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


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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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Tobacco Pesticides & Childhood Leukemia

PestGroup01

Community Tobacco Control Partners Test Results 12/18

Heavy concentrations of pesticide residues in cheap tobacco products being smoked by mothers, fathers or others in the household are likely to be a factor in the high rates of childhood Leukemia (ALL) among Hispanic and Native American children.

I believe these hidden, unregulated pesticides will prove to be a major factor in childhood cancer, once their presence and nature is recognized. It will be seen that simply controlling the most hazardous pesticide residues in tobacco products by imposing reasonable standards on manufacturers could lower the incidence of childhood cancer and many other diseases, perhaps dramatically, especially in the most genetically vulnerable groups of people. 

The reasons the link between tobacco pesticide contaminants and childhood leukemia remains obscure are:

  1. While the link between pesticide exposure of the fetus and development of childhood Leukemia (ALL) is proven, and;

  2. While parental smoking and childhood Leukemia are strongly associated, and;

  3. While Hispanic and Native American children are proven to have higher rates of ALL and;

  4. While marginalized young people are known to be the heaviest consumers of the most heavily contaminated brands, nevertheless;

  5. Nobody seems to know that tobacco products, and particularly those smoked and preferred by young Hispanics and Native Americans, are heavily contaminated with some of precisely the pesticides that are known to cause ALL, and;

  6. Although researchers say that they can see clearly that pesticides, smoking and ALL are linked, they can’t explain the connections because;

  7. There has never been any reference research published showing pesticide contamination of tobacco products, until our little study, and;

  8. Researchers almost never have any reality-based background knowledge of tobacco industry practices to guide their research objectives

Here is what researchers know about Childhood Leukemia that is relevant to tobacco pesticide contamination (journal citations are below the narrative).

  1. In addition to Hispanic and Native American children having higher rates of childhood leukemia (ALL) than other groups, research shows that children with at least 10% Native American ancestry have 59% higher relapse rates after being “cured” of ALL the first time.

  2. Childhood Leukemia is known to be initiated by specific pesticide exposure at specific points in fetal development. There are other causes, but the wrong kind of pesticide exposure at exactly the wrong fetal developmental point initiates genetic processes leading directly to childhood Leukemia.

  3. The relationship between fetal pesticide exposure and increased likelihood of childhood Leukemia in Hispanic and Native American children is proven. The multiple causes of ALL are not clear to researchers, but the associations with pesticides are strong.

Here’s what we want to contribute to the discussion.

We believe that our new data on pesticide contamination of tobacco products offers a novel and powerful even if partial explanation for the association between parental smoking and childhood Leukemia in Hispanic, Native American and other vulnerable populations.

We have just completed our first tests of off-the-shelf tobacco products for pesticide residues (12/18). We randomly selected samples from a universe of tobacco products known to be popular with young smokers.

  1. The pesticides that we identified contaminating tobacco products marketed to and smoked by poor, young non-white people included multiple heavy concentrations of specific pesticides that are known to initiate childhood leukemia disproportionately in Hispanic and Native American babies. We refer specifically to Carbendazim and DDT.

  2. A significant proportion of young, low-income Hispanics and Native Americans smoke little cigars, and because this is a very heavily contaminated tobacco product category, their children are exposed beginning with conception to xenobiotics that are known pathways to childhood leukemia and that show particular virulence in Hispanic and Native American children. Little cigars are by no means the only pesticide-contaminated tobacco products – they are simply the most contaminated of any that we have been able to test so far.

  3. Because childhood Leukemia is known to initiate its growth at specific developmental stages, chronic smoking of tobacco products containing high concentrations of pesticides by the pregnant mother, or by anyone in the household, guarantees that xenobiotics will be present at every critical point for the initiation of development of childhood Leukemia in the growing child.

  4. Since pesticide exposure levels required for initiation of disease processes during fetal development can be very low, concentrations remaining in second-hand smoke might be sufficient to initiate these disease-inducing genetic changes in the fetus even when the pregnant woman does not smoke.

But it’s not just pregnant mothers and smoking family members who give babies Leukemia. A new relationship has just been established between smoking by Hispanic fathers and leukemia in their children. 

Pesticide contamination of the products that young Hispanic fathers are smoking appears to be a novel, powerful and unrecognized connection between their smoking and childhood Leukemia in their children. These findings are further reinforced by recent findings of paternal smoking influence in childhood Leukemia in a non-Hispanic White Australian population. It is therefore highly likely that this link applies to Native American fathers as well.

See for yourself what the research says. Here are some of the core research articles that I believe support a clear link between contaminated tobacco products and childhood Leukemia. 

“Linking Pesticide Exposure with Pediatric Leukemia: Potential Underlying Mechanisms”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4848917/

Leukemia is the most common cancer in children, representing 30% of all childhood cancers. The disease arises from recurrent genetic insults that block differentiation of hematopoietic stem and/or progenitor cells (HSPCs) and drives uncontrolled proliferation and survival of the differentiation-blocked clone. Pediatric leukemia is phenotypically and genetically heterogeneous with an obscure etiology.

The interaction between genetic factors and environmental agents represents a potential etiological driver. Although information is limited, the principal toxic mechanisms of potential leukemogenic agents (e.g., etoposide, benzene metabolites, bioflavonoids and some pesticides) include topoisomerase II inhibition and/or excessive generation of free radicals, which may induce DNA single- and double-strand breaks (DNA-DSBs) in early HSPCs.

Chromosomal rearrangements (duplications, deletions and translocations) may occur if these lesions are not properly repaired.

The initiating hit usually occurs in utero and commonly leads to the expression of oncogenic fusion proteins. Subsequent cooperating hits define the disease latency and occur after birth and may be of a genetic, epigenetic or immune nature (i.e., delayed infection-mediated immune deregulation).

Here, we review the available experimental and epidemiological evidence linking pesticide exposure to infant and childhood leukemia and provide a mechanistic basis to support the association, focusing on early initiating molecular events.”

“Paternal smoking and risk of childhood acute lymphoblastic leukemia: systematic review and meta-analysis”

https://www.ncbi.nlm.nih.gov/pubmed/21765828

OBJECTIVE:

To investigate the association between paternal smoking and childhood acute lymphoblastic leukemia (ALL).

