USDA doesn't test for Roundup. #healthcrisis

No-one in the USA tests for glyphosate residues in food before the food hits our mouths.  Maximum residue levels establish how much glyphosate is allowed on food, but no-one actually checks these levels.

To quote a USDA employee: "Glyphosate was not tested on any commodity in the Pesticide Data Program (PDP) 2010 Survey.  The 2011 PDP Annual Summary, which should be published in early 2013, will show glyphosate findings for soybeans."

Soybeans?  That's all?  Noting that in the last 8 years the residue limit for pasta and bread (wheat) has been increased to higher levels than for GMO foods like soybeans.

Glyphosate used to be expensive to test for. But not any more. As a result of 9/11 and the toxic dusts that enveloped the site, the US government placed a priority on developing extremely good toxin testing machines that could detect traces of chemical and toxic residues to parts per trillion. So today consumers can test.

So why has it not been important to test for glyphosate on food?

The really, really limited research studies (for example in the areas of reproductive and developmental toxicity, and the carcinogenicity studies used to establish the ADI/RfD), are selected and supplied by Monsanto and big agrichemical organisations like Syngenta and Cheminova. So we have 25-35 year old secret, unpublished studies declaring safety of glyphosate at the levels we are exposed to.

The EPA doesn't really look at the results of independent science (searchterm: glyphosate) that work in the public interest and look at toxicity at residue levels at the levels we actually consume.

Therefore companies like Monsanto control the critical studies used for establishing the ADI/RfD, and, as a result, our government considers that glyphosate is not really that toxic. It's fine!  Perhaps consider the last time the USDA assessed glyphosate in the 1993 Reregistration Elegibility Decision , refer to Appendix C and review the names of who put forward the studies.

Monsanto and Co. dominate the submissions, followed by Ciba-Geigy, and then possibly less than 2% of submissions are from other parties.  Imagine if the tables were turned, there was a industry fund that resulted in another independent organisation, acting in the interest of the American (and global) public putting forward the studies without the self interest of potential profits.

Perhaps the USA would be monitoring glyphosate more closely.

The EPA is currently reassessing glyphosate, called the Glyphosate Reregistration Review.  It is critical they review independent studies undertaken in the public interest by scientists and organisations with no financial interest in the result.

To find out about what pesticides the USDA does actually check for, visit the Agricultural Marketing Service or download the actual The 2013 Pesticide Data Program Annual Summary (2013 most recent). Only soybeans.

(Press ‘control+f’ to  search for glyphosate, the most widely used pesticide in the USA.)

Unfortunately - this has a domino effect which can cultivate and excacerbate public misinformation. The Environmental Working Groups well written paper 2015 Shopper's Guide to Pesticides in Produce pulls its information from the USDA PDP summary. But because the USDA PDP doesn't consider glyphosate, we are missing the full picture. The 'Dirty Dozen' and the 'Clean Fifteen' don't give us a broader picture. The EWG and the American public therefore have no idea of Roundup/glyphosate levels in our bread, milk, convenience foods and other staples in modern American diets. I wish someone would whizz McDonalds fries and hamburgers and put them through a glyphosate detection test. A minimum standard should be Single Residue Methods (EURL-SRM) LC-MS/MS. Many testing labs use old equipment so you really need to know. 

People, it is so much more than fruit and vegetables..

This is why we need clever startups like Feed the World - doing what our governments are failing to do. These are great platforms to pressure failing, inept governments and regulatory authorities, and they help change the power base in favour of parents and kids. Because that's who should have the power to limit toxins in food.

Demand your bread is tested, for glyphosate.  Understand what fungicides and insecticides are commonly sprayed on your bread. Testing for abstract fungicides that were commonly used 10 years ago is failure. It is time we were looking at our food staples right across the spectrum, not just fruit and vegetables. It's about understanding that conventionally produced food cannot be safe for our kids as long as the companies control the studies.

Because our governments are not testing for the true elephant in the room.


USDA Agricultural Marketing Service. Science and Technology Program. Pesticide Data Program. Annual Summary. Calendar year 2013. Released December 2014.

Regulatory history of glyphosate carcinogenicity reviews in USA

Of course Monsanto is unimpressed with the IARC classification of glyphosate as a probable carcinogen.  And for good reason. To date Monsanto has submitted nearly every study used by the US EPA to decide glyphosate's carcinogenicity rating. For decades.  Perhaps it is time the IARC, the US EPA and the European Union (and my own country New Zealand) looked at studies other than studies selected by the same corporation that sells the product.

Back in 1985, glyphosate was declared a Class C carcinogen. Why and how did it change?

Carcinogenicity assessments to date appear to include only pesticide company directly-funded studies submitted by the company. I believe that Monsanto has submitted every study.  

NB: When I started documenting glyphosate regulatory assessment and toxicity studies the EPA 1993 Glyphosate Reregistration Eligibilty Decision (RED) document was freely available on the net including references and data for all studies. In the past year it has been removed. Here is a PDF link.

These assessments conveniently exclude a broad swathe of independent studies by scientists working in the public domain. And they never, of course, study the full solution, or formulation, of Roundup.

Very few studies have been used to establish the classification of Group E - non-carcinogenic.  A very small pool to establish this status for the USA population of 314 million people. Please feel free to demand the original documents from the EPA to confirm this.

There are significant effects dismissed - these studies should be publicly released for transparent consultation & peer review by independent scientists.

4 March 1985 :

Toxicology Branch Ad Hoc Committee, comprised of members of the Toxicology Branch of the Hazard Evaluation Division.  The Committee in a consensus review dated 04-MAR-1985 classified glyphosate as a Group C Carcinogen based on an increased incidence of renal tubular adenomas in male mice. According to the consensus review, the tumour is rare, it occurred in a dose-related manner, and the incidence was outside the reported historical control range. The Committee also concluded that dose levels tested in a 26 month rat feeding study were not adequate for the assessment of glyphosate’s carcinogenic potential in this species.

Knezevich, A.; Hogan, G. A chronic feeding study of glyphosate (Roundup technical) in mice. Unpublished Report no. BDN-77420, project no. 77-2061, 1983, submitted to U.S. Environmental Protection Agency by Monsanto Company, prepared by BioDynamics, Inc. Reregistration Eligibility Decision (RED) Glyphosate; EPA-738-F-93-011; U. S. Environmental Protection Agency, Office of Prevention, Pesticides, and Toxic Substances, Office of Pesticide Programs, U.S. Government Printing Office: Washington, DC, 1993.  MRID 00130406

McConnel, R. A chronic feeding study of glyphosate (Roundup technical) in mice: pathology report on additional kidney sections. Unpublished project no. 77-2061A, 1985, submitted to U.S. Environmental Protection Agency prepared by BioDynamics, Inc. Reregistration Eligibility Decision (RED) Glyphosate; EPA-738-F-93-011; U. S. Environmental Protection Agency, Office of Prevention, Pesticides, and Toxic Substances, Office of Pesticide Programs, U.S. Government Printing Office: Washington, DC, 1993.Study:  MRID 00150564

Further content Pp 5 & 6.

Extract from the EPA 1993 Glyphosate Reregistration Eligibilty Decision (RED) P.14 : This is the study that decided the classification of Group C Carcinogen - though it is unclear as it appears under 2 study authors (as above):

A carcinogenicity study in mice was conducted with CD-1mice fed diets containing 0, 150, 750 or 4500 mg/kg/day of glyphosate for 18 months. No effects were observed in the low-doseand mid-dose groups. The following findings were observed in thehigh-dose group: (1) decreased body weight gain in males and females; (2) increased incidence of hepatocellular hypertrophy, hepatocellular necrosis and interstitial nephritis in males; (3)increased incidence of proximal tubule epithelial basophilia and hypertrophy in females; and (4) slightly increased incidence of renaltubular adenomas, a rare tumor, in males. Based on these effects,the systemic NOEL and LOEL were 750 mg/kg/day and 4500mg/kg/day, respectively. The Agency concluded that the occurrenceof these adenomas was spontaneous rather than compound-induced because the incidence of renal tubular adenomas in males was not statistically significant when compared with the concurrent controls. An independent group of pathologists and biometricians alsoconducted extensive evaluations of these adenomas and reached the same conclusion. Therefore, glyphosate was not considered to be carcinogenic in this study.  (MRIDs 00130406, and 00150564End extract.

McConnel, R. (1985) A Chronic Feeding Study of Glyphosate (Roundup Technical in Mice): Pathology Report on Additional Kidney Sections: Addendum to Final Report Dated July 21, 1983: Project No. 77-2061A. Unpublished study prepared by Bio/dynamics Inc. 59 p. MRID 00150564 (Bio/dynamics studies are usually Monsanto paid)

24 Feb 1986:

The kidney slides from the long-term mouse feeding study were subsequently re-examined by several pathologists, and one pathologist diagnosed an additional kidney tumour in the control males. These findings were presented to the FIFRA Scientific Advisory Panel (SAP) which proposed glyphosate be classified into Group D (inadequate animal evidence of carcinogenic potential).  The SAP in their meeting of 11/12 FEB-1986 (report dated 24-FEB-1986), concluded that, after adjusting for the greater survival in the high dose mice compared to the concurrent controls, no statistically significant pairwise differences existed, although the trend was significant.  The SAP further noted that, although comparison of these findings to historical incidences yielded a statistically significant result, this finding did not override the lack of pairwise significance of comparisons to concurrent controls.

The SAP determined that the carcinogenic potential of glyphosate could not be determined from existing data and proposed that rat and/or mouse studies be repeated in order to clarify these equivocal findings.  A new 2 year rat study was performed up to the limit dose of 20,000 ppm. (Stout & Ruecker 1990)

Information:  EPA Memorandum date 17 August 2000 : Glyphosate in/on Alfalfa hay and forage; Field corn forage; Stover and straw of the cereal grains crop group; numerous minor crops; and flax in Northern Dakota. HED Risk Assessment. Page 6.

Information repeated: 30 October 1991 - US EPA Second Peer Review of Glyphosate. Memorandum 1071-83-6.  P.3/4

26 June 1991 - Second Peer Review:

The Health Effects Division (HED) Carcinogenicity Peer Review Committee (CPRC) convened on 26-JUN-1991 to discuss and evaluate the weight of the evidence on glyphosate with particular emphasis on its carcinogenic potential. The Committee concluded that glyphosate should be classified as a Group E chemical (evidence of non-carcinogenic to humans), based upon a lack of convincing carcinogenicity evidence in adequate studies in two animal species.

As part of their consideration the CPRC examined data on the following tumours observed in the second rat study: pancreatic islet cell adenomas in males, thyroid C-cell adenomas and/or carcinomas in males and females, and hepatocellular adenomas and carcinomas in males. None of them were considered to be biologically significant. As for the mouse study, the CPRC concluded that the renal tubular neoplasms in high dose male mice were not compound-related due to the lack of pairwise significance and the lack of pre-neoplastic kidney lesions in males.

This is discussed in a Cornell University paper:

This classification is based on the following findings: (1) None of the types of tumors observed in the studies (pancreatic islet cell adenomas in male rat,thyroid c-cell adenomas and/or carcinomas in male and female rats, hepatocellular adenomas and carcinomas in male rats, and renal tubular neoplasms in male mice) were determined to be compound related; (2) glyphosate was tested up to the limit dose on the rat and up to levels higher than the limit dose in mice; and (3) there is no evidence of genotoxicity for glyphosate. Accordingly, EPA concludes that glyphosate has not been "found to induce cancer when ingested by man or animal." 21 U.S.C.348(c)(3).

Memorandum 30 October 1991 - Second Peer Review of Glyphosate (thank you for retrieving this paper).

Memorandum 1071-83-6

D. Evaluation of Carcinogenicity Data. (Second Peer Review)

1. Lankas, G.R.; Hogan, G.K. (1981) A Lifetime Feeding Study of Glyphosate (Roundup Technical) in Rats: Project No. 772062. (Unpublished study received Jan 20, 1982 under 524-308; prepared by Bio/dynamics, Inc., submitted by Monsanto Co., Washington, D.C.; CDL:246617-A; 246618; 246619; 246620; 246621)   MRID 00093879

Groups of 50 male and 50 female Charles River Sprague-Dawley rats were fed technical glyphosate in their diets at dose levels of 3, 10,or 31 mg/kg b.w./day (males) and 3.4, 11, or 34 mg/kg b.w./day(females) for approximately 26 months.

Discussion of Tumor Data: An increase in the incidence of interstitial cell tumours of the testes was observed in male rats. Because of the absence of a dose-response relationship, the lack of preneoplastic changes, the wide variability in the spontaneous incidence of this tumor, the the similarity in incidences between the high-dose group and the historical controls, and lack of any evidence of genotoxicity, it was concluded by the previous Peer Review Committee that the observed incidence did not reflect a carcinogenic response.

Additionally, there was the question of possible thyroid carcinomas in high-dose females. After a review of the slides by a consulting pathologist, and a reassessment of all relevant data, including the fact that no effect of the treatment on timor latency of the combined incidences of adenoma and carcinoma was apparent, the earlier Peer Review Committee concluded that the data did not demonstrate a carcinogenic response in the thyroid.

Further reading Second Peer Review page 5.

  1. Incidence of tumors of the testes dismissed, primarily because no dose response relationship. Effects on the thyroid dismissed. (EDC?)

2. Stout, L.; Ruecker, F. (1990) Chronic Study of Glyphosate Administered in Feed to Albino Rats: Lab Project Number: MSL- 10495: R.D. 1014. Unpublished study prepared by Monsanto Agricultural Co. 2175 p.    MRID 41643801 (The study 41643801 continued for 2 years - this review is half way through the study) 

This chronic toxicity/carcinogenicity study in the rat was submitted to the Agency as a replacement study for the 26 month 1981 chronic toxicity/carcinogenicity study in the rat. In this study randomised groups of 60 male and 60 female young (8 weeks old) Sprague Dawley rats were fed dietary levels of 0, 2000, 8000, or 20,000 ppm or the equivalent of 0, 100, 400, and 1000 mg/kg/day of technical glyphosate for 2 years. At 12 months 10 animals sex/group were sacrificed.

Discussion of Tumor Data: Age adjusted statistical analyses of the tumor data are presented. The most frequently observed tumors in this study were pancreatic islet cell adenomas in males, thyroid C-cell adenomas and/or carcinomas in males.  Further reading Second Peer Review tumor type page 5-13.

  1. It appears these rats were not dosed until 8 weeks old - adult - doesn't that miss a vital development gap?
  2. The results are unclear - I cannot see the results of the 20 animals sacrificed at 12 months?
  3. Committee interpretation: Dismiss incidences that exceed historical control range. Dismiss effects where no dose related trend. Declare not compound related. How? (pp 7 & 8) (EDC?)

3. Hogan, G.K. (1983). A chronic feeding study of glyphosate in mice. Unpublished report prepared by Bio/Dynamics Inc., dated July 21, 1983. Report No. 77-2061. EPA Acc. Nos. 251007-251009, and 251014.

Also referred to as: Knezevich, A.L. and Hogan, G.K. (1983) A Chronic Feeding Study of Glyphosate (Roundup technical) in Mice: Project No. 77-2061. (Unpublished study received Aug. 17, 1983 under 524-308; prepared by Bio/dynamics, Inc., submitted by Monsanto Co. Accession #251007-251014  MRID 130406

Groups of 50 male and 50 female CD-1 mice were administered glyphosate in the diet at concentrations of 1000, 5000 or 30,000 ppm for 18 months. Glyphosate produced an equivocal carcinogenic response in males characterised by an incidence of renal tubular neoplasms of 1/49, 0/49, 1/50 in the control, low, mid, high dose groups respectively.

