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Internationally, there are an increasing number of reports of glyphosate residues in the human food chain and drinking water sources, and in soil, air and rain, and of its role, alone or in tandem with other chemicals, in diseases in humans, animals and crops.[1] [2]

In March 2015, 17 experts from 11 countries met at the International Agency for Research on Cancer (IARC; Lyon, France) to assess the carcinogenicity of the organophosphate pesticides tetrachlorvinphos, parathion, malathion, diazinon, and glyphosate.[3] [4]

Among other effects, the group found:

Glyphosate has been detected in the blood and urine of agricultural workers, indicating absorption;
Soil microbes degrade glyphosate to aminomethylphosphoric acid (AMPA);
Blood AMPA detection after poisonings suggests intestinal microbial metabolism in humans;
Glyphosate and glyphosate formulations induced DNA and chromosomal damage in mammals, and in human and animal cells in vitro;
One study reported increases in blood markers of chromosomal damage (micronuclei) in residents of several communities after spraying of glyphosate formulations;
Glyphosate, glyphosate formulations, and AMPA induced oxidative stress in rodents and in vitro.

The group classified glyphosate as “probably carcinogenic to humans” (Group 2A).

PSGR calls on New Zealand’s central and local government and regulatory authorities to:

Ban the application of glyphosate-based herbicides;
Ban processed or unprocessed glyphosate-resistant transgenic crops; and
Ban imported glyphosate-resistant feed.

Where it falls within their jurisdiction to:

Establish substantive independent safety studies on all agri-chemicals used in New Zealand, especially glyphosate-based herbicides; and
Rescind approvals and reject future applications for approval for transgenic foods and food additives containing any measure of glyphosate.

Appendix One presents details of glyphosate-related adverse effects, looking at the human, animal and physical environment. The detailed results and/or findings from studies and first-hand experience far from exhaust the material available. It provides reasons why:

Central and local government and regulators should place a total ban on the use of glyphosate to protect the New Zealand environment and to ensure it does not enter the human food chain or animal feed, or drinking or other water sources; and
New Zealand should continue to reject having glyphosate-resistant genetically engineered organisms in the environment.

Appendix Two provides alternatives to the use of glyphosate-based herbicides.

Physicians and Scientists for Global Responsibility New Zealand Charitable Trust

March 2015

Appendix One

What is glyphosate?

When working as a chemist for Monsanto Company, John E Franz invented glyphosate, a broad-spectrum, post-emergence herbicide. It was first registered for use by the United States Environmental Protection Agency (EPA) in 1974.

Glyphosate is the active ingredient in Monsanto’s proprietary herbicide, Roundup®, and an ingredient in proprietary brands marketed by Bayer, Dow, Zeneca and others.[5] Patents continue to be filed for glyphosate and glyphosate-related applications, latterly in respect of genetically engineered glyphosate-resistant crops.[6]

Monsanto’s patent on glyphosate outside the US expired in 1991. In the US, the patent on isopropylamine salt, the most widely used salt form for glyphosate, continued until 2000.[7] The first-generation transgenic Roundup Ready® soybean trait patent expires in 2015.[8]

For decades, Monsanto was the largest US producer of glyphosate herbicides. The company introduced transgenic glyphosate-resistant commercial crops in the mid-1990s and by 2007 glyphosate was the most used herbicide in the US agricultural sector.[9] In 2012, the Asia Pacific market accounted for the largest share in terms of volume.[10]

US patent 7771736 B2 (pub. 2010) covers in vivo use for animals or humans of N-phosphonomethyl glycine, i.e. glyphosate, or a salt, ester or other derivative thereof, in combination with a dicarboxylic acid or a derivative thereof, as an antibiotic for the treatment of pathogenic infections, including infections of mammals by apicomplexan parasites.[11]

Regulatory bodies worldwide have approved many applications involving glyphosate, largely on the basis of decisions made by US regulatory authorities. Glyphosate is used in agriculture, horticulture, viticulture, silviculture and forestry, and in industrial and public sites, aquatic environments, gardens, sports facilities and school grounds. Despite being claimed as less toxic than other herbicides, concerns about its effects on human and environmental health continue to be raised[12] [13] and studies pursued to establish substantive evidence. Increasingly, countries are attempting to ban glyphosate: in Brazil, the Prosecutor General’s office is a pursuing a ban[14]; in Sri Lanka, President Mahinda Rajapaksa issued a directive to ban glyphosate[15]; and in 2013 El Salavador’s National Assembly approved a decree to ban glyphosate[16].

1 - Glyphosate – how it works

Glyphosate is a non-selective herbicide, killing most plants when applied directly to foliage, including grasses, broadleaf, and woody plants. Pre-harvest glyphosate applications are used as a harvest management tool for dry down in addition to or in place of other chemicals for crop desiccation (siccation) to give the appearance of uniform crop maturity.[17] Used in smaller quantities, the sodium salt of glyphosate can act as a plant growth regulator and accelerate fruit ripening.

In actively growing plants, glyphosate-based herbicides are absorbed through foliage and translocated throughout a plant to concentrate in the meristem tissue; the plant tissue whose cells actively divide to form new tissues that cause the plant to grow. Glyphosate inhibits EPSP (5-enolpyruvylshikimate-3-phos-phate), an enzyme involved in the synthesis of the aromatic amino acids tyrosine, tryptophan and phenylalanine which are vital for protein synthesis and plant growth and development,[18] [19] and specific to plants and some micro-organisms. Exposure to glyphosate leads to stunted growth, loss of green colouration, leaf wrinkling or malformation, and tissue death takes from 4 to 20 days, all depending on the application dose.

Plants genetically engineered to be herbicide-resistant - such as Monsanto’s Roundup Ready crops[20] - allow farmers to freely apply glyphosate as a post-emergence herbicide. This practice has seen application rates virtually double since the introduction of transgenic crops, and this over-application is seen as a main contributor in weed species becoming glyphosate-resistant.

2 - Glyphosate – the chemistry

Glyphosate is an aminophosphonic analogue of the natural amino acid glycine, and the name is a contraction of gly(cine) phos(phon)ate.¹ [21]

Glyphosate (N-phosphonomethylglycine) is classified as an organophosphorus herbicide.[22] It and its variants are detailed as herbicides or phytotoxicants. They are materials which control terrestrial and aquatic plants in a given location or selectively control the growth of one or more plant species in the presence of other plants, as with glyphosate-resistant plants.

Formulations of glyphosate include an acid, monoammonium salt, diammonium salt, isopropylamine salt, potassium salt, sodium salt, and trimethylsulfonium or trimesium salt.[23] Generally, references to glyphosate as an herbicide refer to the acid form. The variants can be solids or an amber-coloured liquid. Technical grade glyphosate is used in formulated products, as are the isopropylamine, sodium, and monoammonium salts. Of these, the isopropylamine salt is most commonly-used in formulated products. This is an organic compound obtained, by various processes, from non-renewable fossil fuel resources such as petroleum or natural gas deposits, and to a lesser extent coal.

3 - Glyphosate – registration, additives, interactions and residue levels

To register pesticides in the US, the EPA requires laboratory testing for short-term (acute) and long-term (chronic) health effects. Its website says laboratory animals receive high doses to cause toxic effects to show how overexposure of these chemicals might affect humans, domestic animals, and wildlife. The majority of the tests are carried out by the corporation developing the product.

It is the active ingredient which is safety tested and not usually the other ingredients in a pesticide. These latter, named adjuvants, are often described by the developer as “inert”. In a study published in December 2013, researchers give results from testing the toxicity of nine pesticides involving the active ingredient and in addition the added ingredients. Roundup was shown to be the most toxic of the pesticides tested. The researchers say their results “challenge the relevance of the Acceptable Daily Intake for pesticides because this norm is calculated from the toxicity of the active principle alone. . . . Chronic tests on pesticides may not reflect relevant environmental exposures if only one ingredient of these mixtures is tested alone.”[24]

A study published in January 2014 confirmed the adjuvants, added to glyphosate formulations to increase their effectiveness, may be more toxic than glyphosate itself.[25] For example, studies show that the surfactant polyoxyethyleneamine or polyethoxylated tallow amine used in some glyphosate-based formulations is more toxic by the oral route to animals than glyphosate itself.[26] [27]

The primary purpose of adjuvants is to reduce surface tension and increase penetration. Adjuvants also help the mixing of two or more herbicides in a common spray solution, aid retardants used to decrease the potential for herbicide drift, aid mixing and suspending herbicide formulations in solution, and act as a buffer to change the spray solution acidity. Surfactants (surface active agents) are a type of adjuvant. Their primary purpose is to reduce the surface tension of the spray solution to allow more intimate contact between the spray droplet and the plant surface and thus improve absorption.[28] [29]

3.1 – Glyphosate and chelation

In the 1970s, glyphosate was identified as a chelator of minerals - a compound that combines with other minerals to make them available only under certain conditions. A chelator may be used to extract minerals from ores; e.g. fluoride is used to isolate uranium from the basic rock. Fluoride, found in phosphate fertilizers, chelates calcium and magnesium.

Other recent studies indicate plant uptake systems are susceptible to the chelating effects of glyphosate. For example, short-term experiments showed root uptake and shoot translocation of manganese and iron were severely depressed by glyphosate applications.[30]

A 2014 study[31] hypothesizes that glyphosate, when mixed with hard water, forms a complex with heavy metals like arsenic and cadmium, resulting in the accumulation of the latter in the body. Such metals are naturally present in soil, or may be added through applications of fertilizers. Hard water can contain metals such as calcium, strontium and iron, as well as carbonate, bicarbonate, sulphate and chlorides. The study proposed a link under local conditions between chronic kidney disease and glyphosate. Chronic kidney disease of unknown origin (CKDu) is becoming increasingly common in poor farming communities in some areas of developing countries. The US Centre for Public Integrity found CKDu has killed more people in El Salvador and Nicaragua than diabetes, AIDS and leukaemia combined over the past five years on record. CKDu was identified in the mid-1990s and is now estimated to afflict 15% of working age people in northern Sri Lanka; 400,000 patients with an estimated death toll of 20,000.