METHOD:

We identified 18 published epidemiologic studies that reported data on both paternal smoking and childhood ALL risk. We performed a meta-analysis and analyzed dose-response relationships on ALL risk for smoking during preconception, during pregnancy, after birth, and ever smoking.

RESULTS:

The summary odds ratio (OR) of childhood ALL associated with paternal smoking was 1.11 (95% Confidence Interval (CI): 1.05-1.18, I(2) = 18%) during any time period, 1.25 (95% CI: 1.08-1.46, I(2) = 53%) preconception; 1.24 (95% CI: 1.07-1.43, I(2) = 54%) during pregnancy, and 1.24 (95% CI: 0.96-1.60, I(2) = 64%) after birth, with a dose-response relationship between childhood ALL and paternal smoking preconception or after birth.

CONCLUSION:

The evidence supports a positive association between childhood ALL and paternal ever smoking and at each exposure time period examined. Future epidemiologic studies should assess paternal smoking during well-defined exposure windows and should include biomarkers to assess smoking exposure and toxicological mechanisms.

“Correlates of Prenatal and Early-Life Tobacco Smoke Exposure and Frequency of Common Gene Deletions in Childhood Acute Lymphoblastic Leukemia”

http://cancerres.aacrjournals.org/content/early/2017/03/22/0008-5472.CAN-16-2571

“In summary, we provide evidence that increased tobacco smoke exposure increases the generation of somatic ALL-associated driver deletions. To our knowledge, this is also the first reported application of an epigenetic biomarker to assess the effects of an environmental exposure on leukemogenic alterations.”

“Our findings should be added to an already compelling list of reasons for minimizing the prenatal and early life tobacco smoke exposure of children.” 

“Childhood Leukemia Incidence in California: High and Rising in the Hispanic Population”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5542672/

“Ethnic disparities in children’s exposure to chemicals at home, as well as ethnic disparities in their parents’ exposures to chemicals at work, may contribute to the higher burden of childhood leukemia in Hispanic children.

A more complete evaluation of the role of specific environmental factors that disproportionally affect the Hispanic community in the increased risk of leukemia in Hispanic children is warranted.”

“Native American ancestry linked to greater risk of relapse in young leukemia patients”

https://www.sciencedaily.com/releases/2011/02/110206132908.htm

The study found that ALL cancer was 59 percent more likely to return in patients whose genetic makeup reflected at least 10 percent Native American ancestry.

Investigators also found ALL patients with greater Native American ancestry who received additional chemotherapy as part of a COG clinical trial benefited more from the extra treatment than other children.

“In utero pesticides exposure and generation of acute myeloid leukemia associated translocation (8;21)”

https://medcraveonline.com/MOJT/MOJT-02-00037.pdf

 The present study was set to detect t (8;21) translocation in umbilical cord blood samples from neonates as in utero primary molecular hit in the pathway of childhood leukemia in apparently healthy neonates and to delineate the relationship between generation of this translocation and prenatal pesticide exposure.

Four pesticides were studied including Malathion and Diazinon as organophosphates, and DDT and Lindane as organochlorines. The choice of these four pesticides was based on their popular use in the community under investigation and their well-established role in cancer pathology.”

“Of the studied pesticides, DDT was accompanied by highest risk for carrying the fusion Oncogene [OR 3.55 (95%CI 1.53-8.26), P=0.003].”

“Since pediatric leukemia involves both genetics and environmental interactions, pesticides provide a perfect link in such regard. In this relatively large study we report on a direct relation of prenatal Malathion and DDT exposure and the incidence of leukemia translocation in neonates.”

“To the best of our knowledge, the current study is the first study to evaluate the effect of pesticides on acquiring AML fusion Oncogene in Egypt, where the analyzed Xenobiotics are still used and not banned yet.”  (Published November 28, 2016)

“In Utero Pesticide Exposure and Leukemia in Brazilian Children < 2 Years of Age”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3569673/

 “Our findings suggest that children whose mothers were exposed to pesticides 3 months before conception were at least twice as likely to be diagnosed with ALL in the first year of life compared with those whose mothers did not report such exposure.

Adjusted ORs for AML in the first year of life ranged from 2.75 (95% CI: 0.96, 7.92) for any pesticide exposure in the first trimester of pregnancy, to 7.04 (95% CI: 2.47, 20.10) for exposure during breastfeeding.

Studies conducted in other countries have also reported positive associations between pesticide exposure and hematopoietic neoplasms in children, especially leukemias and lymphomas (Ma et al. 2002Meinert at al. 2000Menegaux et al. 2006Rudant et al. 2007Zahm and Ward 1998).

A systematic review and meta-analysis of 15 studies of the association between residential exposure to pesticides during selected time windows (preconception, pregnancy, and childhood) and childhood leukemia carried out during 1950–2009. (Turner et al. 2010) reported associations with pregnancy exposure to unspecified pesticides (OR = 1.54; 95% CI: 1.13, 2.11), insecticides (OR = 2.05; 95% CI: 1.80, 2.32), and herbicides (OR = 1.61; 95% CI: 1.20, 2.16).

Another meta-analysis of 31 studies of parental occupational exposure to pesticides and childhood leukemia (Wigle et al. 2009) reported associations with occupational exposure to insecticides (OR = 2.72; 95% CI: 1.47, 5.04) and herbicides (OR = 3.62; 95% CI: 1.28, 10.3) during pregnancy.

A French study also examined the association between pesticide exposure and infant leukemia (Rudant et al. 2007). According to use of any pesticide, the observed risk estimates (ORs) were 2.3 (95% CI: 1.9, 2.8) for ALL and 2.2 (95% CI: 1.4, 3.3) for AML. These authors also suggested that a domestic use of pesticides may play a role in the etiology of leukemia, and that prenatal exposure may be a window of fetal vulnerability.

Incidence rates of childhood leukemia in the United States have steadily increased over the last several decades, but only recently have disparities in the increase in incidence been recognized.

“Trends in Childhood Leukemia Incidence Over Two Decades from 1992–2013”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5550103/

In the current analysis, Surveillance, Epidemiology and End Results (SEER) data were used to evaluate recent trends in the incidence of childhood leukemia diagnosed at age 0–19 years from 1992–2013, overall and by age, race/ethnicity, gender, and histologic subtype. Hispanic White children were more likely than non-Hispanic White, non-Hispanic Black or non-Hispanic Asian children to be diagnosed with acute lymphocytic leukemia (ALL) from 2009–2013.