Extract from the EPA 1993 Glyphosate Reregistration Eligibilty Decision (RED) P.14: A carcinogenicity study in mice was conducted with CD-1 mice fed diets containing 0, 150, 750 or 4500 mg/kg/day of glyphosate for 18 months. No effects were observed in the low-dose and mid-dose groups. The following findings were observed in the high-dose group: (1) decreased body weight gain in males and females; (2) increased incidence of hepatocellular hypertrophy, hepatocellular necrosis and interstitial nephritis in males; (3) increased incidence of proximal tubule epithelial basophilia and hypertrophy in females; and (4) slightly increased incidence of renal tubular adenomas, a rare tumor, in males. Based on these effects, the systemic NOEL and LOEL were 750 mg/kg/day and 4500 mg/kg/day, respectively. The Agency concluded that the occurrence of these adenomas was spontaneous rather than compound-induced because the incidence of renal tubular adenomas in males was not statistically significant when compared with the concurrent controls. An independent group of pathologists and biometricians also conducted extensive evaluations of these adenomas and reached the same conclusion. Therefore, glyphosate was not considered to be carcinogenic in this study. (MRIDs 00130406, and 00150564) End Extract.

Further reading Second Peer Review including extensive discussion tumors pp 13-15.

E. Additional Toxicology Data on Glyphosate (Second Peer Review)

1. Metabolism

Ridley, W.; Mirly, K. (1988) The Metabolism of Glyphosate inSprague Dawley Rats--Part I. Excretion and Tissue Distribution of Glyphosate and Its Metabolites following Intravenous and OralAdministration: Laboratory Project No. 86139 (MSL-7215): R.D.No. 877. Unpublished study prepared by Monsanto Co. 587 p.

Howe, R.; Chott, R.; McClanahan, R. (1988) Metabolism ofGlyphosate in Sprague-Dawley Rats. Part II. Identification,Characterization, and Quantitation of Glyphosate and ItsMetabolites after Intravenous and Oral Administration:Laboratory Project No. MSL-7206: R.D. No. 877. Unpublished study prepared by Monsanto Co. 155 p.

2. Mutagenicity - there are no references - however these are the studies held with the US EPA RED 1993 for mutagenicity.

Kier, L.D.; Flowers, L.J.; Hannah, L.H. (1978) Final Report onSalmonella Mutagenicity Assay of Glyphosate: Test No. LF-78-161.(Unpublished study received Apr 25, 1979 under 524-308; submitted by Monsanto Co., Washington, D.C.; CDL:238233-B)  MRID 00078620

Li, A.; Kier, L.; Folk, R. (1983) CHO/HGPRT Gene Mutation Assaywith Glyphosate: EHL Study No. ML-83-155. Final rept. (Unpublished study received Nov 15, 1983 under 524-308; submitted by Monsanto Co., Washington, DC; CDL:251737-B) MRID 00132681

Li, A.; Kier, L.; Folk, R. (1983) In vivo Bone Marrow Cytogenetics Study of Glyphosate in Sprague-Dawley Rats: Study No. 830083. (Unpublished study received Nov 15, 1983 under 524-308; submitted by Monsanto Co., Washington, DC; CDL:251737-D)   MRID 00132683

Shirasu, Y.; Moriya, M.; Ohta, T. (1978) Microbial MutagenicityTesting on CP67573 (Glyphosate). (Unpublished study received Apr25, 1979 under 524-308; prepared by Institute of EnvironmentalToxicology, Japan, submitted by Monsanto Co., Washington, D.C.; CDL:238233-A) MRID 00078619

3. Developmental and Reproductive toxicity. Pp 16 & 17 (studies extracted from US EPA RED 1993 p. 15 & 16)

Rodwell, D.E.; Tasker, E.J.; Blair, A.M.; et al. (1980)Teratology Study in Rats: IRDC No. 401-054. (Unpublished studyincluding IRDC no. 999-021; received May 23, 1980 under 524-308; prepared by International Research and Development Corp.,submitted by Monsanto Co., Washington, D.C.; CDL:242516-A) MRID 00046362

Rodwell, D.E.; Tasker, E.J.; Blair, M.; et al. (1980) Teratology Study in Rabbits: IRDC No. 401-056. (Unpublished study received May 23, 1980 under 524-308; prepared by International Research and Development Corp., submitted by Monsanto Co., Washington, D.C.; CDL:242516-B) MRID 00046363

Street, R. (1982) Letter sent to R. Taylor dated Jul 6, 1982: Roundup herbicide: Addendum to pathology report for a three-­generation reproduction study in rats with glyphosate. (Unpublished study received Jul 7, 1982 under 524-308; submitted by Monsanto Co., Washington, DC; CDL:247793-A) MRID 00105995

4. Structure - Activity Relationships. (No studies submitted)

5. Acute, subchronic and chronic feeding / oncogenicity data. P.17. (studies extracted from US EPA RED 1993 p. 10 & 13)

Birch, M.D. (1970) Toxicological Investigation of CP 67573-3: Project No. Y-70-90. (Unpublished study received Jan 30, 1973 under 524-308; prepared by Younger Laboratories, Inc., submitted by Monsanto Co., Washington, D.C.; CDL:008460-C) MRID 00067039

Reyna, M. (1985) Twelve Month Study of Glyphosate Administered by Gelatin Capsule to Beagle Dogs: Project No. ML-83-137: Study No. 830116. Unpublished study prepared by Monsanto Company Environmental Health. 317 p. MRID 00153374

END OF STUDIES in Second Peer Review Paper.

G. Classification p. 19 (Second Peer Review)

Considering criteria contained in the EPA Guidelines (FR 51:33992-34003, 1986) for classifying a carcinogen, the Committee concluded that Glyphosate should be classified as a Group E (evidence of Non-carcinogenicity to humans), based on lack of convincing carcinogenicity evidence in adequate studies in two animal species.

It should be emphasised, however, that designation of an agent in Group E is based on the available evidence at the time of evaluation and should not be interpreted as a definitive conclusion that the agent will not be a carcinogen under any circumstances.

End discussion Second Peer Review Paper.

26 March 1998

Information retreived from:  EPA Memorandum date 17 August 2000 : Glyphosate in/on Alfalfa hay and forage; Field corn forage; Stover and straw of the cereal grains crop group; numerous minor crops; and flax in Northern Dakota. HED Risk Assessment. P. 6/7

Section:  Dose Response Assessment

On 26 March 1998 the HED Hazard Identification Assessment Review Committee (HIARC) evaluated the toxicology database, selected doses and endpoints for chronic dietary risk assessment, considered the carcinogenic potential and addressed the sensitivity of infants and children from exposure to glyphosate as required by the Food Quality Protection Act (FQPA) of 1996 (HED Doc. No. 12586, W. Dykstra and J. Rowland, 20-APR-1998).

The FQPA Safety Factor Committee (SFC) met on April 6, 1998 and addressed the potential of enhanced sensitivity to infants and children as required by FQPA (HED Doc. 012584 B. Tarplee and J. Rowland  17-APR-1998). The Committee recommended the 10X FQPA Safety Factor be reduced to 1X in assessing the risk posed by this chemical because: 1) the toxicology data base is complete; 2) there is no indication of susceptibility of rats to in utero and/or postnatal exposure to glyphosate (in the prenatal development study in rats, effects in the offspring were observed only at or above the treatment levels which resulted in the evidence of appreciable maternal toxicity), and 3) the use of generally high quality data, conservative models and/or assumptions in the exposure assessment provides adequate protection of infants and children.

An acute dose and endpoint were not selected for any population subgroups because no effects could be attributed to a single exposure (dose) were observed in oral toxicity studies including the development toxicity studies in rats and rabbits.  Therefore a dose and endpoint were not identified for acute dietary risk assessment.

Memorandum Page 6. I believe the studies this was based on are as follows:

CRfD 2.0mg/kg/day based on rabbit developmental study with NOAEL 175 mg/kg/day:
Rodwell DE; Tasker EJ; Blair M; et al. (1980) : Teratology Study in Rabbits. Unpublished. Pre GLP. Monsanto Company. 1980b. Report no. IR-79_018. MRID No. 00046363. IRDC No. 401-056. International Research and Development Corp

4 month mouse carcinogenicity study (NOAEL 750 mg/kg/day):
2 McConnel, R. (1985) A Chronic Feeding Study of Glyphosate (Roundup Technical in Mice): Pathology Report on Additional Kidney Sections: Addendum to Final Report Dated July 21, 1983: Project No. 77-2061A. Unpublished study prepared by Bio/dynamics Inc. 59 p. MRID 00150564  Bio/dynamics studies are almost always Monsanto submitted

1 yr dog study (NOAEL 500 mg/kg/day)
Reyna, M. (1985) Twelve Month Study of Glyphosate Administered by Gelatin Capsule to Beagle Dogs: Project No. ML-83-137: Study No. 830116. Unpublished study prepared by Monsanto Company Environmental Health. 317 p. MRID 00153374

2 year chronic/onco rat study (NOAEL 400 mg/kg/day):
tout, L.; Ruecker, F. (1990) Chronic Study of Glyphosate Administered in Feed to Albino Rats: Lab Project Number: MSL- 10495: R.D. 1014. Unpublished study prepared by Monsanto Agricultural Co. 2175 p.    MRID 41643801

2 generation rat reproduction study (NOAEL 500 mg/kg/day):
Reyna, M. (1990): Two Generation Reproduction Feeding Study with Glysophate in Sprague-Dawley Rats: Lab Project No: MSL-10387. MRID 41621501 Unpublished study prepared by Monsanto Agricultural Co.  1158

Rat development toxicity study (NOAEL 1000 mg/kg/day):
Rodwell, D.E.; Tasker, E.J.; Blair, A.M.; et al. (1980): Teratology Study in Rats: IRDC No. 401-054. MRID 00046362 (Unpublished study including IRDC no. 999-021; received May 23, 1980 under 524-308; prepared by International Research and Development Corp., submitted by Monsanto Co., Washington, D.C.; CDL:242516-A)

An uncertainty factor (UF) of 100 was applied to account for interspecies extrapolation (10X) and intraspecies variation (10X).  The chronic population adjusted dose (cPAD) is equal to the cRfD divided by the FQPA Safety Factor. Because the 10X safety factor was reduced to 1X, the cPAD is equivalent to the cRfD of 2.0 mg/kg/day.
Because of the lack of evidence of carcinogenicity in mice and rats at doses that were judged to be adequate to assess the carcinogenic potential, glyphosate was classified as a ‘Group E’ chemical.

Further reading and link to study outlines released to public.  EPA Memorandum date 17 August 2000

 WHO: studies behind the WHO 2004 carcinogenicity evaluation.




EPA 1993 Glyphosate Reregistration Eligibilty Decision (RED) PDF (EPA has removed this from public access during 2014/2015)

Information for the 1985 & 1991 evaluations has been extracted from an EPA Memorandum date 17 August 2000 for a HED risk assessment for glyphosate.  pp. 5/6

Cornell Paper: Proposed Pesticide Tolerance Glyphosate 5/93.

Information regarding the 1998 evaluations extracted from an EPA Memorandum dated March 13 2002  from an occupational exposure risk assessment. Page 6.

30 October 1991 - US EPA Second Peer Review of Glyphosate. Memorandum 1071-83-6. From William Dykstra and George Z Ghali.

Evaluate the full formulations of pesticides. Our kids depend on it.

Fungicide formulations on our wheat may contribute to gut dysbiosis

I recently attended a presentation by Professor Gilles Eric Seralini at Food Matters Aotearoa Conference 2015. It occurred to me that this study has not received the attention it deserves: Major Pesticides Are More Toxic to Human Cells Than Their Declared Active Principles. R. Mesnage et al 2014.

How does this study impact us?

It demonstrates that the full formulation that is poured on our food can frequently be more toxic than the ‘declared’ (what the pesticides companies tell us) active ‘principle’ or ‘ingredient’.

Corporations have insisted for years that the only thing we need to worry about is the active ingredient.

Yet this study indicates other ingredients (commonly referred to as adjuvants) in the formulations may NOT be inert, but can be active. 

The full formulation is sprayed on our food, but remains unexamined. Over a growing season, as an example, wheat may be sprayed insecticides, fungicides and herbicides. Then at the end of the growing season Roundup may be sprayed on the wheat 7 days prior to harvest, to kill weeds present and dry out the crop (making milling easier).

 Seralini's Food Matters Aoteroa Conference presentation discussed the following:

  • Adjuvants can destroy the cells membrane and interfere with the endocrine system. They help the active chemical/ingredient penetrate the cell.
  • The active chemical is not the most toxic ingredient
  • Benachour et al 2007 – Roundup 1,000 times more toxic than glyphosate alone according to time of exposure.
  • Different adjuvants are in different formulations.

Seralini questioned: What is the compound responsible for toxicity?

Answer: Ethoxylated adjuvants. As a result of this study: Mesnage 2013. (incl. petroleum residue and tallow amines).  A study of 9 Roundup formulations found that every formulation was more toxic than glyphosate (whatever the cell type).  This study found that ethoxylated adjuvants of glyphosate based herbicides are active principles of human cell toxicity - are the ingredients that kill or damage human/mammalian cells. Simply put Roundup adjuvants are necrotic.

Yet because the adjuvants are declared ‘inert’ (safe?) they are not used in regulatory testing.

Seralini noted: As a consequence the human acceptable daily intake (ADI) or reference dose (RfD) and calculated regulatory values are underestimated 1000x in neglecting the effects of adjuvants in the formulation.

None of the regulatory authorities (WHO, US EPA, EC) ever test the full formulation for toxicity, nor do any governments.

Having completed the Benachour et al 2007 study – Seralini and his colleagues then questioned – is this true for all pesticides? A study was then undertaken of the 9 major pesticides (Europe). Major Pesticides Are More Toxic to Human Cells Than Their Declared Active Principles. Mesnage et al 2014.  

Surprisingly, they found the fungicide formulation was most toxic in comparison to its active chemical.

Full formulation of neonicotinoid on seed treatment is not assessed

This should have wide implications for understanding that nowhere in the world are we testing the pesticides we spray on our food, for their true toxicity.

Seralini noted that in all discussions about Confidor, industry (the pesticide producers) do not discuss or refer to the ‘formulation’. Industry very carefully only refer to the active chemical, imidacloprid.

I was aware of Mesnage's 2014 study but had not written too much about it because as a non-scientist, I could not pick it apart accurately in order to clearly present the results. Robin Mesnage, study author, kindly sent me more information about the study.

In short, of the 9 pesticides researched in Mesnage et al 2014  –

Insecticide Pirimor (50% Pirimicarb) – 2 times more toxic than the active chemical (principle).

                 Carbamate that targets aphids

Insecticide Confidor (200gL/Imidacloprid) – 7 times more toxic than its active chemical

                 Neonicotinoid implicated in colony collapse disorder of pollinators

Insecticide Polysect (5g/L Acetamiprid – 21 times more toxic than the active chemical

                 Neonicotinoid implicated in colony collapse disorder of pollinators

Herbicide Matin (500g/L Isoproturon) –the ONLY product with the same toxicity as the active chemical.

                Second most widely used active chemical within herbicides in Europe

Herbicide Starane (200g/L Fluoxypyr) – 85 times more toxic than the active chemical

               Used on wheat, barley, corn & oats.

Herbicide Roundup GT+ (450g/L Glyphosate) – 125 times more toxic than the active chemical

 Sprayed on wheat, barley, corn, oats, sugar, potatoes, legumes (etc) as desiccant and  herbicide. Major feed and food contaminant.

Fungicide Eyetak (450g/L Prochloraz) – 3 times more toxic than the active chemical (however it was the most toxic active chemical tested).

               Most widely used fungicide applied to cereals in Europe

Fungicide Opus (125g/L Epoxyconazole) – 12 times more toxic than the active chemical

              Triazole fungicide applied to field/cereal crops, fruit trees, vegetables & grass growing areas.

Fungicide Maronee (250g/L Tebuconazole) – 1056 times more toxic than the active chemical

              Triazole fungicide widely used on cereal crops.

As the Mesnage noted ‘These experiments have to be done in vivo to conclude on the degree of relevance for humans and animals of these numbers (1056X for tebuconazole), what we have here is more a proof of principle.’

Excepting the active ingredient, the other ingredients (even if they are toxic) are considered inert because they are supposed not to be directly responsible for the pesticide activity. Yet, commercial formulations are designed to have combined toxic effects.

'The fact that glyphosate is active in plants, does not mean that glyphosate is the most toxic ingredient in the mixture.

The secrecy on adjuvants allows manufacturers to change the composition of the formulation without long-term testing, to deal with competition and adapt to market demand.'