Researchers have found copper adsorption decreases in general with increasing concentration of glyphosate in solution, that the concentration of free copper in solution is drastically reduced, and the adsorption of copper in their sample soil lower.[32] Glyphosate reduced seed and leaf concentrations of calcium, manganese, magnesium, and iron in non-glyphosate-resistant soybean.[33] Decreases in seed concentration of iron, manganese, calcium and magnesium by glyphosate were found to be specific and may affect seed quality.[34]

How such effects affect the nutritional content of a food plant are yet to be determined.

3.2 – Testing for glyphosate residues

In the US, the National Pesticide Information Centre Fact Sheet says glyphosate is not included in compounds tested by its Food and Drug Administration's Pesticide Residue Monitoring Programme. Neither is it in its Department of Agriculture's Pesticide Data Programme. A field test found lettuce, carrots and barley contained glyphosate residues up to one year after the soil was treated with 3.71 pounds of glyphosate per acre.[35] USDA data show that glyphosate-based herbicide use increased 6504% between 1991 and 2010. Following a request from Monsanto Company, acceptable tolerances for residues of glyphosate were recently raised again and posted in the US ‘EPA Pesticide Tolerances: Glyphosate’[36] (effective 1 May 2013). These are applied to raw agricultural commodities and hay, oilseed crops, and vegetables, fruits and berries.[37]

4 - Glyphosate in the soil and water

It is claimed that glyphosate residues are immobile and degraded by soil microbes to AMPA and carbon dioxide,[38] and that glyphosate and AMPA (aminomethylphosphonate) are unlikely to move to ground water due to their strong adsorptive characteristics. In fact, glyphosate adsorbs to soil and can potentially contaminate surface waters because it adsorbs to soil particles suspended in runoff.

Glyphosate contamination of surface water is often attributable to urban use.[39] If glyphosate reaches surface water, it is not broken down readily by water or sunlight.[40]

The median half-life of glyphosate in soil ranges from 2 to 197 days, its persistence affected by soil and climate conditions, and can range up to 1699 days under anaerobic conditions in laboratory studies. In water, its median half-life varies from a few days to 91 days.[41] The glyphosate metabolite, aminomethylphosphonic acid, has been shown to have a median half-life of 240-958 days in some soils[42] and persist up to two years in Swedish forest soils.[43]

The French Supreme Court upheld judgements by two previous courts that “Monsanto falsely advertised its herbicide as ‘biodegradable’ and falsely claimed it ‘left the soil clean.’” The French parliament has adopted a law to prohibit private or public non-agricultural use of pesticides in green areas, forests or public space from 1 January 2020.[44] From 1 January 2022, it will be prohibited to place pesticides for non-professional use on the market, to be sold, used or in the possession of someone. This includes glyphosate-based herbicides.

Denmark has banned autumn spraying of glyphosate on sites where leaching is extensive because of heavy rain. Research showed glyphosate had contaminated groundwater from which Denmark obtains drinking water at a rate of five times more than the allowed level for drinking water.[45]

Manuel Tejada (2009) studied the degradation and the effects on biological properties in two soils after the addition of glyphosate, diflufenican and glyphosate+diflufenican and found the application of glyphosate+diflufenican mixture to soil increased the toxic effects of both herbicides in the soil biological activity and the individual soil persistence of each herbicide.[46]

Zabaloya et al (2008) looked at the impacts of post-emergence herbicides on soil microbial communities sampled from agricultural fields with a history of herbicide application in the Argentine Pampas. The herbicides focussed on in the study were glyphosate, metsulfuron-methyl and 2,4-D (2,4-dicholorophenoxyacetic acid). Soil microcosms were treated with one herbicide at a time at a dose 10 times higher than the recommended field application rates causing changes to soil microbial activity, bacterial density and functional richness with the effects of glyphosate most pronounced.[47]

Researchers looking at soil fertility examined the effects of glyphosate with its by-products on growth and viability of microbial models. They found “evidence that Roundup has an inhibitory effect on microbial growth and a microbiocide effect at lower concentrations than those recommended in agriculture.”

Also “these results should be considered in the understanding of the loss of micro-biodiversity and microbial concentration observed in raw milk for many years.”[48]

Researchers recently quantified the biodegradation of glyphosate using standard “simulation” flask tests with native bacterial populations and coastal seawater from the Great Barrier Reef. The half-life for glyphosate at 25°C in low-light was 47 days, extending to 267 days in the dark at 25°C and 315 days in the dark at 31°C. This is the longest persistence reported for this herbicide. The adjuvant AMPA was detected under all conditions. The conclusion was that “glyphosate is moderately persistent in the marine water under low light conditions and is highly persistent in the dark.”[49]

5 – Glyphosate-resistant transgenes in the environment

On the environmental effects of glyphosate, Pesticide Action Network Asia and the Pacific (PANAP) says: “. . . of greatest concern are those that occur at a subtle level, and can result in significant disruption of aquatic and terrestrial eco-systems, including the agro-ecosystem.”[50]

Today the loss of genetic diversity in commercially important crops is acknowledged. Despite crops being bred for superior resistance, genetic uniformity and monoculture practices increase the possibility of pests and diseases evolving to overcome the host plants’ resistance.

Developers claim transgenic crops will help overcome such problems, but scientists cannot easily quantify the exact effect/s novel organisms will have when released into the environment; each may differ to the next. Genes move naturally within a species, by seed dispersal and pollination. This movement is a basic biological principle of plant evolution and is facilitated by insects, wind, animals, humans and other factors. The ecological risks tied to the release of transgenic plants include non-target effects of the crop and the escape of transgenic DNA into wild populations.[51]

Sufficient knowledge existed prior to release of transgenic organisms to demand applying the precautionary principle and early post-release effects warranted cessation. As early as 1998, a researcher at the US Department of Agriculture (USDA) found a resistance gene transferred by pollen from imidazolinone-resistant wheat to jointed goat grass (Aegilops cylindrica).[52] A Canadian study identified pollen transfer as the main means for the development of canola (Brassica napus) with naturally occurring, multiple-resistance to the herbicides glyphosate, glufosinate, and imazethapyr. Study results have indicated “that the pedigreed canola seed production system in western Canada is cross-contaminated with various herbicide resistance traits at a high level.”[53] Cross pollination events are well documented.

A large proportion of the transgenic crop plants developed include glyphosate-resistance: alfalfa, canola/rapeseed, corn/maize, cottonseed, rice, soybeans, sugar beet and wheat. In many locations, transgenic crops have become the dominant crop grown, and pose potential problems as volunteer crops. Glyphosate-resistance and other transgenes have transferred to weeds, and to non-transgenic crops. Called introgression, this is the infiltration of genes from one species into the gene pool of another.

5.1 – Glyphosate-resistant transgenes in weed species

Dr Charles Benbrook, in ‘Genetically Engineered Crops and Pesticide Use in the United States: The First Nine Years’ (2004)[54] said:

“Resistance to glyphosate has emerged as a serious concern across most of the intensively farmed regions of the US. The number of resistant weeds and their rate of spread is not surprising given the degree of selection pressure imposed on weed populations by farmers applying glyphosate herbicides multiple times per year, and sometimes year in and year out on the same field. . . . Resistant weeds typically emerge first on just a few isolated fields, but their pollen, genes, and seeds can travel widely and spread quickly, especially if glyphosate continues to be relied on as heavily has it has been in recent years.”

Farmers use Roundup containing glyphosate on Roundup Ready crops, applying it liberally, and have consequently neglected other weed control measures.[55] [56] Historically farmers used multiple herbicides, which slowed the development of resistance, and they tilled growing land. Roundup Ready crops have reduced those practices and increased the use of glyphosate dramatically.

As early as 2000, in Alberta, Canada, chemical and DNA tests found canola volunteers resistant to three herbicides: Monsanto’s Roundup (glyphosate), Liberty (glufosinate ammonium) produced by Bayer CropScience and BASF’s Pursuit (ammonium salt of imazethapyr). The industry suggested adding the more toxic 2,4-D or similar to a chemical mix to kill these wayward plants.[57]

The more toxic replacement herbicides suggested⁵⁸ include 2,4-D and HPPD-inhibiting herbicides such as Laudis, Impact and Callisto. Callisto’s active ingredient is mesotrione[58] and it has an adjuvant, ethylene glycol. The data sheet of the manufacturer, Syngenta, states Callisto inhibits an enzyme which in turn inhibits carotenoid biosynthesis, that carotenoid pigments protect chlorophyll from decomposition by sunlight and consequently there are restrictions on planting following Callisto applications, from six to 18 months depending on the crop and a withholding period of 70 days from the last application.

Scientists in Nebraska have already found water hemp resistant to 2,4-D[59] and scientists at the University of Illinois have found water hemp resistant to HPPD-inhibiting herbicides.[60] Historically, water hemp is a problematic weed in the US ‘Corn Belt’ because it is aggressive, fast growing and out-competes corn for light, water and nutrients.

In 2005, the Herbicide Resistance Action Committee identified 13 weeds as glyphosate-resistant and common across the Corn Belt states. There is glyphosate-resistant water hemp in Missouri; ragweed in Arkansas; lambs quarters, horseweed and ragweed in Ohio; horseweed in Kansas.[61] Each year, the list of resistant weeds grows. The International Survey of Herbicide Resistant Weeds[62] lists weeds resistant to EPSP synthase inhibitors (G/9) – i.e. glyphosate - and to other herbicides. Today, Palmer amaranth, known as pigweed and wild spinach, is traditionally used as a medicinal plant, and is cooked or used as a salad vegetable. Reports say contaminated pigweed is turning fields of transgenic crops into “weed battlefields”. A pigweed plant produces around 10,000 seeds at a time, is drought-resistant, and has very diverse genetics. It grows as high as three metres and smothers young cotton plants.[63]

A 2010 report from the Third World Network, says:

“The rapid spread of glyphosate-resistant Palmer pigweed constitutes a major agronomic failure of genetically engineered Roundup Ready seeds. This failure was foreseen by critics but dismissed by Monsanto. The critics were right. The failure is prompting US farmers to revert to agricultural practices used in the 1980s and earlier, such as hand weeding and increased tillage.”[64] It continued: “Stricken by a lack of foresight across the conventional agricultural sector, farmers have little choice but to increase use of herbicides, including older chemicals banned in many countries due to their toxicity. These include paraquat and 2,4-D.”