From 1992–2013, a significant increase in ALL incidence was observed for Hispanic White children (annual percent change (APC)Hispanic=1.08, 95%CI:0.59, 1.58); no significant increase was observed for non-Hispanic White, Black or Asian children.

ALL incidence increased by about 3% per year from 1992–2013 for Hispanic White children diagnosed from 15–19 years (APC=2.67; 95%CI:0.88, 4.49), and by 2% for those 10–14 years (APC=2.09; 95%CI:0.57, 3.63), while no significant increases in incidence were observed in non-Hispanic White, Black, or Asian children of the same age.

Acute myeloid leukemia (AML) incidence increased among non-Hispanic White children under 1 year at diagnosis, and among Hispanic White children diagnosed at age 1–4. The increase in incidence rates of childhood ALL appears to be driven by rising rates in older Hispanic children (10–14, and 15–19 years).

More bad news. It looks like we should be concerned about pesticides in tobacco products and childhood brain cancer.

Environ Health Perspect. 2009 Jun; 117(6): 1002–1006.

“Parental Exposure to Pesticides and Childhood Brain Cancer: U.S. Atlantic Coast Childhood Brain Cancer Study”

Cancer Causes Control. 2013 Jul;24(7):1269-78.

“Exposure to pesticides and the risk of childhood brain tumors”

 


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A Community-Level Tobacco Control Strategy

We laugh at the silly idea of Cannabis as a “killer weed” now, but millions believed it and happily allowed the government to send generations of people to prison because they believed it. It seems absurd that anyone would be fooled by that ham-handed government propaganda, but millions were and many still are.

Keeping mind that what has happened in the past could happen again, and could be happening right now, let me ask you to consider this:

What if there is a much more subtle and sophisticated generations-long campaign of disinformation about Tobacco just like there was about Cannabis? What if it’s run by a powerful industry with endless money and not by a bunch of clueless bureaucrats thinking up stupid slogans.  What if the Tobacco industry has known for a long time that it has a severe, possibly fatal problem that it has managed to keep completely out of public view by spending vast sums of money on a combination of public persuasion and widespread, carefully targeted (but increasingly visible) official, scientific and medical corruption?

What if some or even most of the damage being caused in the modern world by commercial Tobacco products is not being caused by the Tobacco in those products but by previously unidentified hazardous toxic substances IN the tobacco products, and what if that means that these products can be controlled at the local level using existing local and state ordinances and laws?

I know that’s it’s a heresy, but fair-minded people will consider the actual evidence and not rest on an unquestioned assumption: maybe it’s not the tobacco in the tobacco products that’s killing most of the people.

The very foundation of the anti-tobacco, anti-smoking faith is that “Tobacco Is Bad Shit”. That’s the firm, unquestioning belief, and every tobacco prevention and control effort in the world is pinned to that article of faith. Tobacco causes illness and death. End of discussion. No questions. Full stop. We already know that Tobacco is bad shit, and we don’t want to hear any more about it. So let’s just move on and figure out how we can keep people from smoking and now vaping the goddamned stuff!

OK, but what if everybody is wrong? Really – what if everyone thinks things are one way, when they are actually another? Is that possible? What if people are all looking in one direction while the answer lies in another? Has there ever been that kind of mass delusion in history? Of course there has been – that’s a central theme in the history of science. People believe something fundamental for generations. It’s obviously wrong, but nobody can see it.  The first one who points this out is attacked. Others speak up and say wait a minute, we should check this out and see if it’s true. They do, and it is. And then everybody says “Whocoulddaknowed?”

The oldest example of “everybody knows” is the flat earth delusion that ruled western minds for centuries. Maps showed the edges of the earth. Then one day – Oops! It’s round. Whocoulddaknowed? Then next the all-powerful church decided to burn heretics who pointed out simple, hard evidence that the world rotated rather than the heavens turning.everyone knew that the earth was the center of the universe and that everything in God’s heavens rotated around God’s earth. Then one day – Oops! Whocoulddaknowed? It took the church centuries to apologize to Galileo.  Then everyone laughed at the idea of invisible bugs causing disease because everyone knows it’s the vapors. Oops! again. Really, Whocoulddaknowed? Little invisible bugs. Well I’ll be damned.

Most of us scoff at that kind of profound ignorance as if we were invulnerable to the same folly. But I’m telling anyone who will listen – it’s not the tobacco that is sickening and killing millions.

I realize that tying those profound historical delusions to a delusion about Tobacco, even if it could be demonstrated, may seem trivial in comparison, but if anything the effect of the delusion about Tobacco has had greater impact than any of those mass delusions just cited. That’s because of our profound collective delusions about tobacco, carefully cultivated by the tobacco industry to shield itself from accountability, have allowed millions of completely preventable deaths in the past and the dying will continue long into the future because of our willful collective ignorance.

The last words attributed to Jesus were “Father forgive them. They know not what they do.” I have always believed that Jesus was using those last words not to comment for all eternity on those who were killing him, but on the one thing most responsible for the suffering and death of mankind.

So, I’ll ask again, what if most of the damage being caused by Tobacco products is actually being caused by pesticide residues that contaminate the Tobacco products? The tobacco products, the manufactured crap, not tobacco itself.

Here’s the thing. We know for sure that pesticide chemicals do exactly what they’re designed to do. They interrupt nerve transmissions, they destroy DNA, they poison internal organs, they mutate little bug babies – the scientists are endlessly creative. So in the end, it really doesn’t matter whether tobacco is bad or not – we know that pesticides are “bad” for sure. They are “xenobiotics” – substances “hostile to life”. But so many people are so tied up arguing the evils of Tobacco so passionately and hatefully that they don’t see themselves as precise  parallels with the Middle Ages “angels on the head of a pin” debate that consumed generations of “wise men”, while the Tobacco companies are snickering all the way to the bank.

There are laws in place in every community to deal with pesticides as toxic substances, although those laws have been rigged by the pesticide manufacturers to cover what they thought was every contingency.