Quoting Mesnage: ‘To praise the efficiency (the toxicity) of their new formulations, manufacturers have no problems claiming that the new is different from the old, with new adjuvants.. When this is about the health effects this is another affair…’

full formulation of herbicides sprayed on wheat needs to be assessed

'What are the consequences of this non-scientific concept?'

Regulatory authorisations of pesticides are based on long-term tests carried with the active ingredient alone.

Are adjuvants sufficiently inert and safe to escape long term testing?

Seralini and Mesnage both maintain that the consequences of this data gap, is that the ADI / RfD of glyphosate (Roundup) - and for pesticides in general - for the human population is underestimated as long as the adjuvants are neglected.

The current approvals throughout the world for the ADI for glyphosate are based on 30 year old, private corporate studies. While the ADI might be eg. 0.3mg/kg/day – scientists today believe due to the – in vivo results – we could be underestimating the ADI by 100,000.

  • Exposure to adjuvants and their presence in the environment are never monitored.
  • Farmers never use an active principle alone.

Pesticides have to be tested for chronic effects, as they are sold and used, as mixtures of active principles (ingredients) and adjuvants.

What are the consequences of this study?

1. The pesticides industry may spend a significant amount of money on PR (above and below the line) to quietly discredit Seralini, Mesnage and the laboratory they work out of to ensure that the facts of this study do not reach mainstream media.

2. People will start to understand that their food may be more toxic than previously thought. They may realise that particularly when it comes to wheat, it may not just be ‘the gluten’.

4. People will place less trust in regulators – these include the World Health Organisation, US Environmental Protection Agency, Europe’s EFSA.

5. People will be less able to trust their individual country regulators that assess toxicity of pesticides within their own country – Eg. NZ EPA.

6. Farmers and pesticides applicators may better understand the source of their illnesses.

7. Greater understanding may result in regards to bee decline and pollinator colony collapse.

8. We may better understand the impact on soils in 2015, Year of Soil.

9. We require open transparent debate. Conventionally farmed cereals can result in higher levels of dangerous moulds/fungi such as fusarium & mycotoxins than organic. Perhaps there is a cost to the consumer that needs to be identified. Perhaps there is a conversation that needs to hit the mainstream.

10. We more clearly understand the sustained growth of the organics sector.


NB. Fungus in cropping situations can be extremely dangerous and damaging to crops. Papers suggest fungal outbreaks may be less common in organic crops.


Less Fusarium infestation and mycotoxin contamination in organic than in conventional cereals. Bernhoft et al 2010.

Sometimes when you hear about pesticides ON food, do you wonder what they are?

The list below gives you an idea of the range and availability of insecticides, fungicides and herbicides available in New Zealand for spraying ON our cereals, pulses, fruit and vegetables. The following list only includes products that are sprayed ON the growing plant - post emergence. RITE just wants to give you a taste of what is available....  This list is simply a selection, and is in no way comprehensive. New Zealand is considered a 'safe' food producer, however there are products listed below that may not be legally used in other countries.

What are the consequences of these sprays on, for example, our daily bread? If you have gluten intolerance of IBS, take a moment to check out the list, then contemplate the fact that wheat isn't likely to get thoroughly washed before production. Rather, wheat will be cleaned without water: magnets, gravity and air currents are used. Water may be added later in the conditioning process, but will be added to slightly increase moisture rather than drain off (and wash). Cereal growing regions with higher rainfall may have higher pesticide residue levels. 

Why the fuss? I'm not necessarily saying these products are bad. What I am saying is the cumulative effects of different products that can be sprayed on the same crop - all for very relevant reasons - are never assessed. These products only ever assessed for a 60kg adult - never a developing foetus or infant.  For example, do we know if these products have similar effects in the digestive system? No. Do we know if these products affect our ability to digest foods? No.  Toxicity assessments are not based on immunological, gastric or endocrine effects. And every study that has proven these products safe by our governments today are supplied and paid for by the same companies that make and sell the product. With no peer review. These studies are private and confidential.  Yet their results directly affect how much can be applied to our food. And of course - remember that no agency or country IN THE WORLD assesses the stronger full formulation (with added stuff to make it work more effectively). Our countries and governments only asses the weaker active chemical.

There are too many data gaps and conflicts of interest. That's all. Conventional food should be safe.

Furthermore the tests that give the operator exposure levels - farmer exposure - are way out of date. It's not just the consumers - it's our farmers trying to get up with cut price demands of duopolist supermarkets.  Most farmers don't have the stretch to avoid chemical fixes that get perfect products to market.  In Australia 'while supermarkets profits have risen at a rate of 4% a year for a decade suppliers profits have flatlined'. (Duopoly Money, Malcolm Knox, The Monthly, August 2014) Our food producers are stressed and the cheap products touted by our supermarkets do not mean healthy products. 

The New Zealand government tests some of these products in its food monitoring programs that assess residue levels in food.

Post emergence herbicides, insecticides and fungicides.
ACL GLYPHOSATE 360: For wheat, barley and oats apply 7-12 days prior to harvest when the grain moisture content is less than 30%. Apply 7-14 days prior to harvesting peas when pods have dried. Use only on peas for threshing. Do not harvest within 7 days after treatment to allow herbicide to translocate into the weed roots. Do not apply to crops which will be harvested for seed. 360 g/litre glyphosate as the isopropylamine salt in the form of a solubleconcentrate
Agritone 750 Selective herbicide for the control of many broadleaf weeds in established pastures, grass playing fields and lawns, and in cereals, grass seed and linseed crops.
Alliacine 40EC: Alliacine is a herbicide for use post-emergence in onions, pre- and post-emergence in lettuce and pre-emergence in carrots, leeks and parsnips.  A carbamate, 400g/litre chlorpropham
Alpha-Scud: For the control of a range of caterpillar pests in vegetable brassicas, maize, sweetcorn and tomatoes, thrips in onions, aphids in stone fruit and tomatoes, and grass grub beetle on non-bearing fruit trees, vines. 100g/L alpha-cypermethrin
Amistar: For the control of a wide range of diseases in wheat, barley, potatoes, ryegrass seed crops, sweetcorn and maize. 250g/L   in the form of a suspension concentrate. Always apply with a triazole fungicide to improve disease control as well as enhance resistance management.
Atranex SC: For post-emergence control of annual grasses and broadleaf weeds in maize, sweetcorn, established lucerne and non crop situations. 500g/L atrazine
Aramo: A selective post-emergent herbicide for the control of annual poa in bulb onion crops. 200g/L tepraloxydim 
Archer Herbicide for the control of certain broadleaf weeds in a wide range of crops. 300g/L clopyralid as the amine salt
Assault: Non-volatile 2,4-D liquid for broadleaf weed control in cereals and pasture.
Attack: A broad spectrum insecticide for use on avocados, citrus, flowers and ornamentals, glasshouse tomatoes and cucurbits, grapes, kiwifruit, persimmons, vegetable and fodder brassicas and fodder beet. 25g/litre permethrin + 475g/L pirimiphos-methyl
Basagran: Selective post-emergence herbicide for use on onions, cereals, clover and grass seed crops, pasture, potatoes, soya beans, peas, lucerne and turf. 480g/L bentazone(present as the sodium salt)
Baton: Non-volatile 2,4-D soluble granules for broadleaf weed control in cereals and pasture.
Beetup Compact: Beetup Compact controls various weeds in sugar and red beets. Provides critical early post-emergent weed control in beets. Carbamate, 80g/litre phenmedipham + 80g/litre desmedipham
Bladex 90 WG: A selective herbicide for the control of various weeds in lentils, lucerne, maize, sweet corn, onion and pea crops. Active Ingredient(s): 500g/L cyanazine
Bonza: A specially formulated blend of paraffinic oil and surfactant to enhance wetting, spreading and uptake of systemic herbicides; with other herbicides and agricultural chemicals to improve wetting and spreading, and as an aid for modifying spray droplet quality and to preserve droplet survival. 450g/L paraffinic oil
Bruno: For selective control of various weeds in maize, onions, peas, potatoes, lentils, lucerne, and sweetcorn. Active Ingredient: 500g/litre cyanazine.
Captan 600 Flo: A fungicide for the control of certain fungous diseases of fruit, vegetables, ornamentals, turf, greenhouse crops and for certain soil borne diseases.
Chlorpyrifos 500EC: Agricultural and horticultural insecticide.
Comet: Systemic cereal fungicide for the control of diseases in barley, wheat and ryegrass. 250g/L pyraclostrobin. Always apply with a triazole fungicide to improve disease control as well as enhance resistance management
Contact Xcel: A non-ionic surfactant which will improve the wetting, spreading and sticking of agricultural and horticultural sprays. 980g/L linear alcohol ethoxylate
Corasil: A plant growth regulator for the improvement of fruit size in oranges and mandarins. 750g/L MCPA as the dimethylamine salt.
Cougar: Selective weedkiller for the control of field pansy and other broadleaf weeds in wheat and barley. Fenoxaprop-P-ethyl 120 g/L
Crest 520: A selective post emergence herbicide for grass weed control in many broadleaf crops, orchards and forestry. 520g/litre haloxyfop-P as the methyl ester
Diquat 200SL : desiccant to allow easier harvesting of certain crops. desiccant in Barley, Green Beans, Lentils, Lucerne, Peas, Red Clover, Soya Beans, Wheat and White Clover and haulm destruction in Potatoes. Bipyridyl, 200g/litre diquat.
Duplosan Super: Systemic post-emergence herbicide for use in wheat, barley, oats, grass crops and grass lawns against a wide range of broadleaf weeds. 130g/litre mecoprop-p, 310g/litre dichlorprop-p and 160g/litre MCPA as dimethylamine salts in the form of a soluble concentrate.
Centric: A selective post emergent herbicide for the control of broadleaf weeds in wheat, barley and oats. CENTRIC is compatible with commonly used cereal herbicides, insecticides and fungicides.  Chlorsulfuron - Sulphonyl urea, 750g/kg chlorsulfuron
Coronet: A selective grass herbicide for use on autumn and spring sown wheat and perennial ryegrass for the control of wild oats and lesser canary grass (Phalaris minor). Carboxylic acid derivative, 69g/L fenoxaprop-P-ethyl.
Cycocel® 750: Plant growth regulant for application to wheat, oats and perennial ryegrass seed crops. 750g/kg chlormequat-chloride in the form of a soluble concentrate
Dew 600 : An insecticide for the control of insect pests of fruit and vegetable crops, cereals, forage brassica and pasture. 600g/L Diazinon
Diazol® 800: For control of insect pests in pasture and kiwifruit and other horticultural crops. 800g/L diazinon
Dictate 480:  Selective contact herbicide for the control of chamomiles, stinking mayweed, cleavers, storksbill, Onehunga weed and other broadleaf weeds in onions, cereals, pasture, clover and grass seed crops, potatoes, soyabeans, peas, lucerne and turf. 480g/L bentazone
Dimilin 2L: An insect growth regulator which disrupts chitin deposition and prevents moulting of porina caterpillar, clover flea of pasture and sciarid fly of mushrooms. 240g/L Diflubenzuron
Downright: A systemic fungicide with protectant and antisporulant activity for the control of downy mildew in grapes, lettuce and onions and early and late blight in potatoes. 500g/L Dimethomorph
Duplosan Super: Systemic post-emergence herbicide for use in wheat, barley, oats, grass crops and grass lawns. 130g/litre mecoprop-p, 310g/litre dichlorprop-p and 160g/litre MCPA as dimethylamine salts
 DuPont Glean: broad spectrum weed control in wheat, barley and oats. Chlorsulfuron
Emblem Flo: A fast acting contact broadleaf herbicide for use in maize, sweetcorn and popcorn. 402g/L bromoxynil, including 393g/L as the butyrate and octanoate esters 402g/L bromoxynil, including 393g/L as the butyrate and octanoate esters
Fenox 240EC: A herbicide for pre-and post-emergence control of broadleaf weeds and some annual grasses in apples, grapes, kiwifruit, stonefruit and forest nurseries. Nitrophenyl ether 240g/litre oxyfluorfen
Foxtrot: Selective grass herbicide for use on autumn and spring sown barley, wheat and perennial ryegrass to control wild oats and lesser canary grass. Active Ingredient: 69g/litre fenoxaprop-P-ethyl.
Jazz: Pre or post-emergence control of weeds in asparagus, carrots, lucerne, maize, lentils, peas, potatoes and tomatoes. Active Ingredient: 500g/litre metribuzin.
Flowable Atrazine: Residual herbicide for the control of certain broadleaf weeds and seedling grasses in maize, sweetcorn, linseed and established lucerne.
Granstar: For control of broadleaf weeds in wheat, barley and oats, and for use in conservation tillage. 750g/kg tribenuron-methyl
Harmony: For control of buttercups and dock in pasture, wheat, barley and oats. 500g/kg thifensulfuronmethyl
Hornet 430SC: A systemic triazole (DMI) fungicide for the control of diseases in cereals, grass seed crops, peas and onions, for the control of brown rot in stonefruit and to control rust and fusarium in pasture. 430g/L tebuconazole 
Hussar®: Selective post-emergence herbicide for the control of certain broad-leaved and grass weeds in autumn and spring sown wheat, durum wheat, triticale, ryecorn and barley. 50g/kg iodosulfuron-methyl-sodium and 150g/kg mefenpyr-diethyl (safener) in the form of a water dispersible granule. IMS and other similar herbicides, work by preventing cell division and plant growth through the inhibition of the necessary amino acids valine and isoleucine.
Kaiso 50WG: A synthetic pyrethroid insecticide for the control of foliar pests in beans, cereals,vegetable and forage brassicas,citrus, grapes, maize, sweetcorn, onions, potatoes, pumpkins, winter squash, tomatoes, ornamentals and amenity turf. 50g/kg lambda-cyhalothrin
Kamba 500: A selective herbicide for the control of difficult broadleaf weeds in cereals, maize, pasture and waste areas. (Controls atrazine resistant fathen in maize). 500g/L dicamba as the dimethylamine salt
Lorsban™ 50EC: Controls insects in agricultural crops and tree and vine fruit. 500g/L chlorpyrifos
Metriphar 48SC: Metriphar is a selective herbicide for pre- and post-emergence weed control in asparagus, carrots, lentils, lucerne, maize, peas, potatoes and tomatoes. Triazinone 480g/litre metribuzin
Moddus: A plant growth regulator to reduce the risk of lodging in wheat, barley and oats and promote seed yield increases in ryegrass seed crops. 250g/L trinexapac-ethyl in theform of an emulsifiable concentrate.
Nu-Trazine 900DF: Residual herbicide for the control of certain broadleaf weeds in maize, sweetcorn, linseed and established lucerne. 900g/kg Atrazine
Opus: Systemic cereal fungicide for the control of diseases in barley, wheat and ryegrass seed crops. 125g/L epoxiconazole in the form of a suspension concentrate. Opus can be used alone or in mixes with a strobilurin fungicide for improved disease control and persistency
Othello: Post emergence herbicide for the control of certain broad-leaved and some grass weeds in wheat. 50g/L diflufenican, 7.5g/L mesosulfuron-methyl, 2.5g/L iodosulfuron methyl sodium in the form of an oil dispersion.
Proline: A systemic fungicide for control of diseases in wheat, barley and ryegrass seed crops. 250g/L prothioconazole
Pulsar: Selective post-emergence herbicide for use in new pastures, peas, clover and cereals. Active Ingredient(s): 200g/L bentazone (present as the sodium salt), 200g/L MCPB (present as the sodium salt). Bentazone not good for wheat
Pulse penetrant: For improved penetration and faster uptake of glyphosate and other herbicides. 800g/L organomodified polydimethyl siloxane
REGLONE is a non-selective, contact herbicide used as a desiccant to allow easier harvesting of many crops.  Diquat dibromide.
ReTain: A naturally occurring plant growth regulator for apples and stonefruit (except cherries) which can improve harvest management, fruit quality and enhance storage potential. 150g/kg aviglycine hydrochloride (AVG)
Saxon: For broad spectrum broadleaf weed control in wheat, barley and oats. Active Ingredient: 200g/litre mecoprop-p + 200g/litre MCPA + 70g/litre fluroxypyr
Seguris Flexi: For the control of a wide range of diseases in barley, ryegrass seed crops and wheat. 125g/L isopyrazam. Apply in a mixture with a triazole fungicide, for curative activity and resistance management
Sprinter 700DS: Non-volatile 2,4-D liquid for broadleaf weed control in pasture and cereal. 700g/L 2,4-D as the dimethylamine and the monomethylamine salts
Stabilan:. 700DS: A plant growth regulator for use on wheat, oats and perennial ryegrass seed crops 750g/L chlormequat-chloride
Starane™ Xtra: Controls broadleaf weeds in cereal and apples. 333g/litre fluroxypyr
Stratos: or the selective control of wild oats in wheat, barley, rye grass and seed crops. Active Ingredient: 200g/litre flamprop-M-isopropyl. 
Tazer: A fungicide for the control of a wide range of diseases in wheat, barley, potato, sweetcorn, maize, onions, grapes, field tomatoes, peas and ryegrass seed crops. 250g/L azoxystrobin
Thistrol Plus: Selective herbicide for controlling broadleaf weeds in young and established pastures, cereals, peas and in white clover and grass seed crops. 25g/L MCPA and 375g/L MCPB, both as the dimethylamine salts
Trimec: A selective herbicide for the control of a wide range of broadleaf weeds in wheat, barley, oats and ryegrass seed crops 600g/L mecoprop, 150g/L MCPA and 18.7g/L dicamba
Troy 480SL: A selective post-emergence broadleaf herbicide for use on onions, cereals, clover and grass seed crops, pasture, potatoes, soyabeans, peas, lucerne and turf.  480g/litre bentazone
Twister: A selective post-emergence herbicide for grass and broadleaf weed control in wheat and winter sown barley. Active Ingredient: 500g/litre isoproturon.
TWINAX : selective post-emergence grass weed herbicide of the DEN chemistry that delivers outstanding control of wild oats, annual ryegrasses and phalaris in wheat and barley.  100 g/litre PINOXADEN
Ultima: Wild oat, Lesser Canary grass and Gnawed Canary grass in Wheat, Triticale, Ryecorn and Durum wheat.  Carbooxylic acid derivative 240g/kg clodinafop-propargyl
Vitaflo 200: Controls the major seed borne and soil borne diseases in wheat, barley, oats and maize.  200g/litre carboxin and 200g/litre thiram.

