminiferous tubule diameter, seminiferous epithelial sloughing, vacuolization, spermatid head retention, germ cell apoptosis, and altered microtubule assembly.”

5.  Environmental Chemistry Letters 14(3) · June 2016 “Toxicity, monitoring and biodegradation of the fungicide carbendazim” 

“We found that carbendazim causes embryotoxicity, apoptosis, teratogenicity, infertility, hepatocellular dysfunction, endocrine-disrupting effects, disruption of haematological functions, mitotic spindle abnormalities, mutagenic and aneugenic effect.”

And the issue isn’t just Carbendazim as you can see looking back in the data. Most of the individual contaminants are concerning by themselves, but they are additive and synergistic in effect and their impact on human health in that regard is absolutely unknown. What is known now, and IMO it ought to be enough, is that young smokers are inhaling a toxic cocktail of chemicals each designed to operate in different ways at the nano-level to disrupt basic life processes.  The dosage of the most advanced pesticides doesn’t matter – they don’t need a “critical mass” to work. A couple of molecules, well below the level of detection, is enough for them to do what they were designed to do to the reproductive systems and genetic materials of bugs, and human teens are simply unfortunate collateral damage in the tobacco industry’s search for increased profits through chemistry.


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Dude! That Shit’s Shrinking Your Balls!

Does your kid, or a kid who you know and care about smoke little cigars or some other kind of cheap, flavored tobacco? Are you frustrated because you can’t stop them? Do they have a major “don’t give a shit” attitude? Even if they are being little idiots, do you understand and still want to help?

I propose some evidence-based reality and an appeal to that little idiot’s well-concealed intelligence. Do you think you can you get this kid to sit with you for one hour and read this post together. In the post I will lay out hard evidence showing how their testicles and genetic materials (and those of their friends) are under stealth chemical attack from contaminated cheap products they are being suckered into smoking. Challenge yourselves to understand the science and read through the references together – they are linked to the original research. This isn’t obscure science – this is about clear evidence of specific chemicals known to attack male reproductive organs in the tobacco brand they smoke that are there because of a cheap, money-grubbing manufacturer’s carelessness and greed. See if your discussion doesn’t trigger an instinct for self-preservation in them and maybe even help them get a clue.

We all know that “please please don’t smoke” doesn’t work, and neither does “smoking is really really bad for you”.  How many millions of dollars are still being wasted on endless repetition of some version of those two “nanny state” themes? Tell a kid that there are 4000 really really bad chemicals in that cigarette, or that he’s going to get lung cancer, and he will sneer to show you how tough he is. Tell him that the cheap-ass manufacturer of that crap he’s smoking is using trash tobacco that’s such shitty stuff that it’s contaminated with totally illegal chemicals that are attacking his balls every time he takes a hit. Tell him that the brands that are poisoned this way are pushed hard to people in poor neighborhoods who can only afford cheap poisoned shit, and to people who have enough money to afford less poisoned brands but are too stupid to know the difference. Show him the data tables below and ask him what he thinks – which brands are pushed to which people in which neighborhoods? Point out, in case he doesn’t get it, that when it comes to tobacco shit definitely rolls downhill.  

BTW this post is for boys. I’m working on one for girls that will be titled “Girl – Those Swisher Things Are Frying Your Eggs!”

So young Dude, you smoke Swisher Sweets. Maybe some other brands too. Lots of people love to smoke Swisher Sweets, especially when they see hotties like Cardi B sucking on their favorite kind of Swisher. But those Swisher Sweets aren’t anything like what the Man behind Cardi B wants you to think they are. No indeed.

Dude, no joke – your balls are at serious risk smoking that shit. If you’re cool with that, no problem. It’s your life. But, for the sake of those who care about you, take a little time and think about a couple of things.

Let’s begin with a reality check on those sweet fruity little cigars. Do you think you’re going to get real tobacco at 2 sticks that weigh 3 grams each for $0.99? Really? Then you must have bought your share of baggies of Oregano thinking you were getting bargain dope, because the math doesn’t work. Even if they didn’t shrivel your nuts, little cigars are not real tobacco. They are worse trash than any toxic Mexican weed you ever smoked, even when you weren’t buying Oregano, and here’s why. Those little 3 gram sticks are made especially for poor kids and stupid kids and are loaded with chemicals that do all kinds of nasty shit, but only to the people who smoke the cheap stuff. Most of those chemicals aren’t even there in the pricier brands, and Swisher Sweet smokers and little cigar smokers in general get special treatment as you can see here. This data is from tests we just ran on off-the-shelf tobacco products popular with young smokers from all kinds of communities.

Community Tobacco Control Partners Test Results 12/18

Keep your eye on that Carbendazim under “Swisher Sweets” in the right-hand column because that’s the ball-shrinker we’re talking about. I’m going to explain the connection in a minute.

To be fair you have to ask why those friendly folks at Swisher Sweet would want to bother to shrink your balls? Well, they don’t actually. They don’t care about your balls, or the kids you may want to make someday with those balls. All they’re doing is spraying their tobacco fields with chemicals that kill off the bugs more effectively by shrinking adult bug balls so they can’t have baby bugs. It’s a new way of controlling bugs, and they will tell you they have to do it. You just can’t kill bugs with pure poisons anymore – they’ve gotten resistant. But their little balls are vulnerable as hell, and that’s what these chemicals are designed to attack and destroy, so you add chemicals like Carbendazim to your chemical cocktail and wham – no bugs, and a lot more valuable tobacco per acre.

OK, bugs don’t have balls, not little ones hanging on the outside anyway, but they do have male reproductive organs and those bug equivalents of your precious balls are what Carbendazim is designed to attack and destroy. 