A January 2014 Dow AgroSciences Press Release[65] stated new data “indicate an astonishing 86 percent of corn, soybean and cotton growers in the South have herbicide-resistant or hard-to-control weeds on their farms. The number of farmers impacted by tough weeds in the Midwest . . . now tops 61 percent. Growers need new tools now to address this challenge.” The “new tools” are their transgenic crops and associated agricultural proprietary chemicals.

Glyphosate-resistant weeds have now been found in 18 countries worldwide, with significant impacts in the US, Brazil, Australia, Argentina and Paraguay.[66] Despite the fact that New Zealand does not grow commercial transgenic crops, glyphosate-resistance has been identified in several locations, the cause given as “over application” of the herbicide.[67]

A study by David Mortensen, a plant ecologist at Pennsylvania State University, University Park, and his team, predicts total herbicide use in the US will rise from around 1.5 kilograms/hectare in 2013 to over 3.5 kilograms/hectare in 2025 as a direct result of growing transgenic crops, and that the new transgenic technologies will also lose their effectiveness.[68]

As stated, to overcome herbicide-resistant weeds Monsanto has suggested applying glyphosate with more toxic chemicals like 2,4-D.

2,4-D is a member of the phenoxy family of herbicides manufactured from chloroacetic acid and from 2,4-dichlorophenol produced by chlorination of phenol. The process creates contaminants; e.g. isomers, monochlorophenol, and other polychlorophenols and their acids.

Developers are now aiming to release transgenic crops resistant to those more toxic herbicides. For example, 2,4-D and dicamba which belong to a chemical class associated with increased rates of diseases, including non-Hodgkins lymphoma. They are highly toxic to broadleaf crops, including many common fruit and vegetable crops, and more prone to air dispersal than glyphosate. Increased use is likely to harm neighbouring farms and uncultivated areas and inevitably result in wider use of these problematic herbicides.

2,4-D is banned in Sweden, Denmark and Norway because it is linked to cancer, reproductive harm and mental impairment. It was an ingredient in Agent Orange, along with 2,4,5-T, the herbicide used in chemical warfare in the Vietnam War. Increased usage will mean increased residues on crops.

In 2013, the USDA's Animal and Plant Health Inspection Service (APHIS) has released a Draft Environmental Impact Statement[69] as part of determining whether to deregulate transgenic corn and soybean plants resistant to several herbicides, including 2,4-D: currently Dow AgriSciences’ Enlist™ corn, Enlist soybean and Enlist E3™ soybean traits.[70] At the same time, the US EPA has to conduct a review of the related herbicides.

In a 2012 report, Dr Charles Benbrook said: “Contrary to often-repeated claims that today’s genetically-engineered crops have and are reducing pesticide use, the spread of glyphosate-resistant weeds in herbicide-resistant weed management systems has brought about substantial increases in the number and volume of herbicides applied.” Approval of transgenic corn and soybeans tolerant to 2,4-D could mean the usage volume of 2,4-D could rise “by another approximate 50%”.[71]

5.2 – Glyphosate-resistant transgenes and the dangers to commercial crops

Gene movement does not always stay within a species. It can occur between species that are closely related within the same botanical family. In 2003, Britain’s advisory committee on releases to the environment (ACRE) identified wild turnip, hoary mustard, wild radish, brown mustard, and wild cabbage as species from which hybrids could be formed with transgenic canola/oilseed rape. In one field trial plot of transgenic oilseed rape/canola, researchers found 46% of seeds in a wild turnip plant were contaminated with novel DNA.[72] The commercialisation of transgenic rice raises potential for gene flow to wild and weedy rice relatives[73] and to traditional commercial varieties.[74]

Other crops with a high risk of contaminating their weedy relatives include sorghum with shatter cane and Johnson grass, canola with mustards, wheat with jointed goat grass and quack grass, rice with red rice, and sunflower with wild sunflower.

Wild radish, wild turnip, wild cabbage and other wild Brassica species grow in New Zealand. Sorghum is grown in warmer areas for summer feed and although rare Johnson grass has been found growing.

For details of weed species check with Key to Weed Species of New Zealand[75], Massey University Weed Species Data Base[76], the Foundation for Arable Research[77] and The Foragers Year[78], and the New Zealand Department of Conservation website.[79]

Brassica crops related to canola are grown in Australia. Volunteer populations of transgenic herbicide-resistant canola have implications for gene flow into weeds species and vegetable crops, and roadside volunteers have the potential to contaminate adjacent crops. Out-crossing rates can result in a substantial number of out-crossed seed per hectare.[80]

Based on studies elsewhere of gene flow into weed species, we can assume interspecific hybridization will occur in certain species combinations.[81] Introgression of herbicide resistant genes or other transgenic traits from B. Napus to the cultivated species B. Rapa and B. Juncea is possible if the species are in physical proximity.[82] [83] [84]

Since its commercial introduction in the mid-1990s, herbicide-resistant canola has been widely grown by Canadian farmers, principally Liberty Link varieties with glufosinate ammonium as its active ingredient and Roundup varieties containing glyphosate. A Greenpeace report in 2005[85] stated that by that time it had become virtually impossible for Canadian farmers to grow canola that was not genetically engineered. Evidence of seed contamination is also given in the Union of Concerned Scientists’ Report, ‘Gone to Seed - Transgenic Contaminants in the Traditional Seed Supply’.[86]

5.3 – Containment of glyphosate-resistant transgenes

Using genetic engineering technology to change one gene does not necessarily change only one function. A variety of changes in transgene expression can occur in a created organism, and each novel DNA sequence is different. The potential for problems starts there.

Glyphosate-resistant and other transgenic crops had been grown commercially for a decade when a Committee under the auspices of the US National Research Council examined the potential consequences of what effect/s transgenes might have on natural or managed ecosystems and human health.

In its report, ‘Biological Confinement of Genetically Engineered Organisms’ (2004) it states: “It is unlikely that 100% confinement will be achieved by a single method.”[87] Studies and reports on transgene transfer are numerous.

5.4 – Glyphosate-resistant transgenes in landraces

Of particular concern is introgression with species known as landraces in areas referred to as ‘centres of origin’. A landrace is a local variety of a plant species which has developed over millennia by adaptation to the natural and cultural environment in which it grows. Landraces are the storehouses of humanity’s basic stock heirloom varieties.

Such natural genetic diversity and crossbreeding has led to gains in agricultural productivity and quality. For example, following the disastrous Southern Corn Leaf Blight in 1970,[88] new hybrids were bred from Mexico’s corn/maize landraces, saving the Southern US states from further significant crop and livelihood losses.

Mexico is the centre of origin of maize/corn[89] and because of potential risks to its landraces cultivation of transgenic corn was banned there from 1998. Despite this precaution, transgenic material has been found in landraces in Mexico’s remote regions, with higher concentrations near major transport arteries. Under the North American Free Trade Agreement, Mexico has moved from exporting to importing corn, corn largely trucked from the US, without being milled, along main highways. Many blame seed spillage from this mode of transport for the landrace contamination.[90] In 2013, a judge threw out the appeals of Monsanto and Mexico’s Environment and Natural Resources Ministry to overturn a court ruling that continued the ban on planting transgenic maize in Mexico.[91] [92] [93]

5.5 – Glyphosate-resistant transgenes in human gut bacteria

Gene flow has even been recorded in the human gut. Transgenic soy represents 77% of soy production globally. The list on http://www.soyconnection.com/soyfoods/product_overview.php demonstrates how easily most consumers could ingest multiple helpings of soy transgenes via food daily. The single study commissioned by the UK Food Standards Agency on human volunteers and carried out at the University of Newcastle demonstrated that transgenic DNA from soybeans in the form of a burger and a milkshake found its way into the gut bacteria of the human volunteers.[94]

6 – Glyphosate – what farmers face

In 2012, the USDA indicated 88 percent of corn/maize grown in country was transgenic. When a study found glyphosate enhances the growth of aflatoxin-producing fungi, lending an explanation for the substantial increase in fungal toxins now found in corn grown in the US,[95] the potential for affecting large areas is plain.

Canadian, Percy Schmeiser, farms in Bruno, Saskatchewan, breeding and growing canola. In 1997, he found Roundup Ready canola plants growing near his farm. To prove this, he sprayed his nearby field with Roundup and found much of the crop was glyphosate-resistant. He saved this harvest separately, and intentionally planted it in 1998. Monsanto approached him to pay a license fee for using their patented technology without a licence. Schmeiser refused, claiming that the actual seed was his because it was grown on his land. Monsanto sued Schmeiser for patent infringement. The case went through the Canadian courts over several years until a Supreme Court 5-4 ruling found in favour of Monsanto. In 1999, Schmeiser filed a separate lawsuit against Monsanto for ten million dollars for “libel, trespass, and contamination of his fields with Roundup Ready Canola.”[96]

Many conventional farmers, on finding transgenic contamination in their fields, have been fined by Monsanto Company, some even losing their livelihood because of financial hardship created by fines and court costs.

In Bowman v. Monsanto Company, a US Supreme Court also found in favour of Monsanto[97] and a Reuters article in January 2014 reported that the Supreme Court upheld Monsanto’s case against the Organic Seed Growers and Trade Association, organic and conventional family farmers, seed companies and public advocacy interests, who had collectively sought a legal standing to prohibit the company from suing farmers whose fields became inadvertently contaminated with its transgenic crops.[98]

In August 2012, conventional farmer, Bob Mackley, spoke in New Zealand about transgenic crops and their effects in his native Australia. He reported that many Australian farmers have suffered significant losses as a result of transgene contamination of their conventional crops, and that legislation favours seed companies, not farmers. Legally without the means to protect his livelihood, Mackley has been forced to time his plantings to avoid contamination from transgenic crops grown by a neighbour. His is a critical balance between profit or contamination and loss.