Pesticides & NZ Herd Fertility. Is it worth asking a few questions?

There appears to be a reluctance somewhat in the mainstream agricultural press ( a few smaller independents may differ) to investigate the potential health outcomes of pesticides and chemicals on stockfeed.

A few years ago an empties rate of 10% would have been shocking – a profound blow. However now state that the average empties rate in New Zealand is now 13%.  And if looking at the top performers, the top 25% of farmers, they achieve an empties rate of 10% based on 2011 figures. 6 Weeks put forward an industry target of 6%.

These figures are New Zealand based, but there is fertility decline internationally. list eight key management areas that affect herd reproductive performance:

1. Calving pattern;  2. Heifer management; 3. Body condition and nutrition; 4. Heat detection; 5. Dealing with non-cyclers;  6. Genetics and artificial breeding practices;  7. Bull management;  8. Cow health.

Kiwi farmers are just as smart as they have always been.  And it's commonly known that if you breed for performance, fertility often suffers - what's known as negative genetic correlations between milk production and reproduction. That is a big one, and it's very difficult to tinker with nature and keep all the 'best bits in'. 

However farmers don’t necessarily have control over quality of inputs – feed quality.

I believe that government authorities and farmer representative organisations haven’t even started to take into account the quality of feed our dairy cows and bulls are exposed to – in particular feed with higher loading of pesticides. Anecdotal reports indicate fertility may be higher for cows raised organically. While that may not be an option, keeping feed as chemical free as possible may be worth consideration. 

NZ doesn’t have maximum residue levels for pesticides on feed, not does it test and monitor our stockfeed.

For over 15 years meat producers have understood that chemical topping can boost stock growth rates and increase clover dominance.  Beef and Lamb have noted: as long as farmers understand some of the limitations such as fertility, pasture composition and effects of the season.’ 

Scientists and researchers have been aware of glyphosate's negative effect on semen quality since 1995.    [1]  [2] [3]

What is not commonly understood are the effects of cumulative chemical exposure on livestock.

Routes of exposure:

1.       Cleancrop HT™ brassica cultivars (leafy turnip, rape, bulb turnip, swede) that are bred to be tolerant to the sulfonyl urea herbicide, DuPont® Telar, active chemical Chlorsulfuron. (China revoked the registration of chlorsulfuron products as of 31 December 2013 and they will be banned as of December 31, 2015. Chlorsulfuron is being banned due to its excessively long residual effect, the high level of skill required to apply it safely and its phytotoxicity to follow-up crops.)

2.       Baleage & silage that has had glyphosate based herbicides (GBH) applied to it.

3.       Pasture spray topped with (for example) GBH or gramoxone (paraquat).

4.       Cereals converted to forage that have been desiccated with Reglone (diquat) or GBH.

5.       Imported GE/GMO feed – most protein meal imported from the USA or South America will be genetically engineered. Over 80% of GE product has a herbicide tolerant trait and will hold higher residues of GBH's. (So therefore French protein meal, for example with less GMO production may be a better bet).

I don’t know if farmers are aware, but vets expect infertility when stock are fed for example, a supplementary diet of HT swedes and herbicide topped baleage.  

Desiccation and spray topping with chemicals is a significant dietary change that has not been properly explored. Scientific literature is now demonstrating that negative effects occur at much lower levels of exposure than previously thought. None of the studies held with any of the big assessment agencies, including NZ EPA consider the effect of the stronger full formulations, commonly applied on feed.

Here are some links that can explain it better than me:

A Danish study recently concluded:

A. Glyphosate can affect the microbial populations (microbiota) in the animal gut with secondary effects on animal production and health

B. Glyphosate can affect animal mineral status with secondary effects on animal production and health

We need farmers to be privy to this discussion. Something mainstream papers in NZ are avoiding. The HT swedes story in Southland is evidence of media shutting up and farmers not hearing the full story.

We need an open discussion within academia. We don’t need discussion to be stifled because corporations don’t want us to engage because their turnover might be impacted.

Feed input quality can only be a part of the story of declining fertility - but it is important to consider it and put money towards research (without financial connections to the corporations that sell the stuff). It’s about productivity. It’s about money. It's about the mix to maximise production and fertility.

As farmers don’t have time to search for information – here are some sites and papers that may be useful.

1. Dr Krüger:

a) Presentation: Collateral damages of the herbicide glyphosate in dairy cows, current possibilities to neutralize this contamination. Monika Krüger (Prof. em.) & Awad Shehata Institute of Bacteriology and Mycology of Veterinary Faculty, University of Leipzig. [4]

b) Glyphosate Increases Birth Defects in Piglets  [5]

d) The Cattle Site – News Further Investigation Needed on the Effect of Glyphosate on Livestock Health.

2. Ib Peterson, a Danish pig farmer, was an early farmer to speak up about stock response to GM animal feed. (Over 80% of GM feed has higher residues of glyphosate based herbicides.)

The Ecologist. Deformities, sickness & livestock deaths: the real cost of glyphosate & GM animal feed? Andrew Wasley. November 2013.

3. Interviews at the China conference on GMOs 2014.

Ib Peterson.    Interview 1.     Interview 2. 

Art Dunham, veterinarian on GMOs and harm to animals 

Howard Vlieger, Farmer and Soil Specialist  

3. Evidence of GMO harm in pig study

4. Other

Healthy Gut Flora: Key to health. Article on how glyphosate can affect ruminant health.

Dr Don Huber : GMO crop pathogen and infertility.

Original letter – Dr Don Huber to the head of the US Dept. Agriculture.

Review by researchers at the University of Adelaide, Flinders University and the Institute of Health and Environmental Research: Not enough evidence that GM crops are safe to eat.

Stuff NZ. No quick answers to stock death mystery

10 Reasons we don’t need GM foods. by Claire Robinson, MPhil, Michael Antoniou, PhD, and John Fagan, PhD

Syngenta Charged for Covering up Livestock Deaths from GM Corn. Sustainable Pulse.

German Poultry Industry Giant Returns to GMO-Free Production



[1] ISIS report. Glyphosate/Roundup & Human Male Infertility

[2]  An acute exposure to glyphosate-based herbicide alters aromatase levels in testis and sperm nuclear quality.  Estelle Cassault-Meyer, Steeve Gress, Gilles-Éric Séralini, Isabelle Galeraud-Denis.  Environmental Toxicology and Pharmacology
Volume 38, Issue 1, July 2014, pp. 131–140

[3] The skinny on Roundup sex and sperm - the studies not held with the US EPA, NZ EPA, WHO and EU.

[4]  Visceral botulism at dairy farms in Schleswig Holstein, Germany - Prevalence of Clostridium botulinum in feces of cows, in animal feeds, in feces of the farmers, and in house dust.  Monika Krüger, Anke Große-Herrenthey, Wieland Schrödl, Achim Gerlach, Arne Rodlof. Anaerobe. 2012 Apr;18(2):221-3. doi: 10.1016/j.anaerobe.2011.12.013. Epub 2011 Dec 21. 

Krüger M, Shehata AA, Schrödl W, Rodloff A. 2013. Glyphosate suppresses the antagonistic effect of Enterococcus spp. on Clostridium botulinum. Anaerobe. 20:74-8. doi: 10.1016/j.anaerobe.2013.01.005. Epub 2013 Feb 6.

Krüger M, Schrödl W, Neuhaus J, Shehata AA (2013) Field Investigations of Glyphosate in Urine of Danish Dairy Cows. J Environ Anal Toxicol 3: 186. doi:10.4172/2161-0525.1000186

[5] Krüger M, Schrödl W, Pedersen Ib, Shehata AA (2014) Detection of glyphosate in malformed piglets. J Environ Anal Toxicol 4: 230. doi:10.4172/2161-0525.1000230


Zdziarski IM, Edwards JW, Carman JA, Haynes JI.  GM crops and the digestive tract: A critical review, Environment International (2014), http://dx.doi/10.1016/j.envint.2014.08.018

Dr Santadino: Glyphosate Destroys Earthworm Eisenia fetida Populations

2015 is the year of soil. So what are our governments going to do?

Provide more than lip service?  Act cautiously and acknowledge the corporations who may have a conflict of interest when it comes to policy advice and investment in research?  Acknowledge that building soil humus, carbon and micro-nutrient availability is a long process without immediate returns?  Longer than even, say, an election cycle?  Will our governments give academics the freedom to research peer reviewed academic literature that may conflict with the mainstream view of soil management? 

Will our agricultural newspapers enable journalists to write honestly and openly about soil quality?  Facilitate a discussion that has the freedom to critically examine how we are managing the biological life in our soils? Despite advertiser preferences and potential conflicts of interest?  Will our newspapers and media outlets act in the best interests of the farmer?

As Franklin D Roosevelt said in 1937: 'The nation that destroys its soil, destroys itself'.

Who can blame farmers when faced with soil fertility decline? I remember watching my dad farm back in the 1970's and thinking, 'you are so good at so many things'. You can drive a tractor, ride a horse, weld up stockyards, drench animals, attend to them, kill and cut up a beast, shear a sheep, plough a field, sow crops - I thought he was pretty amazing. He never stopped. I try to never underestimate the stress placed on farmers to manage a farm. 

But today - it's harder. Forms, obligations, safety standards and other bookkeeping requirements make it harder for a farmer to be outside doing what he/she wants to do - their job. You might think the government doesn't really want farmers outside working.

What adds to the stress? Monopolist/duopolist supermarkets, distributors and exporters have extreme bargaining power. Farmers can't fight this. Their margins are squeezed tighter. They're too busy doing everything else to challenge these big guys. And if farmers are lucky enough to have an effective marketing board that helps them negotiate, the grip that keeps the marketing board together to demand reasonable prices (and not just look after corporate within), seems to often be quite tenuous. Various market mechanisms add to the mix and distort pricing on an international scale.

So there is little stretch in annual farm return to reinvest in something as innocuous as soil improvement. It's not 'urgent'. Soil fertility decline is deceptively slow. Another year can slip by. Farmers have to do everything they can, just to get one crop off and another in the ground to simply pay their mortgage.  

And in the meantime there is little spare cash or focus by government on soil quality. Without time and investment, soil nutrients decrease, soil becomes more friable and less fertile. Unfortunately, if farmers are locked in to pricing structures that means they have no wriggle room, it can be really difficult to question and analyse spray regimes (introduced in the 1980's) that may be depleting their soil and give the microbial life that rebuilds soil, time to recover. (Spray regimes can take away the essential soil bacteria and organisms that traditionally convert organic matter into useable micronutrients for plant vigour and health). But most Ag departments aren't funded to investigate this. Nor the knock on effect on stock health and profitability.  

Farmers can be locked into a system that doesn't provide enough margin to regenerate their land. Many watch this happening, knowing it is, but it's just another cost. Yet quality of soil affects everything from susceptibility of the plant to disease, to how durable a product is on a long voyage. Consequent nutrient availability affects consumer health.

The world is starting to have a discussion about how to farm sustainably. How to go beyond corporate lip service and manage the soil to prevent decline of fertility and loss of arable land. Today's three trace element system (N P K) is not enough. Our soils are more complex than that. And so are we. This discussion is in its infancy and tends to be ignored by most governments (and 'conventional' ag newspapers). Land degradation is occurring on every continent.

It's a well known maxim that all disease starts in the soil. It comes down to lack of nutrients.

Nutrient depletion is reflected in our food quality :

 'A 2003 analysis by Royal Society of British Chemists and the British Ministry of Agriculture of the statistics on the composition of foods from 1940–1991 showed mineral content declines in fruit and vegetables of 16% for potassium to as much as 76% for copper. This trend is confirmed by various other surveys including analysis of USDA food composition data. The surveys show 60% average decline in the vitamin and mineral content of our food.' [1]

How do we 'finance soil'?  Work intelligently and realistically to help farmers nourish their soil. Acknowledge the conflicts of interest within academic funding programs that may inhibit wide ranging and transparent research. How do we act to reduce potential degradation and facilitate complexity in mineral & nutrient availability to enable plants to perform their own insect and fungal disease resistance. Build humus and carbon to prevent erosion.

This takes effort and money to change. It's a cultural shift. Fertile soil makes more food. Healthier food. More transportable food. More nourishing food.

How do we turn the system around? How do we 'finance soil'? 

[1] True Health. Getting fully mineralised soils. Section: The decline and fall. 

Submission to urge the New Zealand government to put in place regulations for zero tolerance for pesticides in baby food

Petition of Alison White and 4276 others. 
Submission by Alison White and Dr Meriel Watts.
Presented by: Mojo Mathers
Referred to: Primary Production Committee.
Date presented 29 May 2014

Following transcription from original submission in parliament.

Petition 2011/112 House of Representatives urge the government to put in place regulations for zero tolerance for pesticides in baby food; specifically that New Zealand match the European Union Directives [1] that processed infant and young children’s food must not contain pesticide residues greater than 0.01ppm (mg/kg).  

Submission by Alison White of Safe Food Campaign:

We've got more than 4,200 people who signed this petition. A common reaction from people was that of course we don't want pesticides in baby food. I'm surprised that they're there anyway. So that was a very common reaction we found when we asked people if they were interested in signing the petition.

In my written submission I gave references to support the fact that different countries around the world, different regulatory authorities have made a special provision for children in regard to pesticide residues in food and baby food in particular. The European Union which is the model that has led the way on this has certain directives which are detailed in the submission with a basic policy of zero tolerance for pesticide residues in food. This is what we want to encourage this select committee to think about doing for New Zealand so we can do this and better protect Kiwi babies. We believe Kiwi babies deserve the same protection as European babies for example.

We would like to draw your attention to this rather startling information. If we compare EU surveys of baby food, We find over 2000 samples in the EC - .04% have pesticide residues – contrast that to NZ in the last survey published 2009, 31.3% have pesticide residues, this is an enormous difference, nearly 800 times more pesticide residues here in NZ.
We’d like some things to be done.

