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Little Cigars And High Liver Cancer Rates In Marginalized Communities

As I continue to mine the data from our December 2018 tests of off-the-shelf tobacco products for pesticide residues I keep running across small surprises that have big implications. Here’s a good example – the data has just shown me a likely connection between little cigar use and the puzzling high rates of liver cancer in Hispanic, Black and Native American communities.

The connection may lie in two of the pesticide contaminants just found in Swisher Sweets – check the carbendazim and cypermethrin in the right-hand data column below. Exposure to either of these chemicals is strongly linked to liver disease; exposure to the two chemicals together appears to have much greater impact than just the simple sum of their effects. They are more than merely additive and they are synergistic. (many additional citations below)

Basic Clin Pharmacol Toxicol. 2012 May;110(5):433-40

“Carbendazim impends hepatic necrosis when combined with imazalil or cypermethrin.”

“Low doses of carbendazim in combination with low doses of imazalil or cypermethrin caused very pronounced hepatic necrosis, more than any of the three individually applied pesticides or combination of imazalil and cypermethrin.”

Community Tobacco Control Partners Test Results 12/18

This study, like the others cited below, is an experiment to see what happens when you combine these two liver toxins. They use mice and rats. They aren’t saying that in the real world you would ever find people exposed to levels of carbendazim and cypermethrin like this at the same time. That would never happen. Except …

If you’re a super-cool young Latino dude smoking Swisher Sweets and fantasizing Carly B, or maybe a young Black mother smoking them because she’s heard they’re less harmful than cigarettes. They’re going to get the full load of carbendazim and cypermethrin together, over and over with every puff. 

Hum Exp Toxicol. 2012 May;31(5):492-505

“Carbendazim combined with imazalil or cypermethrin potentiate DNA damage in hepatocytes of mice.”

“In combination with carbendazim clastogen, properties of imazalils and cypermethrins were potentiated compared to all other treatments and control.

Higher long tail nuclei (LTN) in females indicate that certain cells in females were especially prone to total nucleus disintegration. ‘

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.”

There’s not a single study anywhere that looks at individual pesticides in tobacco products and their impact on human health as inhaled toxins, much less when they are inhaled together day after day in a supertoxic cocktail. I suppose you could call this a simple oversight on the part of thousands of highly trained, highly paid scientists, doctors and regulators. I suppose you could say that.

But that’s exactly what millions of Latino, Black and Native people throughout the Americas are doing – inhaling that carbendazim/cypermethrin cocktail 20-40-60 times a day every day. That’s their only option too, because their only choices are the cheapest most contaminated brands of tobacco products, not the relatively cleaner high-end cigarettes smoked in economically privileged White communities. 

Young Latino, Black and Native American little cigar smokers are also inhaling at least 16 other pesticides in combination with the carbendazim/cypermethrin. No studies exist on what that incredible level of toxic synergy may be doing, but the studies on just the carbenzadim/cypermethrin combination are certainly suggestive. How about if you just add a little DDT to the mix? Done.

Both carbendazim and cypermethrin (and DDT) are potent high-tech Endocrine Disruptors, and they are present here in very significant concentrations, not traces, although endocrine disruptors have been conclusively shown to operate independently of concentration. This characteristic is known as a non-monotonic dose response, and is a much-needed refinement of the standard approach to determining a pesticide’s hazardous levels of exposure. This is especially true with the ED pesticides like Carbendazim and Cypermethrin that appear to have no safe level of exposure at all.

Extraordinarily important work by Dr. Laura Vandenberg of Massachusetts Public Health has shown that the classic way of looking at pesticide toxicity is not only wrong but dangerous in an age of designer pesticides that no longer rely on the brute force of chemical poison. http://dose-response.org/wp-content/uploads/2014/06/Vandenberg-2013-dose-response.pdf

According to Dr. Vandenberg, and these are my words, there is a strong belief among regulators, and way too many scientists, that once you establish a level at which a pesticide does measurable damage you can simply project backwards in a straight line to lower doses and estimate a level where it can’t possibly do any harm.

That makes regulators happy – they have a number. That means they have a full-time job monitoring that number. Above that number – we have a problem and we get to enforce our rules. Below that number – you’re good to go and we’ve done our job protecting the public. Next!

That approach worked great with the first pesticides, which were all heavy-duty poisons. The more poison you use, the more bugs you kill. When bugs develop resistance, use more. If the first spray doesn’t get them all, spray again. But regulators keep people “safe” by limiting the amount that can be used per acre. If you’re a farmer and you reach that amount and the bugs keep eating your crop you yell at the chemical companies and they come up with a newer, stronger, different kind of poison using the same process.

What dose of this new shit kills all the rats? OK, that’s too much. How about a lower dose? Hmmm – still kills a bunch and now it seems to cause tumors. How about this teeny weeny dose? Hey, that seems to work. Look – no bugs, and the rats are alive. Well, most of them. We’re good to go! Off to the tobacco fields! Better living through chemistry.