That’s the beauty of understanding that there are xenobiotic substances ON the tobacco products. It doesn’t matter what you think about tobacco itself, or even what laws and ordinances and regulations say about “tobacco” itself. Hate it or love it – doesn’t matter. These are products, and they are toxic, and they violate all kinds of laws on that basis. If you love Tobacco, you should care. If you hate Tobacco, you should care. Pesticide-free tobacco products would be a major improvement in the life of a community regardless.

So there really doesn’t have to be any argument at all about whether or not tobacco is bad and should be controlled – some of the pesticides on the tobacco products being sold in your community are flat illegal and there are available legal remedies that the law says MUST be applied. Take that to the bank – and to your health department. and don’t let them stonewall you about “lack of authority” – they have it. They have never used it before, and they probably haven’t ever thought about it, but if a toxic substance suddenly falls from the sky into the WalMart parking lot you can bet they won’t be sitting around wondering who is going to handle it. If somebody lets loose a can of DDT in a school you can bet that the local authorities aren’t going to call the state police and then wait. Communities can act when they are in immediate peril, and high concentrations of banned pesticide residues in tobacco products being smoked by children in the community meets that definition in spades.

Pesticides fall into a class of chemicals defined as “toxic substances” in a wide range of environmental and consumer protection regulations and statutes. In every state, there are statutes that empower local, county-level health officials to act when toxic substances threaten local public health. Yes there are pre-emption laws that forbid local communities from imposing greater restrictions on pesticides than state laws do, but in this case we’re talking about local communities using existing state laws on toxic substances in consumer products that, if detected at the any level, can trigger local action by public health authorities without waiting for permission from the state. This strategy may need tweaking in many communities, but because state and federal lawmakers have been incredibly (and perhaps in some cases deliberately) sloppy in writing tobacco product regulations I believe that tobacco product pesticide contamination opens a big wide door for local control.

In Oregon where I live, the credible allegation of the presence of banned “toxic substances” on any property located in the community is supposed to trigger mandatory regulatory responses if the allegation is properly made and supported by evidence. “Property” includes tobacco products sitting on the shelf down at the mini-mart. I’m currently working on educating our local public health administrator on her authority to act in this area.

In most jurisdictions I’ve looked at in California, Colorado, and other Cannabis-legal states, a broad range of “Property” is subject to “toxic substance” regulatory oversight by County public health authorities. 

I can hear the screams from the faithful now – but, but Tobacco is so bad that it doesn’t matter if there’s poison on the leaves! I would only ask the faithful – can you point to one scientific research study that compares the smoke or vapor of 100% pure, organic Tobacco with any Tobacco product on the market? There are none. Zero. And, that’s not one of those famous “distinctions without a difference”. Please think about that – if actual, real Tobacco smoke or vapor has never been tested, and if every report of toxic substances in “tobacco” smoke has been based on rigged “reference cigarettes” supplied by the industry itself, where does that leave the idea that, without any question, Tobacco is horrible, awful, dangerous stuff? It may be true, but there are no studies that prove it one way or another.

Since 1970 virtually every “scientific” study of tobacco products has used industry-supplied “reference cigarettes” that don’t give results relevant to either what is really on the commercial market or to organic or even simply leaf tobacco. At least 25% of those “reference cigarettes” are “reconstituted tobacco”, a synthetic product made from a highly variable mix of tobacco stems, stalks and factory-floor waste called “tobacco dust”. There is no way that the results of smoke stream or vapor stream analysis using “reference cigarettes” has anything to do with tobacco in pure form. I know that anti-tobacco advocates would fear that the results of such testing might clear Tobacco’s name and give people who like to smoke and vape a license to do so. But so what?

I would say to them, if it turns out that it isn’t the Tobacco but the pesticides, since the pesticides are a very controllable harm while people smoking and vaping are not controllable, then forget about your dislike of Tobacco and deal with the problem. Or , I would also ask them, do you secretly agree with that renegade government bureaucrat in the 1920’s who arranged to have bootleg whiskey poisoned with methanol in order to scare people into not drinking? Do you think, I would ask, that this was actually a pretty good idea and those drinkers deserved what they got? Or maybe you aren’t that cold-hearted and simply think that alcohol is so bad anyway, and those drinkers were poisoning themselves anyway, so what’s the big deal?

I would ask them these questions because any person who felt so strongly about alcohol that they would ignore the deliberate poisoning of drinkers by the government wouldn’t be worried about a few pesticides in Tobacco products. By the same reasoning, Tobacco is so bad anyway – who cares about pesticides? 

Think that an example from the 1920’s, a hundred years ago, is a bit irrelevant to today’s enlightened government? Well, remember Paraquat on Marijuana? The DEA came right out and said that regardless of what it did to Marijuana smokers, they were engaged in illegal activity and so it didn’t matter. Besides, from the government’s point of view, a few dead hippies weren’t worth getting worked up over. The idea that was sold to the public is clearly that Marijuana is so bad anyway who cares if the government poisons it – after all, they’re just trying to keep precious little American children from being lured into a life of degradation and crime. 

Workers apply fungicide “Ditio carbamato” to cigar tobacco in Nicaragua every 4 days

So what I’m saying is that the only fair and reasonable way to determine the truth, the relative degree of actual risk, would be to compare (1) commercial tobacco products with (2) organic tobacco smoke and vapor. Otherwise all that science on smoking, and all those horrible components of “tobacco” smoke and vapor, aren’t actually testing “tobacco” smoke or vapor at all. They are testing “Tobacco product” vapor and smoke, and most Tobacco products in America have no relationship to real Tobacco leaf. Again, a distinction with a big difference.

One more heretical question, if you’re with me so far. What if those toxic substances are in Tobacco products for one reason only – because it is more profitable for Tobacco product manufacturers to use these chemicals in Tobacco production than to produce Tobacco without them? Almost as an aside, premium cigars are among the most severely contaminated Tobacco products in the world, because the growers spare no expense in applying pesticides, fungicides and every other kind of chemical to keep bugs and worms 

from eating holes in those incredibly valuable cigar wrapper leaves. And why do they do that? Simple, again. It’s the money. A Tobacco leaf with bug holes can be used for making premium cigars, so once a bug takes a bite that leaf turns from gold into plain old shit. 