Apart from NZ following EU directives, is to do more regular and more extensive surveys of baby food. At the moment we have baby food surveys that are part of the total diet surveys every 5 or 6 years, the last one in done 2009, that was not nearly enough.  They had only 8 samples in 4 different categories of food processed in NZ.

That is not nearly enough. We need to establish a baseline to act from and to compare internationally. 

Submission by Dr Meriel Watts, presenting on behalf of Pesticide Action Network.

Why are children so much more vulnerable to pesticides than we are ourselves?

MRLs that are set for our foods are based on adult tolerances and do not automatically protect children.  In many ways they don’t protect them at all. Children consume much more relative to bodyweight.  Therefore their intake of pesticides relative to adults is much greater. Water is 7 times more, … would be a similar level to food. This at a time when they are particularly vulnerable. When MRLs are set they are only based on one pesticides in that food, and do not look at other avenues of exposure. This can result in much greater exposure. From, air, hand to mouth, those ways results in much greater exposure.

Today babys are born pre-polluted. Mothers who are exposed to pesticides pass it across the placenta. It’s found commonly in placental cord blood, amniotic fluid, in the foetus itself and in the foetus first born faeces. 46 different pesticides are measured in the first borns’ faeces of children. 

When MRLs are set they are only based on one pesticides in that food, do not look at other avenues of exposure. This can result in much greater exposure. From, air, hand to mouth, those ways results in much greater exposure.

They carry a load of pesticides before they hit the world. This is not taken into account when MRLs for food are set.

We have a situation where a lot of these pesticides have additive or synergistic effect – you add one more pesticide the total effect increases.. this is not looked at when the MRL is set.
We are totally underestimating the amount of exposure children have.

What’s really critical is the vulnerability of small children. The developing foetus and newborns – all of their body systems are still in the process of developing, at this stage, particularly the brain and the immune system. During that development process they are acutely, exquisitely sensitive to interference from minute levels of pesticides. This process of development is also not taken into account when MRLs are set for food.

If a child is exposed to an endocrine disrupting chemical at this point it can affect their development for the rest of their lives but also down subsequent generations.

I want to draw your attention to pesticide chlorpyrifos. NZ children are exposed to 100 times more residues of this than for example Japanese children. We know chlorpyrifos is found in a number of our foods. We know from US studies, 4.6 picograms in the cord blood – a tiny amount – far below what we measure in our residue monitoring, 4.6 picogram in the cord blood going through to the developing child is enough to lower their IQ and working memory. 4.6 picograms is 400 million times less than the levels that have been found in our food supply.

Of course not all this is absorbed, and will end up in the brain but a substantial amount is because chlorpyrifos is readily and widely absorbed by humans. I use this just as an illustration – many other pesticides are also found at higher levels in our food and can impact children’s brains and other developing organ systems.

In conclusion, in my book and in my submission I have stated internationally accepted evidence based reasons for why children are very much more vulnerable to pesticides and why they are so much more exposed than we are.  I have illustrated this with just one chemical, chlorpyrifos. Children are exposed to a huge number of chemicals including pesticides on a daily basis …all of which can interact with each other and undermine their ability to contribute to society productively.

Any decrease of IQ in children shifts the whole spectrum of intelligence in society towards the lower end. It means we end up with a huge increase in the number of people who are intellectually challenged and a huge decrease in the number of people who are gifted.
This has a major impact in our society and our ability to get ahead in the world as a country.
This has a big impact on our social systems, because one of the things that goes hand in hand with this is an increase in crime statistics, an increase in suicides, and an increase in difficulties in socialising, as well as of course increases in health problems.

All of which have a huge impact in cost to our society including the health system. So it seems to me it is entirely reasonable to ask that we have zero residues of pesticides in baby food.

I noted a letter in the paper this morning.. a letter..  the government is spending quite a lot of money to subsidise the production of apples with zero residues in the Japanese market. Why can’t we do something to regulate for zero residues. Surely we care about the residues in baby’s food more than we care about residues in the Japanese market.


The conclusion of the Committee can be found here:

Petition 2011/112 of Alison White and 4,276 others. NZ House of Representatives  Report of the Primary Production Committee


[1] COMMISSION DIRECTIVE 2006/141/EC of 22 December 2006 on infant formulae and follow-on formulae and amending Directive 1999/21/EC.  Article 10
1.   Infant formulae and follow-on formulae shall not contain residues of individual pesticides at levels exceeding 0,01 mg/kg of the product as proposed ready for consumption or as reconstituted according to the instructions of the manufacturer.

Poisoning our Future: Children and Pesticides. Dr Meriel Watts. Pesticides Action Network.

Chlorpyrifos as a possible global POP. Meriel Watts PhD. For Pesticide Action Network North America.  August 2012.


Unsafe pesticides assessments. The NZ government & NZ EPA are failing our children, our farmers, & us.

As of 2014, the NZ EPA use toxicological endpoints for assessing toxicity of new pesticides and approving them. These are based on a selection of toxicity studies which give a considered 'safe' NOEL/NOAEL (no observable effect level). These studies are critical in revealing what toxic levels effect the study subject. How dangerous the pesticide is.  These studies help define how much we can be exposed to ie., what the application rate is and how much can be sprayed on our food per acre - our permitted residues. 

In making a request with the NZ EPA to understand what studies they are currently using to assess glyphosate, I was given the application for GF-1280, (with extracts below), as an example. Recently approved new pesticide active ingredient studies become the decision document for the pesticide product. Therefore GF-1280 can now be used as the 'decision document' proving reference points for toxicological safety of glyphosate in New Zealand in 2014. The studies used for risk assessment, to establish toxicological safety are in the Appendices 1 and 2.

EPA noted 'This substance is used in similar ways to other glyphosate-containing herbicides and so the risks associated with these other substances are considered to be similar to the risks associated with the use of GF-1280. Decisions made on more recent glyphosate-containing substances have therefore been primarily based on the findings of the risk assessment performed for GF-1280.'

The studies used are selected and provided by the applicant, Dow Agroscience. 

There are problems:

1. The toxicity studies for glyphosate (Roundup) (Appendix 1) are all private, obtained directly from contracted laboratories that only work with industry – Product Safety Laboratories, Dow, ABC and Covance. They are unpublished and unavailable for review by public sector health representatives or individuals. 
2. The Risk Assessment studies for acceptable exposure levels (Appendix 2) for workers (AOEL) are ancient private studies (Suresh 1993 and Hogan 1981).
3. There are no studies considering the full formulation, no studies looking at the endocrine, neurological or digestive systems.

4. The studies proving safety were all provided by the applicant. This is a conflict of interest.

 It doesn't matter what the mixture - this decision document becomes all the necessary glyphosate studies required for toxicity assessment - whether it goes on our soil our wheat or our potatoes. The studies used within the discussion document to provide safety when assessing risk are located in Appendices 1 and 2.
New Zealand EPA is using studies conveniently supplied directly by the pesticide organisations to prove safety for Kiwis. Refer here to find published and peer reviewed studies currently not considered by the NZ EPA.

Extract from application no ERMA200031 – Application to Import or Manufacture GF-1280 for Release. 
(A maximum application rate of 7.56 kg glyphosate acid/ha per application applies.)

PDF download RITE comment Glyphosate Decision Document

The NZ MPI also refers to the WHO toxicological evaluations to provide a basis for risk assessment in regards to evaluation the safety of glyphosate today.

WHO JMPR Toxicological Assessment Inadequate

The New Zealand MPI states: 'Glyphosate’s toxicity and dietary risk has been reviewed in detail by the Joint World Health Organization/Food and Agriculture Organization Meeting on Pesticide Residues (JMPR), who concluded it is of very low toxicity. MPI has adopted this conclusion in our assessment of the dietary risk of glyphosate to New Zealand and international consumers.'

Let's look at the science covered in the JMPR toxicological evaluations:

The 2011 JMPR glyphosate toxicological evaluation was a smaller Addendum - with a small selection studies submitted to WHO by E.I. du Pont de Nemours and Company, Wilmington, DE, USA. This is not wide ranging science.

The previous WHO JMPR Toxicological evaluation was in 2004, and studies submitted for risk assessment was predominantly supplied by glyphosate producers and marketers, published data was excluded. The new WHO glyphosate ADI that came out of that was from a ancient unpublished corporate study Atkinson et al 1993b - a  2-year study in rats (salivary gland effects) that went on to be the NOAEL that established the ADI of 1.0mg/kg bw (pp127-129). The private, unpublished ten year old study was submitted to WHO by Cheminova A/S, Lemvig, Denmark. It was already old when it was submitted.

The NZ government's rationale is based on narrow unpublished science and ignores all recently released published and peer reviewed research. Possibly the NZ EPA's risk assessment arm has little funding and the scientists are simply unable to undertake a thorough evaluation. Fair enough. However as a result, the NZ government does not consider glyphosate toxic despite a significant amount of science indicating we should not be exposed to it and consequently, it should not be sprayed on our food and animal feed crops.

Update: In March 2015 the IARC condemned glyphosate as genotoxic and a probable carcinogen, scientists have found that the levels of glyphosate in our food that our regulators (Eg. EFSA, US EPA etc) say are safe - have been found by independent scientists to be unsafe - to cause harm. A WHO task force evaluated the IARC findings and in September 2015 advised that 'IARC and JMPR had used “significantly different” databases and that “many studies, mainly from the published peer reviewed scientific literature", that had not been evaluated by JMPR were available to IARC.'

It's time the New Zealand government assessed glyphosate for it's true toxicity - using 21st century, published peer reviewed literature.


Appendix 1: Hazard classification of GF-1280

Table A1.5: Formulation data for GF-1280  Pp 18 - 22

Acute Toxicity
Acute Oral Toxicity. Durando, J. 2005. GF-1280. Acute oral toxicity up and down procedure in rats. Product Safety Laboratories. Dayton, New Jersey, USA. Study ID 050311, 17344.
Acute Dermal Toxicity. Durando, J. 2005. GF-1280 Acute dermal toxicity study in rats- Limit Test. Product Safety Laboratories. Dayton, New Jersey, USA. Study ID 050312, 17345.
Acute inhalation toxicity. Hotchkiss, J. A. et al. 2005. GF-1280 Acute liquid aerosol inhalation toxicity study in F344/DUCRL rats. Toxicology % environmental Research and Consulting. The Dow Chemical Company, Midland, Michigan, USA. Study ID 051151.
Eye irritation. Moore, G E. 2003. GF- 1280 Primary eye irritation study in rabbits. Product Safety Laboratories. Dayton, New Jersey, USA. Study ID 030135, 14416.
Skin Irritation. Durano, J. 2005. GF-1280 Primary skin irritation study in rabbits. Product Safety Laboratories. Dayton, New Jersey, USA. Study ID 050313, 17346
Respiratory Sensitization. Woolhiser M. R. et al, 2006. GF-1280 Local lymph node assay in BALB/cAnNCrl Mice. Toxicology and Environmental Consulting, The Dow Chemical Company, Midland Michigan 48674, USA. Study ID 051095.
Mutagenicity. Mecchi M.S. 2006. Salmonella-Escherichia coli/Mammalianmicrosome reverse mutation assay pre-incubation method with a confirmation assay with GF1280. Covance Laboratories Inc. Vienna, Virginia, USA. Study No 6736-160.
In vivo studies. Charles G. D. et al. 2006. Evaluation of GF-1280 (glyphosate formulation) in the mouse bone marrow micronucleus test. Toxicology & Environmental Research and Consulting. Dow Chemical Company. Midland, Michigan. USA. Study No 061045 (DOW).

Table A1.6: Summary of ecotoxicity data for GF-1280  Pp22-24.

Aquatic organisms
Fish. Hughes C (2006) GF-1280: Acute toxicity to the rainbow trout Oncorhynchus mykiss, determined under static test conditions, ABC study number 50273
Aquatic invertebrates. Hughes C (2006) GF- 1280: Acute toxicity to the water flea Daphnia magna, determined under static test conditions, ABC study number 50276
Algae/Aquatic plants. Hughes C (2006) GF- 1280: growth inhibition test with the unicellular. Green Alga Pseudokirchneriella subcapitata, ABC study number 50274
Soil-dwelling invertebrates. 
Earthworm Eisenia fetida. Mallett MJ (2006) GF-1280 Acute toxicity to the earthworm Eisenia fetida, study number CEMS- 2970.
Soil microflora Carbon transformation NitrogenTransformation. Rix S (2007) GF-1280: Effects on soil microflora respiration and nitrogen transformation, study number CEMS-3310
Terrestrial vertebrates. 
Rat. Durando, J. (2005) GF- 1280 Acute oral toxicity up and down procedure in rats. Product Safety Laboratories. Dayton, New Jersey, USA. Study ID 050311, 17344.
Japanese quail. Gallagher SP, Beavers JB (2006) GF-1280: an acute oral toxicity study with the Japanese quail; project number 379-170

Honey bee. 
Acute Oral. Hughes C (2006) GF- 1280 Acute oral toxicity test with honey bees (Apis mellifera); ABC study number 50275.
Acute Contact. Hughes C (2006) GF-1280 Acute contact toxicity test with honey bees (Apis mellifera); ABC study number 50272

Table A1.7: Summary of ecotoxicity classifications for GF-1280 based on formulation data provided.  P.24

9.1 Aquatic ecotoxicity:   Overall: 9.1B,   Fish: 9.1C,   Crustacean: 9.1C,   Algae: 9.1B 9.2 Soil ecotoxicity: Not triggered based on earthworm data. No data on non target plants are available.
9.3 Terrestrial vertebrate ecotoxicity. Not triggered 9.4 Terrestrial invertebrate. Not triggered.

Appendix 2: Risk Assessment

Calculation of Acceptable Operator Exposure Level (AOEL).  Pp 26-27

The toxicological endpoint for assessment of occupational (worker) and bystander risks is the AOEL (Acceptable Operator Exposure Level). The AOEL is the maximum daily dose considered to be without adverse health effect for operators, workers and bystanders. It is based on the most appropriate NOAEL from relevant studies and is calculated by dividing the NOAEL by one or more uncertainty (safety) factors selected on the basis of the extent and quality of the available data, the species for which data are available and the nature of the effects observed.

3 studies were used to identify AOEL risks. Most likely these studies are:

(1) A developmental study in rabbits was used by the EC review which determined 30% oral absorption and an UF of 100, to derive an AOEL of 0.2 mg/kg bw/day. [The NOAEL value was not given.] (EC,2002)  Page 13. 

AOEL Systemic: 0.2mg/kg bw/day based on:
Suresh, T.P. 1993 : Teratogenicity study in rabbits. Unpublished. GLP – yes. Rallis, India. Study no. TOXI:884-TER-RB. 

For comments on the Suresh study: Roundup and birth defects: Is the public being kept in the dark? It's high mortality level was questioned.

(2) 90 day rat, NOAEL 150 mg/kg bw/day.  Perhaps Dreher, D.M. 1994. Cheminova.

(3) 2 year rat, lowest NOAEL, 31 mg/kg bw/day   - 34 years old and by Monsanto.
 Lankas, G.R.; Hogan, G.K. (1981): A Lifetime Feeding Study of Glyphosate (Roundup Technical) in Rats: Project No. 772062.  Unpublished study received Jan 20, 1982 under 524-308; prepared by Bio/dynamics, Inc., submitted by Monsanto Co., Washington, D.C.; CDL:246617-A; 246618; 246619; 246620; 246621. MRID 00093879.

The EC systemic (the Suresh 1993 study) AOEL of 0.2 mg/kg bw/day was adopted (assuming 30% absorption and an uncertainty factor of 100). Noting that the subchronic and chronic studies reported by the Agency did not lead to classification of glyphosate and taking into consideration the likely duration and frequency of worker exposure, the Agency considers that it is appropriate to use the systemic AOEL value report by the EC (2002) when assessing the risks posed by glyphosate in GF-1280.

Farmers are not safe to use glyphosate / Roundup with the AOEL based on this outdated science.

Note: There is also information on the NZ EPA Chemical Classification and Information Database (CCID). The CCID includes a summary of the data that has led to a particular classification being assigned to the substance. It is not currently updated.

Note: PAN database details GF-1280 is used as a soil treatment and for post-harvest application.