Steve Marsh, an organic farmer in Australia, has sued a neighbour growing genetically engineered crops for compensation after claiming the neighbour’s crop contaminated 70 percent of his property. He is seeking AUD85,000 in compensation and the decision is expected in April 2014.[99]

Over millennia, farmers learned from experience. Like Percy Schmeiser, who spent his farming life developing his canola seed crop, they selected the best seed for next year’s crop to improve yields and quality. Crops were varied and rotated on small acreages, with some land left fallow each year. This method largely solved the potential problems that affect monoculture practices today.

7 - Glyphosate and its effects on human health

With pharmaceuticals a risk benefit judgment needs to be made by a medical professional before any initiation of their use. Pharmaceuticals are clearly distinct and identifiable single agents, whereas food derived using genetic engineering technology contains transgenes, possibly from multiple sources, with unpredictable changes in plant chemistry and often higher levels of accompanying chemical residues. These are multiple, complex and poorly defined alterations compared with those from a food sourced from non-genetically engineered sources.

‘Informed consent’ is a basic of patient-physician and subject-researcher relationship. It involves making the participant aware of and verifying understanding of the risks, benefits, facts, and the future implications of the procedure or test to which they are going to be subjected.[100]

The definition of informed consent used by US Food and Drug Administration (FDA) is complicated, a virtual “get out of jail free” card. After public outcry, US regulators adopted voluntary labelling of products with transgenic ingredients.¹⁰⁰ In contrast, guidelines approved by the Codex Alimentarius Commission allows countries to label transgenic foods and foods containing transgenic ingredients without breaching international free trade laws.¹⁰⁰

What is fact is that consumers – particularly citizens in the US where some 40 percent of transgenic crops are grown – have been guinea pigs for close to two decades, given little choice but to ingest multiple unlabelled transgenic foods or food ingredients on a daily basis, day in day out, year round. With about 94% of US soybean farmers and 72% of corn farmers using Roundup Ready crops, common ingredients in a substantial range of food products, a large majority of foods come from glyphosate-resistant crops to some extent. In addition, animals fed glyphosate-resistant crops will bio-accumulate glyphosate and/or glyphosate metabolites, adding to the human end-user’s intake.[101]

The safety of glyphosate use on herbicide-resistant crops has not been substantiated by rigorous, independent scientific research. Studies used to legitimize approvals are generally industry studies, often neither published nor peer-reviewed, and taken over a too-short timeframe.

Guidelines issued recently by the European Food Safety Authority call for two-year whole food feeding studies to assess the risks of long-term toxicity.[102] This is an improvement on current practices.

7.1 - Glyphosate – exposure for humans

Commonly, people applying glyphosate-based herbicides do not use personal protective equipment and take few other precautions to protect themselves or their families.

Proponents say glyphosate does not easily pass through human skin, that when taken in through the skin or by mouth it is eliminated in less than one day, leaving the body via urine and faeces without changing into another chemical. However, studies with rats showed about one-third of a dose of glyphosate was absorbed by the rats’ intestines, and half found in their stomachs and intestines six hours later. All traces were gone within one week.²⁷

Glyphosate residues are found in the Western diet, particularly associated with transgenic food sources. It is estimated 90 percent of transgenic crops grown worldwide are glyphosate resistant[103] and the four main crops are commonly used as food or food ingredients for the human food chain: soy, corn/maize, cottonseed and canola/oilseed rape. They also commonly appear in animal feed.

Pure glyphosate is claimed as low in toxicity, but there is evidence of numerous adverse effects. Additionally, it is formulated with various adjuvants (agents) added to assist efficacy, sold under many trade names[104], and these adjuvants, while often labelled ‘inert’, can confer additional toxicity.[105] Negative impacts on the body may manifest slowly over time by damaging cellular systems, including oxidative stress, endocrine disruption as general mechanisms of harm that result in insidious effects.

In 2002, Chemical Research in Toxicology, a publication of the American Chemical Society, published a paper about the effect on cell cycle regulation of glyphosate-containing Roundup. It concluded: “... our results question the safety of glyphosate and Roundup on human health.”[106]

Researchers in one study concluded, “The direct effect of glyphosate on early mechanisms of morphogenesis in vertebrate embryos opens concerns about the clinical findings from human offspring in populations exposed to glyphosate-based herbicides in agricultural fields.”[107]

A recent study detected glyphosate in 43.9% of human urine samples taken from participants living in urban areas in 18 European countries. It concluded, “the evidence suggests that a significant proportion of the population could have glyphosate in their bodies – and it is not clear where it is coming from.”[108]

Another recent study found glyphosate in samples of breast milk in lactating mothers in the US. The levels found were 76 ug/l to 166 ug/l. That is 760 to 1600 times higher than the European Drinking Water Directive allows for individual pesticides, but less than the 700 ug/l maximum contaminant level (MCL) for glyphosate in the US decided upon by the EPA based on the false premise that glyphosate was not bio-accumulative. (N.B. Glyphosate is classified as both a pesticide and herbicide).[109]

Independent work has shown that both glyphosate and its metabolite AMPA were eliminated slowly from plasma and, although bioavailability was only 23.21%, it is likely that glyphosate is distributed throughout the body by the blood’s circulation and there may be considerable diffusion of it into tissues to exert systemic effects[110] and where it may accumulate.

Bioaccumulation is a normal process of growth and nurturing of organisms. All animals, including humans, bioaccumulate nutrients, and can bioaccumulate substances in the body to levels that can cause harm. A typical food chain bioaccumulation process is plant uptake from soil or spray, animal eating plant, human eating animal. Each step can result in increased bioaccumulation including toxins where absorption of a substance is at a rate greater than that at which the substance is lost or eliminated.¹⁰¹

Researchers in one study concluded that animals and humans eating transgenic soy “chronically incorporate unknown amounts of this herbicide” and residues of glyphosate in the tissues and organs of food animals that have been fed with transgenic feed are not taken into account in legislation[111] nor studied in detail.

7.2 – Glyphosate – mechanisms of action

In a study published in February 2014, researchers detailed how they evaluated the effect “on hemolysis, hemoglobin oxidation, reactive oxygen species (ROS) formation and changes in morphology of human erythrocytes” (red blood cells) “exposed to different concentrations of glyphosate and its metabolites and impurities (0.01–5 mM) for 1, 4 and 24 h.” They concluded their “results clearly show that the changes induced in the erythrocytes can occur only as a result of poisoning with these compounds” and list AChE, acetylcholinesterase, AMPA, aminomethylphosphonic acid, PMIDA, N-(phosphonomethyl)iminodiacetic acid, ROS, reactive oxygen species, H2R123, dihydrorhodamine 123, and NAC, N-acetylcysteine.[112]

In 2009, researchers published the paper ‘Glyphosate Formulations Induce Apoptosis and Necrosis in Human Umbilical, Embryonic, and Placental Cells’.[113] Apoptosis is the natural process of programmed cell death that allows human foetuses to develop fingers, toes and other features. Necrosis is the premature death of living cells and living tissues. The study evaluated the toxicity of four different glyphosate-based herbicides in Monsanto’s Roundup products range in solutions diluted 100,000 times. This is far below the level at which it is used in agricultural applications and corresponds to levels detected in foods for human consumption and animal feeds.

The researchers tested applications on three distinct human cell types - embryonic, placental, and umbilical – and tested glyphosate alone and the Roundup formula. All of the heavily diluted Roundup formations caused total cell death within twenty-four hours through necrosis, showing Roundup induces apoptosis, causing DNA fragmentation, shrinkage of the nucleus, and fragmentation of the nucleus. It induced complete cell death, whereas glyphosate alone induced only apoptosis. Conclusive evidence proved Roundup adjuvants change the permeability of the three human cells studied, showing they are not inert ingredients as claimed. The researchers concluded: “. . . the proprietary mixtures available on the market could cause cell damage and even death around residual levels to be expected, especially in food and feed derived from (Roundup) formulation-treated crops.”

Researchers tested urine samples from a farmer who sprayed a glyphosate-based herbicide on his land. They included his family as two children were born with birth defects that could potentially be allied to pesticides.[114] Glyphosate residues were measured in samples taken a day before, during, and two days after spraying using liquid chromatography-linear ion trap mass spectrometry. Glyphosate presence reached a peak of 9.5 µg/L in the farmer after spraying, and 2 µg/L were found in him and in one child living 1.5 kilometres from the field, two days after the applications. The researchers noted that oral or dermal absorptions could explain the differential pesticide excretions, even in family members at a distance from the fields. Limits of detection and quantification were respectively 1 and 2 ppb.

In ‘Impacts of environmental toxicants on male reproductive dysfunction’, Wong and Cheng (2011) highlighted the role of endocrine disruptors in embryonic development include epigenetic effects: “Studies in the testis and other organs have illustrated the importance of environmental toxicant-induced oxidative stress in mediating disruption to cell junctions. This, in turn, is regulated by the activation of PI3K/c-Src/FAK and MAPK signalling pathways, with the involvement of polarity proteins. This leads to reproductive dysfunction such as reduced sperm count and reduced quality of semen.”[115] Other researchers have also demonstrated endocrine disruption, concluding “a real cell impact of glyphosate-based herbicides residues in food, feed or in the environment has thus to be considered, and their classifications as carcinogens/mutagens/reprotoxics” discussed.[116]

Researchers Anthony Samsel and Stephanie Seneff have proposed that glyphosate may inhibit cytochrome P450 (CYP) enzymes and that this is an overlooked component of its toxicity to mammals.[117] CYP enzymes play a crucial role in detoxifying xenobiotics.