Tobacco products aren’t contaminated with pesticide residues because the growers and manufacturers want to poison their customers; they’re contaminated because everybody makes more money by using these chemicals and they aren’t being forced to clean up their products, so millions of people are dying just like the bugs and worms in the Tobacco fields. It’s really that simple.

 

The Tobacco industry has produced organic Tobacco products, with no pesticide residue contamination. It knows how. It simply chooses not to. That cost/benefit decision alone impoverishes and drives the loss of millions of lives every year with immeasurable suffering and grief.

Pretty damned grim, right? Well, maybe not.  

All it took to bring down Al Capone was one little charge of income tax evasion, and he wasn’t nearly the magnitude of monster these Tobacco companies are. Al thought he was riding pretty high too. Fancy suits. Expensive wine. Hookers. Blow. The best of everything. But he overlooked that one little crime, and that was enough. 

Who in your County public health structure has the regulatory authority to order inspection of commercial products that are credibly suspected of being contaminated with the residues of banned pesticides? 

Insist that they forget you are talking about Tobacco products.

Ask them what their action would be if you were coming to them with evidence that imported scented candles, or air fresheners, or incense being sold in your community were contaminated with these same pesticides at these same levels?

Geiss, O., Kotzias, D. – Determination of Ammonium, Urea and Pesticide Residues in Cigarette Tobacco. Fresenius Environmental Bulletin (FEB), No. 12 (2003), 1562– 1565

What would they do if they knew that children in the community were going to be inhaling vapors of Endosulfan, 4,4-DDE and Heptachlor over 100 times a day in homes where adults burned these candles?

How about if the issue was air fresheners contaminated with those same nerve toxins? Or maybe incense from China or India full of Chlordane?

What would they do if Tobacco products at the local mini-mart had the same contaminants as the cigarettes on the list you see here.

Oh, and about this cigarette pesticide data being from 2003? See my recent blog post with the Tobacco industry’s own data that shows these same pesticides – and about 100 more – still present on Tobacco worldwide in 2018. Show that data to your county public health department too.

If these two little bits of “income tax evasion” evidence aren’t enough to give your County public health officer “reasonable cause” to order inspection of commercial Tobacco products being sold in your County, let me know.

I’m doing some Tobacco product testing right now (12/18) in three of Oregon’s premier testing labs, and I plan to make the results available as part of a community-level Tobacco product control program.

Local communities have deferred too long to State and federal bureaucrats to protect them from Tobacco products. Simple residue testing of commercial tobacco products being sold in your community will give you ample evidence to insist that your local public health officials use their existing authority to enforce toxic substances regulations against contaminated Tobacco products for sale in your community.

If your community doesn’t have existing qualified pesticide residue testing labs, and most don’t, get in touch and ask for no-cost assistance from the Oregon Community Tobacco Control Partnership. 


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Tobacco Product Risk Reduction

This is a comment that I’ve just submitted to the FDA asking them to enforce their own regulations and conduct appropriate testing, which has not been done to date, to determine whether all current IQOS applications are in compliance with regard to pesticide residues as required by this rule, and then to determine the impact of any discovered pesticide residues on the manufacturer’s many and deceptive “Modified Risk” claims.

You can support a moveon petition to Congress demanding that FDA investigate by clicking on the cute little hummingbird choking on clouds of vaporized pesticides.

To: US FDA December 4, 2018 via Comment Portal

In reference to: 907(a)(1)(B) of Section 907 of the Federal Food, Drug, and Cosmetic Act:

(B) ADDITIONAL SPECIAL RULE.—Beginning 2 years after the date of enactment of the Family Smoking Prevention and Tobacco Control Act, a tobacco product manufacturer shall not use tobacco, including foreign grown tobacco, that contains a pesticide chemical residue that is at a level greater than is specified by any tolerance applicable under Federal law to domestically grown tobacco.

FDA Comment Submission

I am concerned that

  1. The presence of pesticide residues in the Tobacco component of IQOS has not been discussed or referenced in any of Philip Morris’s FDA multiple IQOS applications.

  2. While the IQOS applications offer extensively documented comparisons between toxic substances in the IQOS vapor stream and toxic substances in the smoke stream of combusted Tobacco (reference Cigarettes only, not commercial cigarettes), after performing a keyword search through the submitted IQOS documentation I can find no mention of any comparison of pesticide residues in the IQOS vapor stream with those in a reference cigarette smoke stream in support of the IQOS claim of “modified risk”.

  3. The public record does not show that FDA has yet requested that Philip Morris demonstrate compliance with Special Rule 907(a)(1)(B) with regard to any of its IQOS applications.

  4. To grant any application related to IQOS without first establishing that IQOS can and will comply with Special Rule 907(a)(1)(B) would seriously jeopardize public health in that without demonstrated compliance and published results, the public will not have an opportunity to make a fair and complete comparison of the relative risks the pesticide residue contaminants of the IQOS product vs combustible Tobacco products.

  5. To grant any application related to IQOS that claims “harm reduction” without first comparing the relative harm of inhaling the intact pesticide burden in the IQOS vapor stream to the harm of inhaling the partially combusted, altered and degraded pesticides in a conventional Tobacco smoke stream, would not serve the public’s interest in having full and fair disclosure of all relevant risks associated with the use of IQOS.

Discussion

Because the Tobacco materials, along with any pesticide residues, in the Tobacco component of IQOS will be vaporized well below the point of pyrolytic degradation, and none of any pesticide residues contained in the Tobacco component will be destroyed by combustion, therefore it is reasonable to project that a greater proportion of the original pesticide residue burden on the Tobacco component of IQOS will survive and retain bioactivity in the vapor stream compared with the proportion of surviving and bioactive pesticide residues in a smoke stream that would be generated by combusting that same Tobacco component; and

Because in making its case for “modified risk” Philip Morris, by comparing the toxicant properties of an IQOS vapor stream with the toxicant properties of a Reference Cigarette smoke stream, either by oversight or by design fails to address the differences in potential for harm between (1) delivery of the full original pesticide residue burden in the IQOS vapor stream compared with (2) delivery of a reduced portion of the original pesticide residue burden, of which a portion has been destroyed by combustion, and some or all of the remainder of which has been dry-distilled into altered compounds and/or partially degraded by pyrolytic processes; and,