Note: FSANZ actually set our ADI - acceptable daily intake while NZ EPA receive pesticides applications and approve them for use. 

Does Roundup cause breast cancer?

There are data gaps within our pesticides assessment agencies, the World Health Organisation, US Environmental Protection Agency which trickle through to our own governments that result in very simply, bad and unsafe pesticides assessments.

Every animal study for glyphosate (the pesticide commonly known as Roundup) that the USA EPA and the WHO use to apply the ‘non-carcinogenic to humans’ rating, is sponsored and paid for by an agrichemical company.

 These are the core studies for toxicity which include acute toxicity (shorter term poisonings), and longer term toxicity - reproductive and development toxicity and carcinogenicity studies.

As a result, in this democratic world where we live, no critical study in these vital toxicity assessment areas, that form the parameters used to approve our daily consumption, our RfDs / ADI's, are ever supplied by an independent organisation like, say a university or public interest group.

This agencies are riddled with conflicts of interest.

The very studies that provide the parameters that end up being residue levels, within toxicity assessment, are only ever supplied by the very organisations that require the toxicity assessment to be declared safe.  In the case of glyphosate, the studies for proving non-carcinogenicity are only ever provided by Syngenta, Monsanto and Cheminova.  How can that not be astounding?

Furthermore, no study ever uses the stronger, more effective complete formulation of Roundup, (only the weaker active chemical glyphosate is used).   And I believe this ‘policy’ has profound ramifications for our health.

A recent French university study sent shockwaves through the world when the first (and only) ever long term study of Roundup (the complete formula) on rats at levels we are permitted to be exposed to today. This study by Seralini et al produced tumours on mammary glands of rats. [1] It wasn't meant to be a cancer study, but then cancer does pop up in surprising ways.

This Seralini study should have powerful implications for health policy.

But it is ignored by most governments. To the detriment of women.  I can’t put it any other way.  And the studies our governments and assessment agencies refer to? At this stage every long term study of glyphosate that is held with the EPA, WHO or EU are private corporate studies kept secret under corporate confidentiality agreements.  

Therefore Seralini's long term study showing the ugly photos of mammary gland tumours in rats is staggeringly, the only publicly available, independently prepared long term study of Roundup, ever in the world. 

I find it interesting, or dismaying that when breast cancer support organisations list potential causes of breast cancer, pesticides are rarely included in the mix of possible suspects. Pesticides are designed to kill, after all, and they are to varying degrees, toxins.  And the higher proportions of toxins in our bodies come largely from the food we ingest.  I don’t think that is an outlandish claim.

I believe these cancer organisations should be looking at all these independent studies and lobbying our failing agencies. There shouldn't be international silence.

And that confronting, independent study of Roundup got me thinking -  is there a reason breasts and Roundup never seem to make the same page? 

There is not a great deal of research on glyphosate, or Roundup and the mammary glands.  There is a big gaping hole in the USA research and within the studies held with the EPA and WHO.  For some reason the word ‘mammary gland’ rarely appears in the small portion we are permitted to see of their unpublished (private) research papers held with these organisations. And if you can write an article about the independent science of Roundup better than me, that non-science people can understand (like me), I invite you to, because this is not easy.  So the following information is a meagre attempt to make complex stuff, understandable. I welcome comment and help from people not connected with the pesticides industry.

And I believe there are enough families affected by breast cancer, which will want to try to understand this, tricky as it is. 

What the world is starting to understand, and only through independent (as in non-corporate) studies, is that mammary tumours are mostly estrogen dependent, and Roundup disrupts the balance of sex hormones. The sex hormones, also known as sex steroids, include the androgen testosterone and the estrogens estradiol.  Attempting to clarify as best I can: estrogens are the primary female sex hormones. They originate as cholesterol and become the hormone androstenedione. This stuff is like a pathway that works to become testosterone and then the estrogens estrone and estradiol.  The vital enzyme aromatase is critical in making it all work together. 

 Estradiol is the main estrogen during reproductive years. It also helps with developing breasts and body shape during puberty.  Too much estrogen however can activate oncogenes which can encourage cancers like breast and uterine cancers.  It appears that cancers can grow when the estradiol interacts, or binds with hormone receptors called estrogen receptors (or ERE’s Estrogen Response Elements). These together are called ‘hormone receptor complexes’.  They then bind to specific DNA sequences, potentially causing damage to DNA and hence cell division and DNA replications. Then special cells (eurokaryotic) go into damage control and try to repair the cells. [2] The cells change and you get cell growth. Cancer.     

As Wikipedia notes more elegantly than I: Estrogen receptors are a group of proteins found inside cells. They are receptors that are activated by the hormone estrogen.  Estrogen receptors are over-expressed in around 70% of breast cancer cases.

Some of you may note that aromatase is used in new drugs as an inhibitor to treat breast cancer, these drugs stop aromatase from changing other hormones into estrogen.  So they prevent/reduce the extra estrogen that pretty much acts as food for breast cancers.
Here are some studies that are starting to illustrate just how glyphosate formulations, commonly known as Roundup, may be affecting us:

In 2005 glyphosate was found to disrupt aromatase activity. This French study also noted: Roundup is always more toxic than its active ingredient. [3]   A Brazil study looking at sperm found Roundup made the sperm abnormal and lowered number in 2007. Too much estrogen can lower sperm count.  Of course, scientists have known since 1995 that glyphosate lowered sperm count and damages sperm.  I still don’t know how that study didn’t make the 2002 WHO Toxicity Evaluations… of course it was public! [4]  In 2014 Seralini again studied the full formulation at levels found in water after agricultural spraying. Roundup was found to change gene expression in sperm cells, which could alter the balance of the sex hormones androgen and estrogen.' [5]

And the same year, another French study found Roundup disrupted the synthesising of hormones. The study authors concluded Roundup was an aromatase disruptor at non-toxic doses.  And I quote:  In all instances, Roundup is more efficient than its active ingredient, glyphosate, suggesting a synergistic effect provoked by the adjuvants present in Roundup.  [6]

In 2009, again in France, glyphosate was found to have a disrupting effect on the ERE’s [7]. Remember, how aromatase is critical in the process of synthesising, or making testosterone and estrogen; how the estradiol binds with the EREs, which then bind to the DNA which then leads us to cancer?  It’s all connected and the scientists are trying to link everything up. To understand. 

A very shy US study (because I don’t think you are meant to study glyphosate in the USA) reported that glyphosate disrupted the estrogen-regulated genes relating to tumor formation and tumor growth in hormone dependent human breast cancer MCF-7 cells. [8]

And more recently, a study ignited the internet because it showed how the glyphosate affected the human hormone dependent breast cancer T47D cells.   This 2013 study from Thailand found that glyphosate at low and environmentally concentrations, possesses estrogenic activity.  The study authors believe the estrogenic activity was mediated through the estrogen response element (EREs).  [9]   

These non-industry scientists are starting to demonstrate that glyphosate is very likely a xenoestrogen, or xenohormone, that it can induce the ERE in a way that is similar to the human estradiol.  Simply put, we don’t want xenohormones in our bodies.  Xenoestrogens are pollutants that mimic real estrogen.  Xenoestrogens include DDT, Atrazine, dioxin, PCBs, and BPA.  

Is this how glyphosate can cause breast cancer? 
a.    Glyphosate acts to mimic estrogen.
b.    Too much estrogen can cause early puberty, lower sperm levels
c.    Too much estrogen can cause cancer
d.    Roundup exerts xenoestrogenic effects that promote the growth and spread of breast cancer cells.
e.    At very, very, very low levels.

Pesticides can cause tumours which can lead to breast cancer.  And the non-industry science is starting to join the dots.

These independent studies showing danger aren’t held with the EPA and WHO  – because industry doesn’t want them there. It’s as simple as that. 

It is a rather confronting idea that we are exposed to these xenoestrogens over our entire lifetime.  Pregnant mothers expose their childen to toxins in-utero, a now commonly accepted fact.   “Prenatal exposure to natural and synthetic estrogens is associated with increases in breast and vaginal tumour in humans as well as uterine tumours in animals……….. implications of new findings suggest that causes of endocrine-related cancers or susceptibility to cancer may be a result of developmental exposures rather than exposures existing at or near the time of tumour detection.”[10]  For example, when researchers at the EPA…” dosed laboratory animals with the pesticide atrazine or other EDCs during certain weeks of pregnancy, the offspring never developed fully mature mammary glands, leaving the daughters more vulnerable throughout life to carcinogenesis. [11]

However there is little or no funding for this type of research.  If you look on the sites we all know, the sites that help us raise money for breast cancer research, you may understand something.  The money we raise through the walks and the charity events are only for finding a cure.  It is rare to find on these sites articles about toxicity, and cancer prevention. Sites that raise money for breast cancer rarely, if at all, commit to researching toxins that go in our bodies that contribute to cancer.  I don’t know about you, but I find this chilling.  

Have a look on the most recent EPA approval of glyphosate and search for the word ‘estrogen’.   Or even the WHO paper, you’ll find one reference (page 148). Not these studies only use the weaker active chemical glyphosate, not the stronger formulation that is sprayed on our food [11]. These studies influence world policy.

How do we respond to this, when there are so many public domain studies, not used by the WHO or US EPA that show that the full formulation is genotoxic?

Do we just say, ‘Gee.  Never mind.’?  

I’m not talking about a little used product, something we may rarely be exposed to. Roundup is commonly found on our food, including our wheat.

Then there is the adjuvant factor. Adjuvants are included in the Roundup formulation to make it work more effectively.  A study has recently isolated a formulation ingredient, POE-15 which is actively toxic to humans. This has been quietly taken out of the mix, but what has replaced it? The new ingredient doesn’t have to be listed as an ingredient on product labels [12].  The study authors of course, insist that the full formulation of Roundup must be investigated in long term toxicity trials.  Because stuff like this is in the final mix on our food.

Just who are our assessment agencies protecting?
Just to finish off, here is a list of disorders and disease related to xenohormone exposure :
1.    Increase in reproductive-site cancers (breast, uterine, & ovarian)
2.    Precocious puberty
3.    Decreased fertility in both male and females
4.    Estrogen dominance
5.    Increased incidence of prostate cancers
6.    Polycystic ovarian syndrome
7.    Obesity
8.    Thyroid Disruption
9.    Endometriosis, adenomyosis

I would conclude that corporate financed scientists would declare that Roundup, or glyphosate is not a xenohormone.  I understand that the EPA, WHO and European Commission would declare that there is not sufficient evidence to categorise Roundup as a xenohormone.  Particularly when every study held with the EPA, WHO and Europe for glyphosate reassessment is only of the active substance in the Roundup formulation, not the stronger formulation itself.  

I would conclude that public domain scientists acting in the public’s interest are reaching consensus that Roundup is a xenohormone.

What would you conclude?
What would a public sector endocrinologists, oncologists or fertility experts say?
It’s an interesting conversation.

Help piecing this together more accurately is welcome.

[1] Gilles-Eric Séralini, Emilie Clair, Robin Mesnage, Steeve Gress, Nicolas Defarge, Manuela Malatesta, Didier Hennequin, Joël Spiroux de Vendômois.  Republished study: long-term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize Environmental Sciences Europe. 201426:14. Published June 2014

DOI: 10.1186/s12302-014-0014-5

©  Séralini et al.; licensee Springer 2014

[2] Thomas, Christoforos; Strom A., Lindberg K., Gustafsson J. (22). "Estrogen receptor beta decreases survival of p53-defective cancer cells after DNA damage by impairing G2/M checkpoint signaling". Breast Cancer Research and Treatment 127 (2): 417–427.doi:10.1007/s10549-010-1011-z. PMID 20623183
[3] Richard, S., Moslemi, S., Sipahutar, H., Benachour, N., Séralini, G-E. 2005. Differential effects of glyphosate and Roundup on human placental cells and aromatase. Environmental Health Perspectives 113: 716–20.
[4] Vera Lúcia de Liz Oliveira Cavalli, Daiane Cattani, Carla Elise Heinz Rieg, Paula Pierozan, Leila Zanatta, Eduardo Benedetti Parisotto, Danilo Wilhelm Filho, Fátima Regina Mena Barreto Silva, Regina Pessoa-Pureur, Ariane Zamoner. Roundup Disrupted Male Reproductive Functions By Triggering Calcium-Mediated Cell Death In Rat Testis And Sertoli Cells. Free Radic Biol Med. 2013 Jun 29. Epub 2013 Jun 29. PMID: 23820267
Yousef, M.; et al, “Toxic effects of carbofuran and glyphosate on semen characteristics in rabbits”, Journal of Environmental Science Health, B30, 4, 1995, 513-534
[5]  An acute exposure to glyphosate-based herbicide alters aromatase levels in testis and sperm nuclear quality.  Estelle Cassault-Meyer, Steeve Gress, Gilles-Éric Séralini, Isabelle Galeraud-Denis.  Environmental Toxicology and Pharmacology.  Volume 38, Issue 1, July 2014, pp. 131–140
[6] Benachour, N., Sipahutar, H., Moslemi, S., Gasnier, C., Travert, C., Séralini, G-E. 2007.  Time- and dose-dependent effects of roundup on human embryonic and placental cells. Archives of Environmental Contamination and Toxicology 53, 126–33. 
[7] Gasnier, C., Dumont, C., Benachour, N., Clair, E., Chagnon, M.C., Seralini, G.E., 2009. 499 Glyphosate-based herbicides are toxic and endocrine disruptors in human cell 500 lines. Toxicology 262, 184 -191.
[8] The expression of estrogen-regulated genes relating to tumor formation and tumor growth in hormone dependent human breast cancer MCF-7 cells were reported to be disrupted Hokanson, R., Fudge, R., Chowdhary, R., Busbee, D., 2007. Alteration of estrogen-regulated gene expression in human cells induced by the agricultural and horticultural herbicide glyphosate. Hum. Exp. Toxicol. 26, 747–752.  
[9] Glyphosate induces human breast cancer cells growth via estrogen receptors. Thongprakaisang S, Thiantanawat A, Rangkadilok N, Suriyo T, Satayavivad J. Food Chem Toxicol. 2013 Sep;59:129-36. doi: 10.1016/j.fct.2013.05.057. Epub 2013 Jun 10. Environmental Toxicology Program, Chulabhorn Graduate Institute, Laksi, Bangkok 10210, Thailand.  
[10]  Cancer and Developmental Exposure to Endocrine Disruptors.  Linda S. Birnbaum and Suzanne E. Fenton.   Experimental Toxicology and Reproductive Toxicology Divisions, National Health and Environmental Effects Research Laboratory,   Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA. 
[11] Silent Spring Institute.   EPA:  Raynor JL., et al 2004; Rayner, JL., et al 2005.
[12]  Petit F; Le Goff P; Cravedi J-P; Valotaire Y; Pakdel F. 1997. Two complementary bioassays for screening the estrogenic potency of xenobiotics: Recombinant yeast for trout estrogen receptor and trout hepatocyte cultures. J. Mol. Endocrinol. 19(3): 321-335. [GlyArch1]  [12] Mesnage R., Bernay B., Séralini G-E. (2013, in press). Ethoxylated adjuvants of glyphosate-based herbicides are active principles of human cell toxicity. Toxicology 

National Children's Study". Environ. Health Perspect. 113 (8): 1100 7.  doi:10.1289/ehp.7615. PMC 1280355.  PMID 16079085


Massey University professor claims GM fears 'largely unfounded'.

In response to the NZ Herald article 'GMOs are the way to go - and grow - safely' November 24, 2014 written by Professor Peter Kemp.

Professor Kemp cites the fears regarding GMO food and livestock feed are unfounded.  Perhaps Professor Kemp could consider reviewing current research in published journals or the letters written by independent scientists, outlining international concern regarding the consequences of GMO’s in cropping and food. 

One extract from a 2013 letter stated:  ‘The claim that it does exist is misleading and misrepresents the currently available scientific evidence and the broad diversity of opinion among scientists on this issue. Moreover, the claim encourages a climate of complacency that could lead to a lack of regulatory and scientific rigour and appropriate caution, potentially endangering the health of humans, animals, and the environment.’ [1]

There have been a series of letters from international – independent scientists with no financial connections to the biotech industry, demanding more research and stating that current research does not illustrate that GMO’s are safe. The first statement was written in 1999.  Since then, many more have come forward to declare ‘there is no consensus on GMO safety.