They suggest glyphosate enhances the damaging effects of other food-borne chemical residues and environmental toxins. They also suggest that interference with CYP enzymes acts synergistically with disruption of the biosynthesis of aromatic amino acids by gut bacteria, as well as impairment in serum sulphate transport. They put forward the argument that the consequences are most of the diseases and conditions associated with a Western diet, which include gastrointestinal disorders, obesity, diabetes, heart disease, depression, autism, infertility, cancer and Alzheimer’s disease. The journal Anaerobe published a study which confirms the herbicide’s ability to adversely affect gut bacteria populations, i.e. generate dysbiosis, in particular predispose to increased botulism in cattle.⁴⁴ [118]

7.3 - Acute effects

Glyphosate in spray form may cause eye or skin irritation, and/or irritation in the nose and throat. Swallowing it can increase saliva, burn the mouth and throat, cause nausea, vomiting, and diarrhoea, and death; it is used as a suicide agent in some countries. If pets touch or eat plants wet with spray from glyphosate-containing products they may drool, vomit, have diarrhoea, lose their appetite, or seem sleepy.²⁷

Since 2000, a US government backed programme has been funding the Colombian government to aerial spray coca and opium crops.[119] In 2006, 171,613 hectares were sprayed with Roundup-Ultra which is 43.9 percent glyphosate, with adjuvants POEA and Cosmo-Flux 411 F.[120] PANAP says this has resulted in widespread animal deaths and food crop losses.

Human ailments commonly include: vomiting; diarrhoea; abdominal pain; gastrointestinal infections; itchy, burning skin; rashes and infections (particularly in children); blisters; burning or weeping eyes; blurred vision; conjunctivitis; headaches; fever; rapid heartbeat; palpitations; raised blood pressure; dizziness and balance disorders; chest pains; numbness; insomnia; depression; debilitation; breathing difficulties; respiratory infections; dry cough; sore throat; an unpleasant taste in the mouth; reduced cognitive capacity; seizures; impaired vision, smell, hearing; drop in blood pressure; twitches and tics; muscle paralysis; peripheral neuropathy; loss of gross and fine motor skills; excessive sweating; severe fatigue.⁵¹

7.4 – Glyphosate – associated allergic reactions

Novel DNA introduced into a plant’s genome can result in the production of proteins that may be new to the human diet. The more transgenic plants present in the food chain, the more people will potentially be consuming proteins new to their diet. Allergic reactions to these may not reveal themselves immediately.

Many symptoms identified in a UK study into allergic reactions to transgenic soy may be related to glyphosate exposure; e.g. irritable bowel syndrome, digestion problems, chronic fatigue, headaches, lethargy, skin complaints. Other glyphosate-tolerant crops may potentially present similar results.[121]

7.5 - Glyphosate – reproductive health

Exposure to glyphosate-based herbicides, even at very low doses may result in reproductive and hormonal problems, miscarriages, low birth weights, pre-term deliveries, and birth defects.⁵¹

Laboratory studies have shown that very low levels of glyphosate, Roundup, POEA, and the metabolite AMPA all kill human umbilical, embryonic and placental cells. Roundup can reduce sperm numbers, increase abnormal sperm, retard skeletal development, and cause deformities in amphibian embryos.⁵¹

Some 95% of Argentina’s annual crop of 47 million tonnes of soybean is transgenic Roundup Ready soybean on which 200 million litres of glyphosate are applied annually, mainly by aerial spraying.⁵¹ Two years after widespread aerial spraying of Roundup onto transgenic soybean crops bean in 2002, human birth malformations were reported in rural areas.

Professor Andres Carrasco was an embryologist at the University of Buenos Aires Medical School. He and researchers from the UK, US, Brazil and Argentina have shown glyphosate causes malformations in frog and chicken embryos at doses far lower than those used in agricultural spraying and well below maximum residue levels in products presently approved in the European Union (20 mg/kg for soy).[122] The test animals used by Carrasco’s group share similar developmental mechanisms with humans.

The researchers concluded their results “raise concerns about the clinical findings from human offspring in populations exposed to Roundup in agricultural fields.” Professor Carrasco stated, “The findings in the lab are compatible with malformations observed in humans exposed to glyphosate during pregnancy.” He claimed, “The toxicity classification of glyphosate is too low. In some cases this can be a powerful poison.”

In 1997, the maximum residue level (MRL) allowed for glyphosate in soy in the EU was raised 200-fold from 0.1 mg/kg to 20 mg/kg. Carrasco found malformations in embryos injected with 2.03 mg/kg glyphosate. Soybeans can typically contain glyphosate residues of up to 17mg/kg. Levels of up to 97 mg/kg have been reported in seven of 11 maize samples in Argentina, tests three months later producing the same results. At that time the MRL was 20 mg/kg. This has since been raised by the US FDA to 40 mg/kg.[123]

7.6 - Glyphosate – genotoxicity and cancer

Exposure to glyphosate-based herbicides, even at very low doses may result in various cancers - especially haematological cancers such as non-Hodgkin’s lymphoma, and hormonal cancers such as breast cancer. Several epidemiological studies have linked exposure to glyphosate with non-Hodgkin’s lymphoma, hairy cell leukaemia, multiple myeloma, and DNA damage.⁵¹

Studies have demonstrated that glyphosate and/or Roundup cause genetic damage in human lymphocytes and liver cells; bovine lymphocytes; mouse bone marrow, liver, and kidney cells; fish gill cells and erythrocytes; caiman erythrocytes; tadpoles; sea urchin embryos; fruit flies; root-tip cells of onions; and in Salmonella bacteria.⁵¹

Other studies have shown that it causes oxidative stress, cell-cycle dysfunction, and disruption to RNA transcription, all of which can contribute to carcinogenicity.⁵¹

In 2001, 200 cases of cancer were reported in the Argentinean village of Ituzaingo which has 5000 residents. By 2009 there were 300, 41 times the national average. The community has also seen many malformed babies born. After documenting the tragedies, a group took their case to court. In 2006, the provincial Supreme Court ruled toprohibit the use of agrochemicals within 1000 metres of residential areas in the province of Cordoba.[124]

7.7 - Other health impacts

There is emerging evidence that glyphosate can affect the nervous system, and in particular areas of the brain associated with Parkinson’s disease. In one case study glyphosate exposure was linked to ‘symmetrical parkinsonian syndrome’. An epidemiological study of children identified a link with Attention-Deficit/ Hyperactivity Disorder (ADHD). Under other effects, a PANAP report says: “Glyphosate damages liver cells and interferes with a number of enzymes important in metabolism.”⁵¹

Jasper et al (2012)[125] found exposure to Roundup, even at low doses and for a relatively short period of time, can induce serious hepatic and haematological damage. Long-term exposure from contaminated soil or water, even at low concentrations, can lead to serious human health problems, including liver damage, anaemia, and conditions associated with ROS, such as different types of cancer and neurodegenerative diseases.

A 2013 study found the effects of pure glyphosate on estrogen receptors mediated transcriptional activity and their expressions. Results indicated that low and environmentally relevant concentrations of glyphosate possessed estrogenic activity, in particular causing the growth of breast cancer cells, and there was an additive estrogenic effect between glyphosate and genistein, a phytoestrogen in soybeans.[126] Brief exposure to a Brazilian glyphosate formulation caused liver damage in rats the researchers concluded indicated irreversible damage to liver cells. [127] [128]

A 2013 review paper on glyphosate prepared for the Scottish Parliament can be viewed on http://www.gmwatch.org/index.php/news/archive/2013/15047-glyphosate-destructor-of-human-health-and-biodiversity. The findings detail the impact of glyphosate on human health and the environment.

As of April 2014, despite such findings of adverse, or at least questionable, effects, there remains no official monitoring of the consequences to the human population ingesting transgenes or from glyphosate-based herbicides, and consumers have no official notification of risks.

8 - Glyphosate – the conclusion

Glyphosate may be one of the most biologically disruptive chemicals in the human and physical environment, in part because of its wide range of effects at the cellular level and in part because the extraordinary extent of its use and its insertion into our daily diet means constant exposure to it of virtually everyone. The range of diseases now associated with glyphosate-based herbicides should ring alarm bells. Their biological effects are primary. Virtually every bodily system can be adversely affected.

In their study, researchers Anthony Samsel and Stephanie Seneff state¹²²:

“Our systematic search of the literature has led us to the realization that many of the health problems that appear to be associated with a Western diet could be explained by biological disruptions that have already been attributed to glyphosate. These include digestive issues, obesity, autism, Alzheimer’s disease, depression, Parkinson’s disease, liver diseases, and cancer, among others.

“While many other environmental toxins obviously also contribute to these diseases and conditions, we believe that glyphosate may be the most significant environmental toxin.”

The toxic effects of glyphosate take a considerable time to manifest overtly and no health or regulatory body is officially looking for what effects may have occurred, making it easy to claim glyphosate is not harmful, and allow usage and sales to continue.

There is no need to take risks with glyphosate-resistant transgenic crops when there already exists effective, sustainable solutions to the problems that this novel technology is claimed to address. Conventional plant breeding, in some cases helped by safe modern technologies like gene mapping and marker assisted selection, continues to outperform genetically engineered crops in producing high-yield, drought-tolerant, and pest- and disease-resistant plants that can meet present and future food needs.[129]

Agro-ecological methods of farm management render the use of glyphosate redundant. Numerous methods exist to manage weeds without recourse to chemicals that undermine both human health and ecological stability.

Physicians and Scientists for Global Responsibility New Zealand Charitable Trust

March 2015

Reviewed by Meriel Watts, PhD; Coordinator Pesticide Action Network Aotearoa NZ

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Further material

‘Introducing Glyphosate, the world’s biggest selling herbicide’, Friends of the Earth Europe, June 2013 http://www.foeeurope.org/sites/default/files/press_releases/foee_1_introducing_glyphosate.pdf

GeneWatch UK and Greenpeace International maintain a register of documented releases of transgenic organisms and contaminated foodstuffs on www.gmcontaminationregister.org.

‘Who Owns Nature? Corporate Power and the Final Frontier in the Commodification of Life’ on www.etcgroup.org/sites/www.etcgroup.org/files/publication/707/01/etc_won_report_final_color.pdf.

Glyphosate Effects on Crops, Soils, Animals and Consumers, Europe – UK 31 October 2011, Don M Huber, Emeritus Professor of Plant Pathology, Purdue University, Lafayette, IN, http://www.nvlv.nl/downloads/Powerpoint_presentatie_lezing_Don_Huber_25_okt_2011.pdf

‘Glyphosate: The Elephant in the Room’ a power-point presentation http://people.csail.mit.edu/seneff/, scroll down and click on “(Powerpoint Slides) (PDF Version)”.