Because Special Rule 907(a)(1)(B) requires that manufacturers “shall not use” tobacco of any origin containing pesticide residues “at a greater level” than “any tolerance” specified under Federal law; and

Because in addition to pesticides registered for use on Tobacco with established tolerance levels, Federal law also specifies certain pesticides that are banned for use on Tobacco; in the context of US Special Rule 907(a)(1)(B) this requires that manufacturers shall not use any Tobacco containing those banned pesticides “at a greater level” than zero; and

Because current Tobacco industry documentation shows that certain pesticides not registered for use on Tobacco in the United States are present in the world Tobacco supply, and certain pesticides banned in the US are also present in the world Tobacco supply (https://www.coresta.org/agrochemical-guidance-residue-levels-grls-29205.html ); and

Because Philip Morris is a large importer of Tobacco stem and waste materials from Brazil, a Tobacco exporter with documented heavy use of pesticides on Tobacco crops; (https://www.zauba.com/Buyers-of-tobacco-stems) and

Because imported Brazilian Tobacco stems and waste that are likely to be contaminated with pesticides residues, some of which may violate the “greater level” condition of  Special Rule 907(a)(1)(B), are used in large quantities (millions of kilograms/year) by Philip Morris in its Tobacco product manufacturing in the US and are therefore, in the absence of any statement by the manufacturer to the contrary, likely used in its IQOS manufacturing processes; however, without testing for the presence and concentration of pesticide residues in the IQOS Tobacco component there can be no demonstration of IQOS compliance with Special Rule 907(a)(1)(B) regarding any such “imported tobacco”; and

Because Brazilian Tobacco pesticide use includes the documented use of pesticides for which US EPA and USDA have established that there are no safe levels, and that are either not registered or banned for use on Tobacco in the US ( https://www.hindawi.com/journals/omcl/2018/7017423/ ); therefore,

I am requesting that FDA suspend further consideration of the Philip Morris MRTP application, and any other Philip Morris application that can result in approval by the FDA for sale of IQOS in the US, until the issues I raise here are addressed under the FDA’s 907(a)(1)(B) authority and any other applicable enabling authorities.


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Stone Killers

If you want a new way to control the damage that Tobacco products do to your community, then this may interest you.

This post offers credible tobacco industry data showing all of the pesticides that contaminate Tobacco products worldwide. It is published by CORESTA, the tobacco industry’s captive science & research institute. This information alone can empower local initiatives by offering credible evidence that banned toxic substances may be contaminating locally-sold Tobacco products.

If your local health department has regulations that allow it to investigate whether a product being sold in your community is contaminated with banned pesticide residues, then this list will give them probable cause to sample locally-sold Tobacco products and test for the presence of banned pesticide chemicals.

It is important for you to keep in mind, when making such a request, that (1) it doesn’t matter that the products are Tobacco – they are just like pesticide contaminated candles, air fresheners or incense – and (2) these contaminants are present because of negligence by the manufacturer and lack of regulatory oversight by any superior authority, so the local authorities have to act in the interest of public health and safety.

So this is it – the official (but highly confidential) June, 2018 tobacco industry guide to the pesticide chemicals used on tobacco worldwide. It’s an industry list cautioning manufacturers to ‘watch out’ for these chemicals that remain on Tobacco from the fields, which means that it’s a list of what the industry knows is potentially present in any Tobacco product anywhere.

Many of these pesticides are damaging to human health at very low levels of chronic exposure – just like a smoker gets 100-200 times a day, 365 days a year puffing away and inhaling the pesticide residues invisibly contaminating the tobacco in their cigarette. (Except that it isn’t really tobacco, but that’s another post.)

But the really severe public health threat created by pesticides on Tobacco lies in the industry’s attempt to pivot toward vaporizing. Imagine that instead of being at least partially destroyed by combustion and smoking, all those pesticides are now being gently vaporized and delivered full-strength to your lungs as IQOS Tobacco vapor.

While the tobacco industry publishes pesticide standards for its members, it makes clear that nobody actually has to follow this industry guidance. The tobacco companies are safe from accountability because there is no testing of commercial cigarettes in the United States for the presence of any of these chemicals, and what little testing the FDA, EPA and USDA do perform almost seems deliberately designed to shield the tobacco industry from investigation. It’s not as if the FDA doesn’t have the authority to demand that Tobacco companies at least keep the contamination down a little. 

907(a)(1)(B) of Section 907 of the Federal Food, Drug, and Cosmetic Act:

(B) ADDITIONAL SPECIAL RULE.—Beginning 2 years after the date of enactment of the Family Smoking Prevention and Tobacco Control Act, a tobacco product manufacturer shall not use tobacco, including foreign grown tobacco, that contains a pesticide chemical residue that is at a level greater than is specified by any tolerance applicable under Federal law to domestically grown tobacco.

Please keep that language in mind as you browse the list below. Chronic low-dose exposure to any one of the pesticides on this list, just by itself, is enough to cause serious damage to human adults, children and babies. The US government, along with the health authorities of every state, seem collectively uninterested in knowing what dozens of these violent chemicals, all being either burned or heated, smoked or vaporized and then inhaled actively or passively are doing to smokers or vapers, their families and everybody else downwind every day of their lives.

One last thing – notice that there are a lot of banned pesticides on the list. That’s because the Tobacco industry recognizes that large stores of these chemicals still exist and farmers still use them for one simple reason – they  kill bugs. It might also be that these chemicals are still being made in black factories in India and China.

Whether using banned pesticides or not, most small farmers in the Third World can’t even read the labels, if there are any, so all they care about is killing bugs and fungus. Every pound of tobacco that bugs eat and fungus destroys is one less pound the farmer has to sell to feed his family, which doesn’t mean that the kids just go without a snack for a day or two.

So of course hundreds of thousands of small tobacco farmers worldwide are going to use triple-witching stuff like Endrin, Heptachlor, Aldrin, and Dieldrin whenever they can get it or whenever they are told to use it. Because while manufacturing of these incredibly toxic chemicals is banned almost everywhere, ‘black’ factories in China and India are churning out the oldies but goodies by the ton and selling them in countries where 50% of all pesticides are used on just one crop – tobacco.