Scientists with no financial connections to the bottom line.

Kemp states that ‘no human health problems have been proven after decades of use’. He quotes a ‘well known’ study which originates from the University of California, Davis, which has a Seed Biotechnology Center.  This centre 'received funding from biotech companies like Monsanto. The University runs a student Fellowship funded by Monsanto'. This is just the first of many concerns with the paper, documented in the study: Review of paper by Alison Van Eenennaam and AE Young (2014): Prevalence of impacts of genetically engineered feedstuffs on livestock populations. J Anim Sci, 92:4255-4278 – A compilation of critiques by scientists

There are problems too in securing research. When Dr Huber, a soil scientist with years working in the US government researching nuclear fallout was repeatedly contacted by vets who kept finding a mysterious organism in ill livestock. He found the same organism in GMO plants and immediately contacted the head of the USDA requesting urgent research. He was ignored. Over two years later, following Huber’s letter to the head of US agriculture, following directions - USDA personnel have not been permitted to be involved. 

There is simply not enough funding - and the research that actually demonstrates harm appears, for some reason, to be ignored by governments and assessment agencies. Research by Professor Giles-Eric Seralini and Dr Judy Carman come immediately to mind. It is surprising that an independent, agricultural focussed university such as Massey has not considered these independent studies.

To date, 99% of GM crops publicly released hold insecticide or herbicide tolerant traits.  They have resulted in a net increase in herbicide use. This increased herbicide use is implicated in soil degradation as well as demonstrated negative effects regarding plant and animal health, particularly concerning the effects of glyphosate based herbicides as heavy metal chelators.

It may be worth reading the Sribd article, The So-Called Scientific "Consensus": Why the Debate on GMO Safety is Not Over. Also consulting GMWatch’s Myths and Truths. This paper is written by scientists with no financial connections to biotech.  They are independent.

The question for many independent scientists, is why can’t we follow the precautionary principle?  Test this food that is consumed by both our livestock and children, test also for the effects of Roundup and glyphosate based herbicides that are sprayed on the over 80% that is herbicide tolerant - investigate the long term effects on our soil – and then proceed. Because to date a notion called ‘substantial equivalence’ – has been adopted by our governments and assessment agencies. It means that there is no need for feeding studies to assess toxicological safety. This is the ticket for ‘no research needed’.

If there weren't such enormously high barriers to researching the safety perhaps GMO food have gained a different acceptance level with everyone from independent scientists to mothers.  Perhaps a professor from Massey wouldn't have to write and article to NZH to help boost 'consumer confidence'.  I note there was no room for comments below the article to provide evidence of 'consumer confidence'.

With so many concerns being raised regarding the digestive system, people may want to know if drought tolerant ryegrass will have the same impact on the gut as Carman’s pig study. To date, drought tolerant GM traits have been found to be underwhelming.

Let’s talk about the money. Europe does not want GMOs in its food. So there is no premium in a GM content for export to the wealthiest continent. Europe has also found that varieties of non GMO corn are producing greater yields thank GMO varieties. Our farmers in NZ are feeding their stock GM protein meal because it is the cheapest available stuff available. Are there any effects of this?  No research available. China is currently rejecting GM DDGS - a protein meal we are importing to feed our NZ livestock, they have quarantined US alfalfa/lucerne imports that are GM contaminated. China has also banned the herbicide chlorsulfuron (Telar), implicated in the HT swede Southland cow deaths, the results of which are yet to be made public.

Europe and China are very cautious about GMO, for good reason.

To date we still don’t have feeding studies for the thousands of tonnes of GMO’s that are currently imported into New Zealand. For processing into Kiwi food and for our livestock.
If you want to talk about greenhouse gas emissions – the increased pesticide use has led to a direct reduction in micro-organisms in soils. Micro-organisms help maintain fertile soil. Increased pesticides use associated with current GMOs create unhealthier soils and result in less carbon sequestration. A natural effect of good management that has traditionally gone hand in hand with farming for centuries. 

Generate some independent GMO feeding studies, and release them in public journals Massey University and we’ll talk. The tragedy with GM technology acceptance is that, from the start, the actual product was never subject to feeding trials to prove safe. Ever. 

You say step one must be to increase consumer confidence. To facilitate this, GM production should be underpinned by rigorous independent science demonstrating long term safety.  Not just a fancy dream that sounds appealing.   

And right now it’s not. 

A version of the above article was submitted to NZ Herald but remained unpublished, as was the following 200 word letter: 

Regarding the article by Professor Peter Kemp.

Kemp states that ‘no human health problems have been proven after decades of use’.  Independent scientists internationally state ‘ there is no consensus on GMO safety’.

This means GMOs have not been proven safe. The study Prof Kemp quotes have been repudiated by scientists as having conflicts of interest, missing important data etc.

Not safe. Premium markets like Europe reject GM content in food. China is rejecting GMO’s we import to feed our livestock.

GM varieties have been found to be less drought tolerant than conventional. If there are not feeding studies for existing GM our livestock & children are exposed to how is a drought tolerant ryegrass going to be tested? In the paddock?

Regarding greenhouse gas emissions, over 80% of current GM farmed is herbicide tolerant, resulting in degraded land sequestering less carbon than traditional farming.

Professor Kemp is correct, 'step one must be to increase consumer confidence'. Generate independent GMO feeding studies for GM lines imported into NZ as livestock & human food today, release them in public journals Massey University, and we’ll talk.

Create an international model in safety assurance that will meet with the approval of independent scientists and health specialists.

GM production should be underpinned by rigorous science demonstrating long term safety.  Not just a fancy dream that sounds appealing.   For our kids, livestock & land.

Impacts of genetically engineered crops on pesticide use in the U.S. -- the first sixteen years
Charles M Benbrook

The missing link in herd reproductive performance?

The elephant in the room.

The elephant in the room.

Stock Feed: Roundup levels ramped up but no testing available.

Nowhere in New Zealand do they test for glyphosate, or Roundup, on stock feed.

Nor does New Zealand have feed residue limits for pesticides for livestock.

I believe this is the same for most countries.

Yet the use of glyphosate on stock feed has increased astronomically in the last decade because glyphosate based herbicide (GBH) formulations, commonly known as Roundup, have been rapidly adopted as late harvest aids on cereal crops and to increase the metabolisable energy (ME) in animal feed crops. 

When Roundup was originally released it was as a weed killer.  Spray the paddock out to clean it up and then reseed.

There are three major ways we have increased Roundup levels on stockfeed across New Zealand.

Firstly, Roundup is sprayed on our cereals: our wheat, oats and rye among others (to levels higher than GMO Roundup Ready crops as a harvest maturation aid.  Sprayed up to 7 days before harvest, these sprays can help cereal crops dry out (mature) uniformly before harvest and help get rid of weeds. 

Livestock get the chaff and remnants after the cereal grains (for human consumption) are extracted.  The external dry matter has much higher levels of Roundup than the interior grains we humans eat.

Secondly, New Zealand is also actively importing hundreds of thousands of tonnes of GMO protein meal for livestock consumption.  It’s cheap. It’s unmonitored and untracked.  99% of genetically modified (or genetically engineered) protein meal has higher levels of insecticides and/or herbicides. Most of this is Roundup (or GBH) tolerant and will carry higher Roundup residues.  

(Many scientists and farmers believe that GM stockfeed / protein meal is unsafe for livestock for reasons other than high pesticide/insecticide residues, however the NZ government has not invested money in evaluating GM feed safety).

Unless stated otherwise by the producer, include poultry feed in this calculation as GMO because this is frequently the cheapest option.

Finally, we have higher residues on our stock feed because of the practice of increasing metabolisable energy in the feed through desiccation of our hays and silage and pasture topping.  These Roundup (or glyphosate based herbicide GBH formulation) applications ‘bring out the sugars’, so the animal can extract more energy per kilogram of feed.  But it’s not just hay and silage that can be desiccated before bailing for later use.  Stubble from a recently harvested crop  can be sprayed out with Roundup and then later, finished off. Once again, higher residues of Roundup.

Fair enough.

However, there are no tests in NZ, in the farmer’s interest, advising how high these residues are.  So we don’t know the levels our livestock are exposed to.  And the agricultural/farm newspapers aren’t talking about it.

The public are worried about glyphosate passing into the milk, and the meat that we sell on our export markets.  A valid concern.

But there is something else: the New Zealand dairy herd, and our replacement stock.   There has been a decline in dairy herd fertility (the term in NZ is reproductive performance) across the world over the last twenty years.

Even the critical studies that the pesticide industry supplies to the major assessors of glyphosate/Roundup toxicity, the EPA, WHO and Europe, find ‘undesirable’ effects in the reproductive and developmental toxicity tests. [1].  These are not university based scientific studies working in the public interest.  These are private, unpublished corporate studies. That’s what the big assessment agencies, the World Health Organisation, the US EPA and Europe use to arrive at the permitted daily levels of exposure. And as a result these studies are used by the NZ EPA. The agencies don’t use public (independent) university research to arrive at the ‘acceptable daily intake’ ADI.

Why would these corporations put forward studies showing harm?

This is because initially, the industry studies were only looking at supplying the studies for human consumption purposes.  When these ancient (read – out of date) studies were supplied, desiccation hadn’t been thought of.  And of course, none of these studies dose animals year after year.  Most of these studies (from where the below symptoms have been extracted), don’t go beyond rodent pregnancy and don’t dose in the lead up to pregnancy and the first trimester in developmental studies. Therefore a two generation study can easily take less than 60 days.  These aren’t long term studies.

Of course, most farmers understand that the Roundup formulation is stronger than glyphosate (over a 100 times stronger), which is the active chemical – but farmers don’t know this formulation is never tested.  Testing the complete formulation for toxicity is not ‘industry standard’. So there is no study held for the complete formulation with the WHO, let alone the NZ EPA.

To give a benchmark, (since NZ doesn’t have one): the level permitted in the USA  [2] for grass forage, fodder and hay is 300ppm; and for clovers and lucerne - 400ppm (in the US lucerne is alfalfa). There are no major studies equating daily feed consumption with the desiccated feed residue levels we pour on our stockfeed today, in 2014.

The following target/critical effects/symptoms of glyphosate / Roundup happen in industry studies dosed at or below 400 mg/kg per bodyweight per day.

These effects are extracted from the reproductive and developmental studies directly funded by pesticide corporations and held with the USA EPA, the World Health Organisation and the European Commission.:

·         Decreased pregnancy rate

·         Decreased litter size

·         Decreased survival rate – increased postimplantation loss.

·         Distocia/abortions/reabsorptions

·         Lower growth rate (diarrhoea, soft stools, decreased food consumption)

·         Gastrointestinal disturbances/congested stomach

·         Liver weight increases;

·         Changes in salivary glands

·         nephrocalcinosis

·         Focal tubular dilation of the kidneys.  Reduced kidney weights.

·         Heart malformations & abnormalities including: Dilated heart, interventricular septal defect.

Skeletal (teratologic) variations, anomalies and malformations include:

·         Unossified transverse processes of seventh lumbar vertebra

·         Ossified transverse processes of the seventh vertebra

·         Unossified or partially ossified sternebrae

·         Extra 13th rib


I recently retrieved another neurotoxicity study that added more symptoms to this list.   This neurotoxicity study is not listed on the EPA Glyphosate Reregistration but in EPA files dated 13 May 1994, it discusses a study AR 5425 for acute mammalian neurotoxicity [3].  The following symptoms were at 300 mg/kg bw/day. These signs included:

·         ptosis

·         decreased activity

·         shaking

·         hunched posture

·         upward curvature of the spine

·         reduced splay reflex

·         sides pinched in

·         labored or irregular breathing

Please note, non-industry studies by scientists working in the public domain, find damage at levels way below those permitted for human consumption (0.5 parts per million) [4].  Additionally, every one of these studies only show effects for glyphosate.  There is not one study held by the major assessment agencies using the complete glyphosate formula farmers apply on crops today.

It is not commonly understood that New Zealand doesn’t have maximum residue limits.  America, Australia and the USA have them.  I don’t believe the NZ government regards this as a concern. But most politicians do not rely on farm income.  

So, we don’t have limits on Roundup on animal feed, and we don’t test and monitor levels on animal feed either?  No. We don’t consider glyphosate based formulations as a possible contributor to decline in reproductive performance of the NZ dairy herd, either.

If you are choosing to feed desiccated hay/silage/cereals fodder to your animal I would recommend you track closely:

1.       Veterinary fees

2.       Replacement ratios

3.       Birth weights

4.       Incidental illnesses often dismissed. Eg. Diarrhoea

On a final note, it would be interesting to see if breeders supplying to LIC are steering away from desiccated feed or imported soy/corn/cottonseed protein meal.  Scientists have known for years that glyphosate, at sub-lethal doses damages sperm quality and reduces sperm levels. A recent 2014 study demonstrated that Roundup can damage sperm at levels found in water after agricultural spraying.  Please understand neither the NZ EPA nor any NZ government departments will investigate this study. Our agricultural newspapers will ignore it.

When are GBH as a potential contributor to reproductive performance loss going to be researched and when are we going to commit research funding and conduct trials to evaluate this?

Because isn’t it about the money?


[1] The critical studies that the pesticide industry supplies to the major assessors of glyphosate/Roundup toxicity, the EPA, WHO and Europe

1.       EPA REDReassessment Eligibility Decision Glyphosate 1993. PDF

2.       WHO/FAO Pesticide Residues in Food.  2004 Toxicological Evaluation Glyphosate

3.       European Commission Studies supplied for the Reproductive & Developmental Toxicity of Glyphosate Document No 6511/VI/99-final

[2]   USA Government Printing Office Electronic Code of Federal Regulations.  Title 40: Protecting The Environment. Part 180 Tolerances and exemptions for pesticide chemical residues in food. Subpart C – Specific Tolerances.  S. 180.364 Glyphosate; tolerances for residues.

[3] EPA Acute Mammalian Neurotoxicity Study.  13 May 1994.  Discusses a study AR 5425 and provides a list of symptoms (page 8) at the high dose of 300 mg/kg bw/day.

[4] Current levels human consumption (sub-agricultural doses): Gasnier C, Dumont C, Benachour N, Clair E, Chagnon MC, Séralini GE.  Glyphosate-based herbicides are toxic and endocrine disruptors in human cell lines. Toxicology. 2009 Aug 21;262(3):184-91. Epub 2009 Jun 17.

[5] Yousef, M.; et alToxic effects of carbofuran and glyphosate on semen characteristics in rabbits”, Journal of Environmental Science Health, B30, 4, 1995, 513-534

[6] An acute exposure to glyphosate-based herbicide alters aromatase levels in testis and sperm nuclear quality.  Estelle Cassault-Meyer, Steeve Gress, Gilles-Éric Séralini, Isabelle Galeraud-Denis.  Environmental Toxicology and Pharmacology.   Volume 38, Issue 1, July 2014, pp. 131–140

US scientist that exposed glyphosate dangers to livestock, to speak at Food Matters Aoteroa Feb 2015

Head of USDA suppressing research on Roundup.

Click here to watch Professor Huber's talk.

Click here to watch Professor Huber's talk.

Traditionally we understand that the work of scientists in the public laboratories and universities our tax dollars pay for, is thorough and the research completed with great integrity and thought. 

We understand that with no financial interest in research outcomes, the results we see from these publicly funded institutions are for the benefit of the general public.

So what happens if one of these gatekeepers sounds an alarm which is simply ignored?

In February 2011 an extremely conservative and internationally respected soil scientist, Dr. Don Huber, wrote a letter to Tom Vilsack the US Secretary of Agriculture [1].  He didn’t mean for the letter to be leaked by the USDA but this happened, and the letter became public.

You could say Don Huber’s career is no less than distinguished.  He has a blue chip C.V.. As military scientist, in early years he researched the impact of nuclear warfare, later the impact of fallout on agriculture. While in command of a specialised Strategic Medical Intelligent Detachment (MIDS) he assisted with the formation of what is now, the NCMI.  His final military position was as Associate Director of the Armed Forces Medical Intelligence Centre.  Alongside and after this employment he works as Emeritus Professor at Purdue University. [2]

Traditionally Americans call people like Huber a ‘patriot’. He has an extensive service record.