‘Glyphosate poisoning’, Bradberry et al, 2004, Toxicol Rev. 2004;23(3):159-67 http://www.ncbi.nlm.nih.gov/pubmed/15862083

US National Pesticide Information Centre http://npic.orst.edu/factsheets/glyphotech.html and

US Environmental Protection Agency - Technical Factsheet on: GLYPHOSATE

http://www.epa.gov/safewater/pdfs/factsheets/soc/tech/glyphosa.pdf

Glyphosate fact sheet - Pesticide Action Network UK http://www.pan-uk.org/pestnews/Actives/glyphosa.htm

Glyphosate Facts 2013 Industry Task Force on Glyphosate http://www.glyphosate.eu/glyphosate-basics/what-glyphosate

Avoiding Glyphosate Resistance in New Zealand, A Ministry for Primary Industries Sustainable Farming Fund Project - http://www.groundworkassociates.co.nz/glyphosate/

NZ Grassland Association www.grassland.org.nz/ ‎

Human contamination by glyphosate, Friends of the Earth Europe, June, 2013

http://www.foeeurope.org/sites/default/files/publications/foee_4_human_contamination_glyphosate.pdf

Glyphosate Factsheet - Critical Habitat Project of the Centre for Ethics and Toxics: http://environmentalcommons.org/glyphosate.pdf

World Health Organisation - Chemical hazards in drinking-water - glyphosate and AMPA

http://www.who.int/water_sanitation_health/dwq/chemicals/glyphosate/en/

Organic Consumers Association Comments on New Study Showing Glyphosate Found in Mothers' Breast Milk, 7 April 2014, http://www.organicconsumers.org/articles/article_29697.cfm

Food and Agriculture Organization of the UN - GLYPHOSATE N-(phosphonomethyl)glycine) http://www.fao.org/fileadmin/templates/agphome/documents/Pests_Pesticides/Specs/glypho01.pdf

Sierra Club Canada – Glyphosate N-(phosphonomethyl)glycine

http://www.sierraclub.ca/national/programs/health-environment/pesticides/glyphosate-fact-sheet.shtml

Glyphosate-tolerant crops in the EU, pub. 30 October 2012, compiled by agricultural economist Dr Charles Benbrook for Greenpeace http://www.greenpeace.org/international/en/publications/Campaign-reports/Genetic-engineering/Glyphosate-tolerant-crops-in-the-EU/

Appendix Two

Alternative non-chemical weed management

There is a need to develop effective and sustainable methods for weed control that address the needs of territorial authorities and the public.

1 - Alternative methods to conventional herbicide application technologies – major areas

Saturated super-heated steam and hot water are cost effective and environment-friendly. They can be used in practically all weather conditions and are safe to be used in close proximity of children, adults, shops, and wildlife.

They are methods used successfully by a number of New Zealand Councils in urban and rural areas.

A study which looked at thermal weed control compared with the herbicide glyphosate on the efficacy of weed kill found hot water was equally as effective as glyphosate.[130]

In Auckland, hot water control of roadside vegetation costs no more than glyphosate-based herbicides.

Salt - Killing weeds with readily available salt is effective and inexpensive. Salt dehydrates plants, disrupts the internal water balance of plant cells, and makes ground unsuitable for future plant growth.

Dunedin City Council treats weeds on footpaths, kerbs and channels with salt water.

Mowing - turn areas of noxious and invasive plants into mowable areas suitable for re-vegetation

Weeds for erosion and weed control work – some weeds left to grow in gullies can reduce the risk of erosion, exclude other weeds, and act as a nursery for native tree regeneration. .

Non-spray techniques[131] for selective weed control in ecologically sensitive areas or in dense bush canopies where potential for collateral damage with foliar applications of herbicides:

*Simultaneous application of herbicidal gels to cut stems of shrubs and saplings during pruning;

*Rolling herbicidal gels onto crushed plants;

*Injection of herbicidal gels or solutions into rhizomes, bulbs, corms or fibrous tissue;

*Pressure-injection of herbicide solutions or pathogens into trunks of trees.

2 - Alternative methods to conventional herbicide application technologies – small, specialist areas

Hand weeding in special areas where only unwanted plants need to be removed. It can be done with tools such as weed-eaters and grubbers, or by digging up the weeds by hand. Some weeds can sprout from fragments, so all plant material (including roots) should be removed from the site.[132]

For some species, vegetation should be tied in light-proof bags to rot for 12-18 months before adding to compost, or they can be dried and/or incinerated.

Weed mats to stop weed germination; either as a blanket cover over an entire area or as one square metre around individual plants. Use natural fibre carpet or woollen weed matting as natural materials help to retain moisture and offer control. Polythene is not biodegradable, has to be removed after the plants have grown, and prevents rain from penetrating the soil.
Mulch - spread organic material at least 100mm thick around the base of plants to prevent weed invasion and to stop soil drying out. Mulch helps retain moisture and provides long-term weed control. Ideal mulch materials are bark and untreated sawdust. Add fertiliser as the mulch decomposition process takes nitrogen from the soil.

For more information on non-chemical weed control, visit the Weed Management Advisory at https://weedmanagementadvisory.wordpress.com/.

What are New Zealand Councils doing?

The former Auckland and North Shore City Councils had successful non-chemical management of roadside vegetation for many years. Auckland Council has adopted a Weed Management Policy in which herbicides are supposed to be used only as a last resort. Auckland Transport has maintained non-chemical vegetation management in most of those areas in which it was previously used, with a variety of methods, including hot water, steam, plant-based herbicides (pine oil, coconut oil, palm oil), weed eaters; but appears to have ideological problems rolling it out to the rest of the region.

Waiheke Island Local Board and its advisory panel for weed management have called for non-chemical vegetation management on the island.

Waiheke’s Eco-village has undertaken massive native bush and wetland restoration over 20 years without any use of herbicide.[133]

Taupo District Council has reduced the use of chemicals by an average of approximately 30 percent per year since 2006. TDC reserves the right, through the Council resolution process, to identify areas under its jurisdiction that are to be “No-Spray” geographical areas.[134]

Falling within Council areas

KiwiRail controls weeds and reduces infestations with guidance from Regional Councils[135], which may be able to effectively install no-spray policies.

NZ Transport Agency maintains roads only that are part of the state highway network.[136] It undertakes to control plant pests in accordance with regional plant pest management strategies and within its road reserve boundaries. Chemical herbicides used include the active ingredients glyphosate, metsulfuron, terbuthylazine and triclopyr.

The Department of Conservation offers:

http://www.doc.govt.nz/getting-involved/run-a-project/restoration-advice/weed-control/

http://www.doc.govt.nz/getting-involved/run-a-project/restoration-advice/weed-control/control-methods/

http://www.doc.govt.nz/getting-involved/run-a-project/our-procedures-and-sops/biodiversity-inventory-and-monitoring/

[1] For example: ‘Glyphosate-Based Herbicides Produce Teratogenic Effects on Vertebrates by Impairing Retinoic Acid Signaling’, Paganelli et al, Chem. Res. oxicol., 2010, 23 (10), pp 1586–1595 DOI: 10.1021/tx1001749, August 9, 2010, http://pubs.acs.org/doi/abs/10.1021/tx1001749. *Roundup and birth defects: Is the public being kept in the dark? Earth Open Source, 2011, http://www.scribd.com/doc/57277946/RoundupandBirthDefectsv5. *‘Differential Effects of Glyphosate and Roundup on Human Placental Cells and Aromatase’, Richard et al Environ Health Perspect. Jun 2005; 113(6): 716–720. Feb 25, 2005. doi: 10.1289/ehp.7728 PMCID: PMC1257596 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1257596/.* ‘Pre- and postnatal toxicity of the commercial glyphosate formulation in Wistar rats’, Dallegrave et al, Arch Toxicol. 2007 Sep;81(9):665-73. Epub 2007 Jul 19. http://www.ncbi.nlm.nih.gov/pubmed/17634926

[2] ‘Pesticides in Mississippi air and rain: a comparison between 1995 and 2007,’ Majewski et al, Environ Toxicol Chem. 2014 Jun;33(6):1283-93. doi: 10.1002/etc.2550. Epub 2014 Apr 4. http://www.ncbi.nlm.nih.gov/pubmed/24549493. See page 5 of this PSGR document.

[3] ‘Carcinogenicity of tetrachlorvinphos, parathion, malathion, diazinon, and glyphosate’, Guyton et al, published online, 20 March 2015 DOI: http://dx.doi.org/10.1016/S1470-2045(15)70134-8. The assessments will be published as volume 112 of the IARC Monographs (http://monographs.iarc.fr; monographs identifying environmental factors that can increase the risk of human cancer. National health agencies can use this information as scientific support for their actions to prevent exposure to potential carcinogens. Since 1971, more than 900 agents have been evaluated, of which more than 400 have been identified as carcinogenic, probably carcinogenic, or possibly carcinogenic to humans.

[5] http://en.wikipedia.org/wiki/Glyphosate.

[6] http://en.wikipedia.org/wiki/John_E._Franz. See early patent applications by scrolling down to Patents and/or see http://www.google.com/patents/US3799758. See also http://www.greenpeace.de/fileadmin/gpd/user_upload/themen/pat ente_auf_leben/greenpeace_patente_von_monsanto_englisch.pdf ‘Monsanto’s Patents: A List of seed monopolies’

[7] http://en.wikipedia.org/wiki/Monsanto and http://www.frost.com/prod/servlet/market-insight-print.pag?docid=JEVS-5N2CZG

[8] http://www.monsanto.com/newsviews/pages/roundup-ready-patent-expiration.aspx. For Monsanto Company patents see http://www.monsanto.com/products/pages/product-patents.aspx.