But of course regulatory authorities in the ‘advanced’ countries like the US don’t test for these banned pesticides in anything anymore, much less in tobacco products like cigarettes, because “nobody uses them anymore and all the old stores have been used up or destroyed long ago”.


Table 1.   Crop Protection Agent (CPA) Guidance Residue Levels (GRL)

This is not a list of recommended CPAs (Crop Protection Agents) for tobacco. That is a matter for official and/or industry bodies in each country.

  • GRLs have not yet been set for all CPAs registered for tobacco. Setting GRLs is an ongoing process based on a list of priorities decided by frequency of use and importance to leaf production.
  • The presence of a compound does not imply endorsement by CORESTA
  • The entries in the list do not replace MRLs (Maximum Residue Levels) set by the authorities. Compliance with MRLs is a legal requirement for countries that have set them for
No. CPA GRL

(ppm)

Residue definition Notes
1 2,4,5-T 0.05 2,4,5-T
2 2,4-D 0.2 2,4-D
3 Acephate 0.1 Acephate
4 Acetamiprid 3 Acetamiprid
5 Acibenzolar-S-methyl 5 Acibenzolar-S-methyl
6 Alachlor 0.1 Alachlor
 

7

 

Aldicarb (S)

 

0.5

sum of Aldicarb, Aldicarb sulfoxide and Aldicarb sulfone, expressed as Aldicarb
8 Aldrin + Dieldrin 0.02 Aldrin + Dieldrin
9 Azinphos-ethyl 0.1 Azinphos-ethyl
10 Azinphos-methyl 0.3 Azinphos-methyl
11 Benalaxyl 2 Benalaxyl
12 Benfluralin 0.06 Benfluralin
 

13

 

Benomyl (a)

sum of Benomyl, Carbendazim, and Thiophanate-methyl expressed as Carbendazim  

see Carbendazim

14 Bifenthrin 3 Bifenthrin
15 Bromophos 0.04 Bromophos
16 Butralin 5 Butralin
17 Camphechlor (S) (Toxaphene) 0.3 Camphechlor (mixture of chlorinated camphenes)
18 Captan 0.7 Captan
19 Carbaryl 0.5 Carbaryl
 

20

 

Carbendazim (a)

 

2

sum of Benomyl, Carbendazim, and Thiophanate-methyl expressed as Carbendazim
 

21

 

Carbofuran (S)

 

0.5

sum of Carbofuran and 3- Hydroxycarbofuran expressed as Carbofuran
22 Chinomethionat 0.1 Chinomethionat
23 Chlorantraniliprole 10 Chlorantraniliprole
24 Chlordane (S) 0.1 sum of cis-Chlordane and trans- Chlordane
25 Chlorfenvinphos (S) 0.04 sum of (E)-Chlorfenvinphos and (Z)-Chlorfenvinphos

 

No. CPA GRL

(ppm)

Residue definition Notes
26 Chlorothalonil 1 Chlorothalonil
27 Chlorpyrifos 0.5 Chlorpyrifos
28 Chlorpyrifos-methyl 0.2 Chlorpyrifos-methyl
29 Chlorthal-dimethyl 0.5 Chlorthal-dimethyl
30 Clomazone 0.2 Clomazone
31 Cyfluthrin (S) 2 Cyfluthrin (sum of all isomers)
32 Cyhalothrin (S) 0.5 Cyhalothrin (sum of all isomers)
33 Cymoxanil 0.1 Cymoxanil
34 Cypermethrin (S) 1 Cypermethrin (sum of all isomers)
 

35

 

DDT (S)

 

0.2

sum of o,p’- and p,p’-DDT, o,p’-

and p,p’-DDD (TDE), o,p’- and p,p’-DDE expressed as DDT

 

36

 

Deltamethrin (b)

 

1

sum of Deltamethrin and Tralomethrin expressed as Deltamethrin
 

 

37

 

 

Demeton-S-methyl (S)

 

 

0.1

sum of Demeton-S-methyl, Oxydemeton-methyl (Demeton-S- methyl sulfoxide) and Demeton-S- methyl sulfone expressed as Demeton-S-methyl
38 Diazinon 0.1 Diazinon
39 Dicamba 0.2 Dicamba
 

40

 

Dichlorvos (c)

 

0.1

sum of Dichlorvos, Naled and Trichlorfon expressed as Dichlorvos
41 Dicloran 0.1 Dicloran
42 Diflubenzuron 0.1 Diflubenzuron
 

43

 

Dimethoate (d)

 

0.5

sum of Dimethoate and Omethoate expressed as Dimethoate
44 Dimethomorph (S) 2 sum of (E)-Dimethomorph and (Z)-Dimethomorph
 

45

 

Disulfoton (S)

 

0.1

sum of Disulfoton, Disulfoton sulfoxide, and Disulfoton sulfone expressed as Disulfoton
 

 

 

 

 

 

 

 

46

 

 

 

 

 

 

 

 

Dithiocarbamates (as CS2) (e)

 

 

 

 

 

 

 

 

5

 

 

 

 

 

 

 

 

Dithiocarbamates expressed as CS2

In countries where fungal diseases such as blue mould are a persistent problem in the field throughout the growing season, the use of dithio- carbamates (DTC) fungicides may be an essential part of the season-long disease management strategy and in keeping with GAP as a means of ensuring crop quality and economic viability for the producer. Under high disease pressure residues of dithio- carbamates (DTC) fungicides slightly in excess of the specified GRL may be observed.   In countries where there is not a field fungal disease problem the use of fungicides is not necessary, and there should be no residues detected. Consistent with GAP, dithiocarbamates (DTC) fungicides must be used only according to label instructions to combat fungal diseases in the seedbed and in the field.