Don Hubers’ work today at Purdue University is in soil science. Huber is an internationally recognized expert on nutrient-disease interactions. 

The letter he wrote to Vilsack described the worrying growth of an organism, a pathogen that is significantly impacting the health of plants, animals and possibly human beings.  He wrote that this pathogen was identified in much higher quantities on Roundup ready soybeans and corn, querying a link with the RR gene or with the presence of Roundup, or glyphosate.  The pathogen was found in high concentrations in Roundup Ready soybean meal and corn, distillers meal, fermentation feed products, pig stomach contents, and pig and cattle placentas.

Veterinarians were coming to Professor Huber because the laboratory tests confirmed that this organism was in a wide variety of livestock experiencing spontaneous abortions and infertility, and it was somehow connected to the feed source.

Huber explained to Vilsack that the pathogen may explain the escalating frequency of infertility and spontaneous abortions over the past few years in US cattle, dairy, swine, and horse operations. These include recent reports of infertility rates in dairy heifers of over 20%, and spontaneous abortions in cattle as high as 45%.

Many of these animals where eating wheatledge, which has a 100mg/kg (or 100ppm) maximum residue level (MRL) of Roundup herbicide (or glyphosate based herbicides – GBH).

Very high Roundup levels may be found on (1) GE/GMO protein meal imported into NZ (2) Desiccation, or pre-harvest sprays on NZ cereals (including wheat), and (3) Animal feed (hay and silage).  Roundup is sprayed on animal feed in NZ to increase its metabolisable energy. On our own cereals (up to 7 days before harvest), to dry off the weeds and mature the harvest.

In 2006 international maximum levels permitted on cereals were increased to reflect this practice.

And while New Zealand has no residue limits on Roundup (or glyphosate based herbicides) on animal feed, in the USA today the federal regulations advise that MRLs for animal feed can be as high as 300mg/kg and 400mg/kg.  [3] The US feed limits provide an indication of how high residues can be. These are levels that demonstrate show toxicity and harm in animal studies.

Just to contrast, the permitted level for soybeans for human consumption is 20mg/kg. [4]

When it comes to the EPA and the toxicity assessments that decide how risky Roundup is, the studies are dominated by one company.  If we consider the last assessment for re-registration of glyphosate, completed in 1990 (dated 1993) you will see, under ‘developmental and reproductive toxicity’, only four research studies.  Every one of these research studies was submitted by Monsanto [5].

None of these research studies for developmental and reproductive toxicity gave the animals doses of glyphosate leading up to pregnancy or in the first trimester of the rodent, the test animal.  

Every chronic toxicity and carcinogenicity study is supplied by Monsanto.  These, and studies by Cheminova and Syngenta, appear to be the studies that the EPA bases their ‘Group E (evidence of non-carcinogenicity for humans)’ classification for glyphosate/Roundup.

None of these research studies used the stronger, complete formulation of Roundup that is applied to plants on farms today.  Every international assessment agency in the world only evaluates the pesticide (in this case glyphosate) in its (less effective) pure form. 

There may be plenty of smart scientist and corporate blog types out their choosing to sneer at Don Huber, or simply ignore him.  Get them to show me one single study of the complete formulation of Roundup held with the EPA. Show me one lifetime study held at the levels our farm animals are exposed to every day.

Or with the NZ EPA, or the WHO or Europe's EFSA. 'Our' assessment agencies simply don't want these studies.

There’s a massive data gap.  And scientists unfettered by shareholder demands are trying to fill it.  So snide scientific types go mad – but you are missing the big picture.

And of course, every one of these industry funded studies supplied to the US EPA (also WHO, NZ EPA etc etc) are unavailable to scientists outside of Monsanto & the EPA to read and evaluate.  They are kept secret under commercial confidentiality agreements.   Is that in the national interest?  No oncologist, toxicologist, neurologist working in the public sector can examine them.  Where’s the transparency?  So scientific types who choose to criticise can ask people they love who suffer from long term illness if they would prefer public domain science form the studies that establish our reference dose for pesticides.  Not Monsanto, as is current policy.

Problems in reproductive and development toxicity industry studies include a high maternal death rate [6].  If you take a look at some of the work done by independent scientists outside of the agrichemical industry sponsored studies and you will find problems at much lower MRLs than the Monsanto sponsored studies [7].  If you look at the European toxicity results you will find that the level of 20mg/kg is concerning [8].  And that was an industry study.

Huber has reason to be concerned.  Many people are aware that in general, industry studies tend to find no toxicity at lower levels, when non-industry, or scientists working in the public domain, find danger.  Industry and non-industry studies for Bisphenol A clearly demonstrate this. [9]

Don Huber is a scientist working in the public domain.  In the public interest.   This is the difference. 

Huber is not connected to shareholders.

Huber wrote to Vilsack and explained that these diseases and problems are reaching epidemic proportions and asked Vilsack to bring the USDA in to conduct a multi-agency investigation, and combine that with a moratorium on the deregulation of Roundup ready crops until the relationship with glyphosate can be worked out or ruled out so that greater harm doesn’t happen.

How did Tom Vilsack, the Secretary for Agriculture in the USA respond? 

He did nothing.

Mr Vilsack has repeatedly demonstrated a preference for large industrial farming and genetically modified crops. As Iowa state governor he originated the seed pre-exemption bill which blocked local communities from regulating where GMO crops could be grown.  Mr Vilsack was the founder and former chair of the Governor's Biotechnology Partnership, and was named Governor of the Year by the Biotechnology Industry Organization, an industry lobbying group. [10]

Why would Tom Vilsack listen to a professor of 50 years standing, highly respected by his peers and follow this one up? 

 It is simply not in Mr. Vilsacks interest.  

And New Zealand follows the same model. The greater bulk of the imported soy/corn/cottonseed protein meal that Kiwi farmers feed to the NZ herd is Roundup Ready. We spray out our silage, pasture top with Roundup and accept Roundup as an important tool in farming. Our farming papers and the NZ EPA avoid this conversation. And then question declining herd fertility.

Glyphosate is the herbicide that Roundup Ready crops can tolerate in the form of Roundup.  It is an essential aid to the biotech industry. 

How do the livestock farmers that are watching animals become infertile, or then abort, become sick through diarrhoea for no apparent reason, seeing malformations,  and facing higher veterinary bills feel about this, or farmers with a lower than expected crop yield ... react?

I think it makes them stressed, depressed and deeply worried.  Because the mainstream agriculture and farming newspapers won’t talk about it.  This conversation simply doesn't happen.  Quietly talk to journalists.  Ask them.

 As of 2014, over two years later, following Huber’s letter to the head of US agriculture, following directions - USDA personnel have not been permitted to be involved. Independent scientists (working in the public interest) have not submitted proposals because of fear that the researchers will be shut down if their efforts become public knowledge (and some have been told by their administrators that they shall not research the area) – but the research is going forward, internationally, with private funding. 

Professor Don Huber: presentation at Food Matters Conference  - 14/15 February 2014, Te Papa, Wellington. 



[1] Letter to Secretary Vilsack from Dr. Huber.   Interview.

[2]  Research, academic and military background of Dr. Don M. Huber.

[3] US GPO:  Electronic Code of Federal Regulations.  Title 40 Protecting the Environment. Section 180.373.


[5]  EPA Reregistration Eligibility Decision (RED) Glyphosate 1993. PDF

[6] Rodwell, D.E.; Tasker, E.J.; Blair, M.; et al. (1980): Teratology Study in Rabbits: IRDC No. 401-056. MRID 00046363(Unpublished study received May 23, 1980 under 524-308; prepared by International Research and Development Corp., submitted by Monsanto Co., Washington, D.C.; CDL:242516-B)

 [7] Antoniou M, Habib MEM, Howard CV, Jennings RC, Leifert C, et al. (2012) Teratogenic Effects of Glyphosate-Based Herbicides: Divergence of Regulatory Decisions from Scientific Evidence. J Environ Anal Toxicol S4:006. doi:10.4172/2161-0525.S4-006

[8] vom Saal FS, Hughes C 2005. An Extensive New Literature Concerning Low-Dose Effects of Bisphenol A Shows the Need for a New Risk Assessment. Environ Health Perspect 113:926-933.

[9] Roundup & Birth Defects:  Is the public being kept in the dark?

[10] Wikipedia, Tom Vilsack.



The NZ health policy that could get to the guts of the matter.

It's an election year and there is one health policy I want to see that none of the parties are publicly considering.

It is a policy I believe nearly every Kiwi would support. Especially women, whom this issue disproportionately affects.  A common sense policy to help us maintain our commitment to a health expenditure as a proportion of GDP at under 11%. 

It's a research funding commitment. Not to developing some new flash drug, some silver bullet, a 'sure fix'. It's not a sexy issue, quite the opposite in fact. It's down and dirty and rather, errr, fecal.

We need to understand what makes our gut lining and digestive system - degrade. Breakdown.

What are the environmental triggers that lead to a permeable bowel? What are the main dietary and environmental factors that result in a reduced gut microbiota – reduced bugs and bacteria in our gut?

We really don’t know.

This is a massively important area. Why? Because a permeable gut wall is usually present before onset of illness. Let me repeat: Before.  So when you descend into illness after a traumatic event, losing a parent for instance, in most cases your gut was already sick.  Your body didn't have enough 'ooomph' to get you through unscathed. Your gut wasn't working properly, you couldn't extract enough nutrients to boost your immune system in a time of stress. Then you got sick. And we all get sick in different ways as we have different genetic predispositions, according to the environmental challenges our ancestors faced.

What illnesses are related to permeable (leaky) bowel? Many cancers, type 1 diabetes, rheumatoid arthritis, coeliac disease, irritable bowel, allergies, asthma, autism, ADHD & ADD, depression and ankylosing spondylitis to name a few. Yes, this list covers a lot of illness. I find it stunning, myself. And when your family is presenting with ongoing immune related maladies, coughs, colds, the flu etc, it can be pretty surprising to come to terms with this. 

Yet, a huge part of our immune system depends on a healthy digestive tract. Vitamin C is only part of it. We need a heck of a lot of other nutrients to be absorbed by our bodies – using a healthy digestive system. Without that the system breaks down.

There is a reason, 2,400 years ago, Hippocrates considered that all disease began in the gut.

When we walk into the doctors, the symptoms doctors see are the tip of your own private iceberg.

The gut is not often considered, it is hidden away. How do we learn about this? We need research.

Doctors are time poor and this is a relatively new field. Is there a corresponding relationship between New Zealand's extremely high rate of antibiotic use and it's correspondingly stunning rate of asthma? How do pesticides sprayed on our food affect our digestive system?  Herbicides, insecticides and fungicides kill plant based bacteria, bugs and fungus, after all. Is it no surprise that a little town of Te Puke in New Zealand with its population of 7,500, its orchards and sprays just happens to have an arthritis support group? Why do I know a mum with 2 autistic kids who spent their early years surrounded by 3 different orchards with three different spray regimes?

Why are people starting to believe there is a correlation between the Roundup that is sprayed on our wheat, soy, vegetable oils and other cereals, and on the feed that our intensively farmed animals (particularly pork and poultry), which together comprise a huge part of our staple food groups – and growing illness rates. It doesn’t seem all that spurious, when you think about it. Particularly when you think that not a single study held with the NZ EPA, US EPA, WHO & EU investigating the effects of pesticides as environmental triggers to illness - on the gut. At all.

There's more... you could say I am generalising or you could say we need to commit the cash for the research.

The pharmaceutical industry is embracing the big new field of 'prebiotics' and even 'fecal transplant medicine' to help us rebuild our digestive systems. These guys know something is wrong.  My call is that we need to practice prevention. In a country where the medicine is taxpayer funded, the only logical situation is to reduce illness in the first place.

There is no point having a poo transplant to improve your gut bacterial profile and then go home and eat a big lunch of bread that has been desiccated (pesticides sprayed on our wheat to dry it out and get rid of weeds) with Roundup (a patented antibiotic, I kid you not).

Yes, our cereals can have Roundup sprayed on them.  Combine that with a dose of antibiotics.  Killing all those desirable bugs of generously donated healthy fecal matter.

What a …waste…  I reckon we can be smarter.

Because the NZ tax system isn't a money pit.

Can we afford to hop on a ridiculous taxpayer funded bandaid roundabout?  That's why this call for research funding is simple Kiwi common sense.

Let's get to the bottom of this problem. Digest some facts.

Doctors are often between a rock and hard place. Distressed parents demanding antibiotics to fix baby Sam's illness walk into their clinic every day. But I don't know a single doctor who wouldn't appreciate independent research (with no ties to the pharmaceutical industry) to get to the guts of the matter.

This initiative covers an incredibly broad spectrum of the non-communicable illnesses whose costs to our healthcare system are spiralling. We have blockbuster drugs on our pharmaceutical scheme the likes of which we have never seen before, tied of course, to problems related to a permeable gut.

Sadly, researching environmental triggers for gut breakdown are probably not patentable, which is why the commercial sector aren't here already. This needs to be publicly funded.

Call my bluff, tell me I'm generalising, but I urge you to demand that your political parties think strongly about this research.

The gut is sick before the descent into illness. Without the sick gut would we get sick? Probably not.

We need to understand this. We need to do more than apply expensive pharmaceutical bandaids. Our bodies are delicately balanced systems.

We have over three times the bacterial cells in our bodies than human cells. Our immune systems and body bacteria are interdependent.

Our bodies have evolved to need and use these bacteria every day. We evolved from bacterial sea dwelling slime, we are them and they are us. We get rid of our evolutionary partner and we get sick.

Increased city based populations have resulted in us living in a cleaner, more hygienic environment, reducing our early exposure to germs and dirt. But it’s more than that. Our illnesses are accelerating faster than they ever did before.  There are environmental triggers behind this illness explosion.

A needle in a haystack? Perhaps. But while our governments continue to ignore this pressing need to understand the toxins in our diets, the situation will only get more expensive. (I could say distressing but we are talking policy here). It's the twenty first century. We have the technology and the scientists.

Does it make sense that we should direct a significant funding commitment to researching gut health? Support groups for people with the above-listed illnesses may agree.  And many sufferers have more than one problem, which often include mental health disorder - both relating back to the digestive system. The gut and brain are intricately interconnected through our immune and endocrine systems, among other things, inextricably tied to gut health.

Primarily this is about reducing onset of disease. A no-brainer.  It's tied to a healthy diet (of which lunches in lower decile (‘less fortunate’) schools could only aid), reduced dietary toxins and perhaps amending our medical practices (with independent science based recommendations) to understand what our bodies can actually cope with.

We are in the dark ages when it comes to the science of understand how our we end up with leaky guts and a reduced ability to extract the healthy nutrients we need to live active, happy, well balanced lives.

We need to ensure our kid’s food is safe (perhaps follow European policy with their no pesticides in baby food mandate) and if necessary, legislate in practical ways to protect our kids physical and psychological futures. Keep toxins out of their bodies as long as we can.

On the plus side, where there is tragedy there’s opportunity.  Mass illness?  Mass niche based opportunities!  The science could boost small start-ups in New Zealand. Like suppliers of natural prebiotics. Let's not let all those big overseas pharmaceutical corporations make all the money. We are the land of raw milk and raw honey, after all.  Develop home grown organic baby foods. There is international market demand for these products. 

Let’s reduce the barriers to small food based businesses and let our foodies develop the stuff they know will sell. Let our producers diversify with smart incentives.

These problems aren't going away quickly. Let's make some cash while we fix the situation.

I know an entrepreneur or two that may be able to help out….

Conflicts of interest & unsafe drinking water.

Conflicts of interest & unsafe drinking water.

Independent scientists have been churning out research for years that declares that the current levels of pesticides that we are exposed to are unsafe. The big 3 agencies simply choose to ignore them or dismiss them. And we return to a simple fact, the effect of this ‘lower toxicity status’ conferred by only using corporate studies is the excuse provided by governments to not test for the most common pesticide used on earth.

Without government financing and support, independent scientist’s hands are tied. 

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