[9] Stephen O. Duke and Stephen B. Powles (2008) Glyphosate: a once-in-a-century herbicide: Mini-review. Pest Management Science Pest Manag Sci 64:319–325. http://en.wikipedia.org/wiki/Glyphosate. US EPA 2007 Pesticide Market Estimates, http://www.epa.gov/opp00001/pestsales/07pestsales/usage2007_2.htm#3_6 and http://www.epa.gov/opp00001/pestsales/07pestsales/usage2007_3.htm#3_7

[10] https://archive.org/details/GlyphosateMarketGlobalIndustryAnalysisSizeShareGrowthTrendsAndForecast2013-2019 and http://www.economist.com/node/14904184

[11] http://www.google.co.uk/patents/US7771736, Invented by William Abraham, Original Assignee Monsanto Technology Llc.

[12] http://www.huffingtonpost.com/2011/06/24/roundup-scientists-birth-defects_n_883578.html

[13] http://www.huffingtonpost.com/2013/04/25/roundup-herbicide-health-issues-disease_n_3156575.html?utm_hp_ref=mostpopular

[14] http://news.agropages.com/News/NewsDetail---11886-e.htm

[15] http://www.dailymirror.lk/news/44366-glyphosate-to-be-banned-in-sri-lanka.html

[16] http://en.centralamericadata.com/en/article/home/El_Salvador_Use_of_53_Chemicals_Banned

[17] ‘The agronomic benefits of glyphosate in Europe’, Monsanto Europe SA. February 2010.

[18] http://www.purdue.edu/newsroom/releases/2014/Q1/plants-use-unusual-microbial-like-pathway-to-make-essential-amino-acid.html

[19] http://www.pnas.org/content/99/18/11567.full

[20] http://www.monsanto.com/products/Pages/monsanto-agricultural-seeds.aspx. Monsanto’s transgenic Roundup Ready crops include alfalfa, canola, corn, cotton, sorghum, soybeans, sugar beets and wheat.

[21] http://npic.orst.edu/factsheets/glyphotech.pdf for detailed information on glyphosate. See http://npic.orst.edu/reg/state_agencies.html for a list of (US) products containing glyphosate and search by active ingredient.

[22] See Classification of Herbicides http://www.alanwood.net/pesticides/glyphosate.html. When glyphosate is used as an ester or salt, its identity should be stated: glyphosate-diammonium, glyphosate-dimethylammonium, glyphosate-isopropylammonium, glyphosate-monoammonium], glyphosate-potassium, glyphosate-sesquisodium, glyphosate-trimesium [81591-81-3].

[23] http://npic.orst.edu/factsheets/glyphotech.pdf. See also http://npic.orst.edu/reg/state_agencies.html for US products containing glyphosate (search ‘active ingredient’) and http://npic.orst.edu/factsheets/glyphotech.pdf for more on glyphosate.

[24] ‘Major pesticides are more toxic to human cells than their declared active principles’, Mesnage et al, http://www.hindawi.com/journals/bmri/aip/179691/

[25] ‘Glyphosate commercial formulation causes cytotoxicity, oxidative effects, and apoptosis on human cells: differences with its active ingredient’, Chaufan et al, Int J Toxicol. 2014, PMID: 24434723 http://www.ncbi.nlm.nih.gov/pubmed/24434723?dopt=Abstract

[26] http://www.panap.net/sites/default/files/monograph_glyphosate.pdf

[27] Mesnage R, Defarge N, Spiroux de Vendômois J, Séralini G-E. Major pesticides are more toxic to human cells than their declared active principles. Biomedical Research International, 2014. http://www.hindawi.com/journals/bmri/aip/179691/

[28] http://extension.psu.edu/pests/weeds/control/adjuvants-for-enhancing-herbicide-performance

[29] http://www.agroconsultasonline.com.ar/ticket.html/ucsu2062205591998internet.pdf?op=d&ticket_id=4874&evento_id=9969

[30] ‘Foliar-applied glyphosate substantially reduced uptake and transport of iron and manganese in sunflower (Helianthus annuus L.) plants’, Eker et al, J Agric Food Chem. 2006 Dec 27;54(26):10019-25, http://www.ncbi.nlm.nih.gov/pubmed/17177536.‘Relevance of glyphosate transfer to non-target plants via the rhizosphere[, Tesfamariam, Bott, Cakmak, Römheld, Neumann, Euro J Agro 31 (2009), http://wyofile.com/wp-content/uploads/2011/07/2009_Glyphosate_Rhizosphere_Waitingtimes_Bindingformsinsoils_Tesfamariamaetal.pdf

[31] ‘Glyphosate, hard water and nephrotoxic metals: are they the culprits behind the epidemic of chronic kidney disease of unknown etiology in Sri Lanka?’ Jayasumana C1, Gunatilake S2, Senanayake P3. Int J Environ Res Public Health. 2014 Feb 20;11(2):2125-47. doi: 10.3390/ijerph110202125. http://www.ncbi.nlm.nih.gov/pubmed/24562182

[32] ‘The effect of dissolved glyposate upon the sorption of copper by three selected soils’, Morillo et al, December 2001. Chemosphere, Volume 47, Issue 7, May 2002, Pages 747–752, http://dx.doi.org/10.1016/S0045-6535(01)00338-1. http://www.sciencedirect.com/science/article/pii/S0045653501003381.

[33] ‘Glyphosate Interactions with Physiology, Nutrition, and Diseases of Plants: Threat to Agricultural Sustainability?’ Cakmak et al, European Journal of Agronomy, Volume 31, Issue 3, October 2009, Pages 114–119, http://www.sciencedirect.com/science/article/pii/S1161030109000665

[34] ‘Glyphosate reduced seed and leaf concentrations of calcium, manganese, magnesium and iron in non-glyphosate resistant soybean, Cakmak et al. http://research.sabanciuniv.edu/13147/1/2009_Glyphosate_reduced_seed_and_leaf_concentrations_of_calcium_etc.pdf

[35] National Pesticide Information Centre Technical Factsheet on: GLYPHOSATE http://npic.orst.edu/factsheets/glyphogen.pdf

[36] http://www.epa.gov/fedrgstr/EPA-PEST/1997/April/Day-11/p9231.htm

[37] Summary of Monsanto petition is on http://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPP-2012-0132-0009.

[38] http://maps.thefullwiki.org/Glyphosate

[39] Botta F, Lavison G, Couturier G, Alliot F, Moreau-Guigon E, Fauchon N, Guery B, Chevreuil M, Blanchoud H (September 2009). "Transfer of glyphosate and its degradate AMPA to surface waters through urban sewerage systems". Chemosphere 77 (1): 133–9. doi:10.1016/j.chemosphere.2009.05.008. PMID 19482331. http://www.sciencedirect.com/science/article/pii/S0045653509005852

[40] "Registration Decision Fact Sheet for Glyphosate (EPA-738-F-93-011)" United States Environmental Protection Agency. 1993.

[41] http://npic.orst.edu/factsheets/glyphotech.html

[42] US EPA 1993

[43] Ecotoxicology and Environmental Safety, Volume 18, Issue 2, October 1989, Pages 230–239 ‘Influence of climatic and edaphic factors on persistence of glyphosate and 2,4-D in forest soils’ Torstensson et al, www.sciencedirect.com/science/article/pii/0147651389900845

[44] http://www.env-health.org/news/latest-news/article/new-french-law-will-ban-non

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[47] ‘An integrated approach to evaluate the impacts of the herbicides glyphosate, 2,4-D and metsulfuron-methyl on soil microbial communi-ties in the Pampas region, Argentina’ Zabaloya et al (2008) http://www.sciencedirect.com/science/article/pii/S092913930800036X

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[52] http://www.ianrpubs.unl.edu/epublic/live/g1484/build/

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[56] ‘The Rise of Superweeds—and What to Do About It’ Union of Concerned Scientists USA

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[57] www.gene.ch/genet/2000/Feb/msg00053.html

[58] http://css.cals.cornell.edu/extension/cropping-up-archive/wcu_vol12n06-2002a1mesotrione.pdf

[59] http://cropwatch.unl.edu/web/cropwatch/archive?articleID=4669108

[60] ‘Resistance to HPPD-inhibiting herbicides in a population of waterhemp (Amarathus tuberculatus) from Illinois, United States’, Hausman NE et al, Pest Manag Sci. March 2011;67(3): 258-61, epub Jan 262011, www.ncbi.nlm.nih.gov/pubmed/21308951

[61] http://cornandsoybeandigest.com/ag-issues/glyphosate-resistance-rising-0201.

[62] http://www.weedscience.org/summary/home.aspx,http://www.weedscience.org/summary/MOA.aspx?MOAID=12,

[63] ‘Explosion Threatens Monsanto Heartlands France,’ 2 May 2009, www.scoop.co.nz/stories/WO0905/S00064.htm; “'Superweed' explosion threatens Monsanto heartlands,” 9 April 2009, www.france24.com/en/20090418-superweed-explosion-threatens-monsanto-heartlands-genetically-modified-US-crops, http://tiny.cc/vTMid; ‘Monsanto's GM crops spawning superweed epidemic in US.’ www.organicconsumers.org/articles.

[64] Genetically Engineered Backslide: The Impact of Glyphosate-Resistant Palmer Pigweed on Agriculture in the United States, © Edward Hammond 2010, http://www.twnside.org.sg/title2/biosafety/pdf/bio12.pdf

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[91] ‘Mexican Judge Throws out Monsanto Appeal to Confirm GM Maize Ban’, 30 December 2013, Sustainable Pulse

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[96] Percy Schmeiser Wikipedia various

[97] http://en.wikipedia.org/wiki/Bowman_v._Monsanto_Co.

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[103] Powles (2008) Glyphosate: a once-in-a-century herbicide, Pest Manag Sci 64: 319-325 http://onlinelibrary.wiley.com/doi/10.1002/ps.1518/abstract

[104] See http://en.wikipedia.org/wiki/Glyphosate for trade names. Those other ingredients can make the product more toxic.