 

No. CPA GRL

(ppm)

Residue definition Notes
 

47

 

Endosulfans (S)

 

1

sum of alpha- and beta-isomers and Endosulfan-sulphate expressed as Endosulfan
48 Endrin 0.05 Endrin
49 Ethoprophos 0.1 Ethoprophos
50 Famoxadone 5 Famoxadone
 

51

 

Fenamiphos (S)

 

0.5

sum of Fenamiphos, Fenamiphos sulfoxide and Fenamiphos sulfone expressed as Fenamiphos
52 Fenitrothion 0.1 Fenitrothion
 

53

 

Fenthion (S)

 

0.1

sum of Fenthion, Fenthion sulfoxide and Fenthion sulfone expressed as Fenthion
54 Fenvalerate (S) 1 Fenvalerate (sum of all isomers including Esfenvalerate)
55 Fluazifop-butyl (S) 1 Fluazifop-butyl (sum of all isomers)
56 Flumetralin 5 Flumetralin
57 Fluopyram (g) 5 Fluopyram
58 Folpet 0.2 Folpet
59 HCH (a-, b-, d-) 0.05 HCH (a-, b-, d-)
60 HCH (g-) (Lindane) 0.05 HCH (g-) (Lindane)
 

61

 

Heptachlor (S)

 

0.02

sum of Heptachlor and two Heptachlor epoxides (cis- and trans-) expressed as Heptachlor
62 Hexachlorobenzene 0.02 Hexachlorobenzene
63 Imidacloprid 5 Imidacloprid
64 Indoxacarb (S) 15 Sum of S isomer + R isomer
 

65

 

Iprodione (S)

 

0.5

sum of Iprodione and N-3,5- dichlorophenyl-3-isopropyl-2,4- dioxoimidazolyzin-1-carboxamide expressed as Iprodione
66 Malathion 0.5 Malathion
 

 

 

 

 

67

 

 

 

 

 

Maleic hydrazide

 

 

 

 

 

80

 

 

 

 

Maleic hydrazide (free and bounded form)

In some instances, where GAP is implemented and label recom- mendations with regard to application rates and timing are strictly adhered to, residue levels may exceed the current GRL of 80 ppm as a result of extreme weather conditions and the current technology available for application. However, as with all CPAs, all efforts should be made to strictly follow label application rates, and use should be no more than necessary to achieve the desired effect.
68 Metalaxyl (S) 2 sum of all isomers including Metalaxyl-M / Mefenoxam
69 Methamidophos 1 Methamidophos
70 Methidathion 0.1 Methidathion
 

71

 

Methiocarb (S)

 

0.2

sum of Methiocarb, Methiocarb sulfoxide, and Methiocarb sulfone expressed as Methiocarb

 

No. CPA GRL

(ppm)

Residue definition Notes
 

72

 

Methomyl (f)

 

1

sum of Methomyl, Methomyl- oxime, and Thiodicarb expressed as Methomyl
73 Methoxychlor 0.05 Methoxychlor
74 Mevinphos (S) 0.04 Mevinphos (sum E and Z isomers)
75 Mirex 0.08 Mirex
76 Monocrotophos 0.3 Monocrotophos
 

77

 

Naled (c)

sum of Dichlorvos, Naled, and Trichlorfon expressed as Dichlorvos  

see Dichlorvos

78 Nitrofen 0.02 Nitrofen
79 Omethoate (d) sum of Dimethoate and Omethoate expressed as Dimethoate see Dimethoate
80 Oxadixyl 0.1 Oxadixyl
81 Oxamyl 0.5 Oxamyl
82 Parathion (-ethyl) 0.06 Parathion
83 Parathion-methyl 0.1 Parathion-methyl
84 Pebulate 0.5 Pebulate
85 Penconazole 1 Penconazole
86 Pendimethalin 5 Pendimethalin
87 Permethrin (S) 0.5 Permethrin (sum of all isomers)
88 Phorate 0.05 Phorate
89 Phosalone 0.1 Phosalone
90 Phosphamidon (S) 0.05 Phosphamidon (sum of E and Z isomers)
91 Phoxim 0.5 Phoxim
92 Piperonyl butoxide 3 Piperonyl butoxide
93 Pirimicarb 0.5 Pirimicarb
94 Pirimiphos-methyl 0.1 Pirimiphos-methyl
95 Profenofos 0.1 Profenofos
96 Propoxur 0.1 Propoxur
97 Pymetrozine 1 Pymetrozine
 

98

 

Pyrethrins (S)

 

0.5

sum of Pyrethrins 1, Pyrethrins 2,

Cinerins 1, Cinerins 2, Jasmolins 1

and Jasmolins 2

99 Tefluthrin 0.1 Tefluthrin
 

100

 

Terbufos (S)

 

0.05

sum of Terbufos, Terbufos sulfoxide and Terbufos sulfone expressed as Terbufos
101 Thiamethoxam 5 Thiamethoxam
 

102

 

Thiodicarb (f)

sum of Methomyl, Methomyl- oxime, and Thiodicarb expressed as Methomyl  

see Methomyl

103 Thionazin 0.04 Thionazin
 

104

 

Thiophanate-methyl (a)

sum of Benomyl, Carbendazim, and Thiophanate-methyl expressed as Carbendazim  

see Carbendazim

 

No. CPA GRL

(ppm)

Residue definition Notes
 

105

 

Tralomethrin (b)

sum of Deltamethrin and Tralomethrin expressed as Deltamethrin  

see Deltamethrin

 

106

 

Trichlorfon (c)

sum of Dichlorvos, Naled, and Trichlorfon expressed as Dichlorvos  

see Dichlorvos

107 Trifluralin 0.1 Trifluralin

 

 

  • Carbendazim is the degradation product of Benomyl and Thiophanate-methyl. In the case the same sample contains residues of both Carbendazim and/or Benomyl/Thiophanate-methyl, the sum of the residues should not exceed 2
  • Deltamethrin is the degradation product of Tralomethrin. In the case the same sample contains residues of both Deltamethrin and Tralomethrin, the sum of the two residues should not exceed 1
  • Dichlorvos is the degradation product   of  Naled  and     In the case the same sample contains residues of both Dichlorvos and/or Naled/Trichlorfon, the sum of the residues should not exceed 0.1 ppm.
  • Omethoate is the degradation product of Dimethoate. In the case the same sample contains residues of both Dimethoate and Omethoate, the sum of the two residues should not exceed 0.5
  • The Dithiocarbamates Group includes the EBDCs: Mancozeb, Maneb, Metiram, Nabam and Zineb – as well as Amobam, Ferbam, Policarbamate, Propineb, Thiram and
  • Methomyl is the degradation product of Thiodicarb. In the case the same sample contains residues of both Methomyl and Thiodicarb, the sum of the two residues should not exceed 1
  • Fluopyram added to GRL list June

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