But, unfortunately, those chemicals in the tobacco fields don’t only bust bug balls, they retain the chemical potency to twist and shrink the balls of every creature they touch, like human Swisher Sweet smokers. That would be you, young Dude, wouldn’t it?

Well hey, as long as you keep buying their shit why should they worry about a few chemicals you don’t seem to mind even if they are attacking your balls? Nobody says it’s illegal for them to have ball-busting chemicals in their little cigars, so why worry about it. Nobody inspects tobacco products for pesticides anyway because they think that anyone who smokes deserves anything that happens to them and this means that everyone from doctors to FDA to inspectors to anti-tobacco crusaders all totally ignore the presence of pesticides in tobacco products and what they would have to admit that means.

OK, this has all been trash talk. Now I’m going to assume that you understand regular English and basic science. I’m also going to assume that if you’ve read this far maybe you’re ready for some straight talk, and that you may, secretly even, be starting to give a shit. So here’s just a taste of the straight science behind your shrinking balls in regular English, with links for you to follow and make up your own mind what you’re going to do about it. 

This first reference just about says it all for any young man who smokes little cigars and expects to have children:

Why Carbendazim has been banned in the EU since 2014

Then there are all these peer-reviewed scientific findings:

“Although the exact mechanism of action is unclear, carbendazim appears to bind 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.” (translation: it shrinks your balls.)

The Link: https://pubchem.ncbi.nlm.nih.gov/compound/Carbendazim#section=GHS-Classification

“The fungicide Carbendazim Methyl-2-benzimidazole carbamate (MBC) is known to produce male reproductive toxicity.” (translation: there is no doubt.)

The Link: https://www.ncbi.nlm.nih.gov/pubmed/17479253?dopt=Abstract

“Administration of carbendazim induced significant decrease in testis weight, diameter, and germinal epithelial height of the seminiferous tubules. Histological results revealed degeneration of seminiferous tubules, loss of spermatogenic cells, and apoptosis.

Moreover, carbendazim caused elevation of testicular malondialdehyde (MDA), marker of lipid peroxidation, and reduced the activity of the antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT).” (translation: it shrinks them and totally fucks them up.) 

The Link: https://www.ncbi.nlm.nih.gov/pubmed/22903170?dopt=Abstract

“2,5-Hexanedione (2,5-HD), a taxol-like promoter of microtubule assembly, and carbendazim (CBZ), a colchicine-like inhibitor of microtubule assembly, are two environmental testicular toxicants that target and disrupt microtubule function in Sertoli cells.” (translation: testicle toxins work together.) 

The Link: https://www.ncbi.nlm.nih.gov/pubmed/15141104?dopt=Abstract

“Due to synergistic effects, low environmentally present concentrations of imazalil and cypermethrin in food, and especially their mixtures with carbendazim have genotoxic potential that could be particularly dangerous over prolonged exposure in mammalian organism.”(translation: prolonged exposure destroys the genetic materials in your balls.) 

The Link:  https://www.ncbi.nlm.nih.gov/pubmed/21868589?dopt=Abstract

If you want to read more on other linkages between pesticide contamination of tobacco products and disease please follow these links to other recent posts:

Obesity & Obesogens: The Toxic Chemical Connection

https://wp.me/p48Z9A-nJ4

Tobacco Pesticides & Childhood Leukemia

https://wp.me/p48Z9A-nIL

Tobacco Road – Brazilian Tobacco, Nerve Agents, and American Cigarettes

https://wp.me/p48Z9A-nyp

DDT, Little Cigars, & Dropouts

https://wp.me/p48Z9A-nIk

Organic Tobacco Is Safer Tobacco & Here’s Why

https://wp.me/p48Z9A-nH5

Do You Want To Make Little Cigars Illegal In Your Community?

https://wp.me/p48Z9A-nEY

Smoking & Health – Fake Science Kills

https://wp.me/p48Z9A-nxW

 


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DDT, Little Cigars, & Dropouts

Students who smoke are at significantly heightened risk of school failure, but nobody can explain the clear connection. In the latest, large 2016 study of child smokers over one-third of Late Starters (35.8%) and almost half of Continuous Users (44.4%) dropped out of high school. Go figure.

We’ve shown through lab analysis that there are high concentrations of DDT and other endocrine-disrupting pesticides present in tobacco products.

PestGroup01

Community Tobacco Control Partners Test Results 12/18

These pesticides are proven to cause severe developmental and cognitive deficiencies. (Peer-reviewed journal links at end of post). 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?

Research On Pesticides, Kids & Learning

Prenatal DDT and DDE exposure and child IQ in the CHAMACOS cohort.

“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.”

In Utero p,p′-DDE Exposure and Infant Neurodevelopment: A Perinatal Cohort in Mexico

“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.”

In utero exposure to dichlorodiphenyltrichloroethane (DDT) and dichlorodiphenyldichloroethylene (DDE) and neurodevelopment among young Mexican American children

“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.”

Prenatal organochlorine exposure and behaviors associated with attention deficit hyperactivity disorder in school-aged children.

“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.”

Increased risk of attention-deficit/hyperactivity disorder associated with exposure to organophosphate pesticide in Taiwanese children.

“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.”

Association of pyrethroid pesticide exposure with attention-deficit/hyperactivity disorder in a nationally representative sample of U.S. children.

“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.”

Developmental neurotoxic effects of two pesticides: Behavior and neuroprotein studies on endosulfan and cypermethrin.

“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.”

Developmental pesticide exposure reproduces features of attention deficit hyperactivity disorder

 “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.”

Prenatal exposure to organophosphate pesticides and reciprocal social behavior in childhood.

“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.”

Pesticide exposure in children.

“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.”