But then all the poisons stopped working. Well, not entirely, but you had to keep piling them on and it got to the point where all those organochlorine pesticides were causing some alarm. Some may remember Rachel Carson’s “Silent Spring”. The tobacco industry, from the very beginning the world’s heaviest users of these poisons because bugs love tobacco leaves more than any other plant, realized that they needed something better. Not safer, just better. They already owned all the regulators and were in the process of owning the scientific community so nobody was looking at pesticides in tobacco products, even though cancer was beginning to explode and everybody knew it was “smoking-related”. Nobody ever asked “smoking what?” because “everybody knew” it was tobacco. The fact that the tobacco pesticides were beginning to be identified as super-toxic environmental carcinogens somehow escaped attention, and gave the chemical industry time to develop other kinds of “Crop Protection Agents”.

Endocrine disruptors break out of the old poison/dose relationship completely, but regulators haven’t even thought of keeping up. Endocrine disruptors are the ag industry’s answer to poison fatigue. You don’t have to keep using more and more, and the numbers don’t set off any regulatory alarms because you’re using stuff that nobody understands. All we know is that it takes care of our bug problem.

ED’s are designed to work at any level – in the latest ones all it takes is a couple of molecules at the right place at the right time and – voila – no baby insects or, more commonly, “non-viable offspring”. The bugs have babies but they don’t survive to eat those valuable cops like tobacco – their fave in the whole world.

A Swisher Sweets smoker, whether they are smoking the little cigar intact or just using the wrapper as a blunt, is inhaling a blend of carbendazim and cypermethrin with every puff. Since smoking patterns vary, let’s just say that little cigar smokers are exposed through inhalation multiple times a day every day. Since these chemicals operate independently of dose, their concentration matters for other reasons but not to explain what they so to the smoker’s liver. What they are likely to do to smokers when they are inhaled together seems pretty clear, even though these studies are only on rats and the rats are eating the cancerous combo, not smoking it.

Here are a few of the studies that seem to make the connection – what do you think? There are lots of related refs – but how many do we need to begin asking questions about the safety of some of these tobacco products?

Int J Exp Pathol. 2012 Oct;93(5):361-9

“Effect of cypermethrin, carbendazim and their combination on male albino rat serum”

Alpha-cypermethrin and carbendazim are synthetic; α-cypermethrin belongs to a class of synthetic pyrethroids and carbendazim belongs to the class of carbamate fungicides. The current study was carried out to evaluate the low-dose exposure of individual and mixed forms of cypermethrin and carbendazim.

The experimental results indicate that even low-dose use of the synthetic pyrethroid carbamate and their combined form results in consequential negative effects on cell function.

Toxicol Sci. 2015 Sep;147(1):116-26.

“Oral Exposure of Mice to Carbendazim Induces Hepatic Lipid Metabolism Disorder and Gut Microbiota Dysbiosis”

Carbendazim (CBZ) has been considered as an endocrine disruptor that caused mammalian toxicity in different endpoints. Here, we revealed that oral administrations with CBZ at 100 and 500 mg/kg body weight for 28 days induced hepatic lipid metabolism disorder which was characterized by significant increases of hepatic lipid accumulation and triglyceride (TG) levels in mice.

The serum cholesterol (TC), high-density lipoprotein, and low-density lipoprotein levels also increased after CBZ exposure.

Correspondingly, the relative mRNA levels of some key genes related to lipogenesis and TG synthesis increased significantly both in the liver and fat.

Moreover, the increase in serum IL-1β and IL-6 levels by the treatment of CBZ indicated the occurring of inflammation.

Furthermore, the levels of bioaccumulation of CBZ in the liver and gut were very low as compared in the feces, indicating that most of CBZ stayed in gastrointestinal tract and interacted with gut microbiota until excreted.

At phylum level, the amounts of the Bacteroidetes decreased significantly in the feces after 5 days CBZ exposure. High throughput sequencing of the 16S rRNA gene V3-V4 region revealed a significant reduction in richness and diversity of gut microbiota in the cecum of CBZ-treated mice. UniFrac principal coordinates analysis observed a marked shift of the gut microbiota structure in CBZ-treated mice away from that of the controls.

More deeply, operational taxonomic units’ analysis identified that a total of 361 gut microbes were significant changed. In CBZ-treated groups, the relative abundance of Firmicutes, Proteobacteria, and Actinobacteria increased and that of Bacteroidetes decreased.

Our findings suggested that CBZ could lead to hepatic lipid metabolism disorder and gut microbiota dysbiosis in mice

Toxicol In Vitro. 2014 Dec;28(8):1507-20. 

“Potential involvement of chemicals in liver cancer progression: an alternative toxicological approach combining biomarkers and innovative technologies.”

Pesticides as well as many other environmental pollutants are considered as risk factors for the initiation and the progression of cancer. In order to evaluate the in vitro effects of chemicals present in the diet, we began by combining viability, real-time cellular impedance and high throughput screening data to identify a concentration “zone of interest” for the six xenobiotics selected: endosulfan, dioxin, carbaryl, carbendazim, p’p’DDE and hydroquinone.

Endosulfan, was able to strongly modulate all the studied cellular processes in HepG2 cells, followed by dioxin, then carbendazim.

Our in vitro data indicate that these xenobiotics may contribute to the evolution and worsening of hepatocarcinoma, whether via the induction of the EMT process and/or via the deregulation of liver key processes such as cell cycle and resistance to apoptosis.


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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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