[105] National Pesticide Information Centre, General Fact Sheet, Glyphosate http://npic.orst.edu/factsheets/glyphogen.pdf

[106] ‘Pesticide Roundup provokes cell division dysfunction at the level of CDK1/cyclin B activation’. Marc et al, 2002, Chem Res Toxicol. 2002 Mar;15(3):326-31. http://www.ncbi.nlm.nih.gov/pubmed/11896679. Glyphosate-based herbicides are toxic and endocrine disruptors in human cell lines’, Gasnier et al, 2009, Toxicology 262 (2009) 184–191, http://www.gmoseralini.org/wp-content/uploads/2013/01/Gasnieral.TOX_2009.pdf

[107] ‘Glyphosate-Based Herbicides Produce Teratogenic Effects on Vertebrates by Impairing Retinoic Acid Signaling’, Paganelli et al, Chem. Res. Toxicol., 2010, 23 (10), pp 1586–1595 DOI: 10.1021/tx1001749, Copyright © 2010 American Chemical Society, http://pubs.acs.org/doi/abs/10.1021/tx1001749

[108] http://www.foeeurope.org/sites/default/files/press_releases/foee_1_introducing_glyphosate.pdf

[109] Honeycutt Z, Rowlands H. 2014. Glyphosate Testing Report: Findings in American Mothers’ Breast Milk, Urine and Water. Moms across America and Sustainable Pulse. http://www.momsacrossamerica.com/glyphosate_testing_results. See 100 for bioaccumulation.

[110] Anadón et al 2009

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[112] ‘The effect of metabolites and impurities of glyphosate on human erythrocytes (in vitro)’, Marta Kwiatkowskaa, Bogumiła Hurasb, Bożena Bukowskaa, Pesticide Biochemistry and Physiology, Volume 109, February 2014, Pages 34–4,3http://dx.doi.org/10.1016/j.pestbp.2014.01.003.

[113] Benachour and Séralini, University of Caen, Laboratory Estrogens and Reproduction, France, Chem. Res. Toxicol., 2009, 22 (1), pp 97–105 DOI: 10.1021/tx800218n, © 2008 American Chemical Society http://pubs.acs.org/doi/abs/10.1021/tx800218n

[114] ‘Glyphosate Exposure in a Farmer’s Family’, Mesnage et al, 2012, Journal of Environmental Protection, Vol. 3 No. 9 (2012) , Article ID: 22645, DOI:10.4236/jep.2012.39115. http://file.scirp.org/Html/3-6701610_22645.htm

[115] E. W. Wong and C. Y. Cheng, “Impacts of Environmental Toxicants on Male Reproductive Dysfunction,” Trends in Pharmacological Sciences, Vol. 32, No. 5, 2011, pp. 290- 299. doi:10.1016/j.tips.2011.01.001, http://www.ncbi.nlm.nih.gov/pubmed/21324536.

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‘Occupational Exposure of Forest Workers to Glyphosate during Brush Saw Spraying Work,’ Jauhiainen et al, American Industrial Hygiene Association Journal, Vol. 52, No. 2, 1991, pp. 61-64. doi:10.1080/15298669191364334, http://oeh.tandfonline.com/doi/abs/10.1080/15298669191364334?queryID=%24{resultBean.queryID}&#.U1bO-KKVrSM

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Several past members have greatly contributed to PSGR, and their biographies are listed below.

Dr Mike Godfrey (1938-2024)

Mike Godfrey qualified LRCP.MRCS (England) and MBBS (London) in 1963. He joined a General Practice in Mt Maunganui, New Zealand in 1971, after seven years in various hospital posts in England. He left general practice in 1986 to establish an environmental health and chelation clinic in Tauranga.

Dr Godfrey is a founding member and past-President of the NZ Academy of Oral Medicine and Toxicology, and a Clinical Associate of the Graduate School of Integrative Medicine, Swinburn University, Melbourne.

Established the Bay of Plenty Environmental Health Clinic (1986), which operates in 2024 as Clinical Thermography NZ.

Post-graduate qualifications and appointments:

1989 Diploma American Board of Chelation Therapy. Recertified 1994,1999
1991 Fellow of American College of Advancement in Medicine (FACAM)
1996 Fellow of Australasian College of Nutrition and Environmental Medicine (FACNEM)
2000 Clinical Associate (visiting lecturer) Swinburne University, Melbourne
2003 Board member of International Board of Clinical Metal Toxicology

Conference presentations:

Dr Godfrey has presented 14 clinical papers at post-graduate medical conferences in America, Australia, Germany, India and New Zealand between 1989 and 2007. He was a lecturer for chelation and heavy metal toxicity at Fellowship training courses for the ACNEM, Melbourne, 1998-2004, and Auckland Medical School GP CME training in 1999.

Dr Godfrey published widely on environmental toxicology and therapeutic interventions to reverse symptoms. A major focus concerned dental amalgam and mercury poisoning, and increasing evidence that environmentally relevant levels of mercury could promote conditions chronic fatigue, depression and memory loss.

Link to Dr Godfrey's publications/CV.

Dr Godfrey was an early adopter of infra-red breast thermal imaging (thermography) technology, importing a $40,000 American system using a Military-developed Infra-red camera and proprietary software some 20 years ago. Breast thermal imaging or thermography started over 100 years ago as a non-touch and non-invasive method of potential early detection of breast cancer. As of 2024, some 9,000 women (and some men) had elected to include thermography as part of their breast health monitoring strategy. In 2023, publishing a review of the Bay of Plenty based clinic's work:

Godfrey, M. and Godfrey, P. (2023) Breast Thermography: A 20-Year Retrospective Review of Infra-Red Breast Thermal Imaging in New Zealand and Its Potential Role in Breast Health Management. Advances in Breast Cancer Research , 12, 129-141. DOI: 10.4236/abcr.2023.124010

Assoc Prof Peter Wills.

Theoretical Biologist in the Department of Physics, University of Auckland.

BSc in Chemistry and Biochemistry in 1973. PhD in Biochemistry in 1977. Held full time positions at a variety of leading overseas institutes.

Dr Wills’ most recent research has been concerned with the early stages of biological evolution, especially the origins of genetic coding and biological information processing. Some of his collaborative research work into prions - the infectious agents active in transmissible spongiform encephalopathies - has involved the contained laboratory use of microbial genetic engineering for gene amplification and functional protein analysis.

In 2022 Dr Wills and colleagues commenced research to explore the theory that RNA and peptides – chains of amino acids that are essentially smaller and simpler versions of proteins – evolved together to create the first genetic code.

He has published widely in the international scientific literature covering a number of different fields: biochemistry, theoretical physics, molecular genetics and complexity theory.

Since the mid-1980s, Dr Wills has written and spoken extensively about genetic engineering, both in New Zealand and abroad. His analysis has been published internationally. He was an invited speaker at the 1994 Third World Network Conference in Penang that resulted in the scientists’ statement, “The Need for Greater Regulation and Control of Genetic Engineering” and in 1999 he was the only foreign invitee to the first Australian Consensus Conference on “Gene Technology in the Food Chain.”

He was a Witness to the Royal Commission on Genetic Modification on behalf of PSRG and a number of other New Zealand organisations. He has also been a Witness on genetic engineering to the Waitangi Tribunal.

Dr Wills was Co-founder of Scientists Against Nuclear Arms (1983), and Chair of Greenpeace New Zealand (1993-1996).

Dr Wills held a trustee position until 2020

Links:

University of Auckland profile.

Google Scholar

How did life on Earth begin? This scientist will test a novel theory

Dr Elizabeth Harris

MBChB, Dip.Obs, Cert. NZ Sports Med., Cert. Proficiency Child Health, Cert. Family Planning, Dip. Musculoskeletal Med., FRNCGP. General Practitioner, Trustee PSGR. Region: Otago

Dr Harris trained in Dunedin, completing her MBChB in 1991. Dr. Elizabeth Harris has worked in general practice for 20 years and holds further qualifications in complimentary health and functional medicine. Her organisation, The Brain Health and Biofeedback Clinic assists patients with brain health measures and interventions to manage Traumatic Brain Injury (TBI), Fibromyalgia, Posttraumatic Stress Disorder (PTSD) and chronic unexplained illness,. Elizabeth Harrris held a trustee position 2009-2020

Dr Robert Anderson

Sadly, Robert Anderson (Bob) died on 5 December 2008.

In recognition of his decade of service to PSGR, and to many other organisations, PSGR hosts his public lectures. Other work and lectures can be found on www.connected.gen.nz, sponsored by The Blase Company, Auckland.

In 2010, Amnesty International Tauranga Moana established the Robert Anderson Memorial Award to honour the contribution Bob made to Peace, Human Rights and Social Justice. It is presented annually to a recipient equally committed to these issues. Read more on https://www.connected.gen.nz/robert-anderson-memorial-award.

Robert Anderson held a combined honours degree in Physics and Chemistry, and a PhD in Science Education.

Prior to taking his degree, Robert worked at the University of Birmingham, England, as a research technician in the Department of Biochemistry, under Dr John Teal from the University of Cambridge, studying fluorescence of proteins in neutral solution. He also worked under Professor Brian Perry from the University of Cambridge, investigating the actin/myosin relationship in muscle protein.

Robert and his wife, Jean, emigrated to New Zealand in 1968, where Robert taught Chemistry, Physics, Laboratory Technology and Nuclear Medicine at tertiary level.

In retirement, Robert gave public lectures on genetic engineering, other scientific and environmental issues, and peace and social justice, in support of the public’s right to be independently informed. He authored eleven books, including two co-authored with Dr Mike Godfrey, Director of the Bay of Plenty Environmental Health Clinic, Tauranga. He contributed regularly to New Zealand periodicals.

Robert was a Trustee of PSRG from its inception as a Charitable Trust and change of name to PSGR.

In 2010, Amnesty International Tauranga Moana established the Robert Anderson Memorial Award to honour the contribution that its member, Robert (Bob) Anderson, had made to Peace, Human Rights and Social Justice.

You can find out more on http://connected.gen.nz/robert-anderson-memorial-award.

Dr John R Clearwater

Researcher and consultant. John Clearwater was a founding member of PSRG in 1998, and one of six initial Trustees. Ill health forced John to relinquish his Trusteeship in 2008. It was with sadness we accepted his resignation. John has consistently made valid contributions and supported PSRG. We will miss his involvement and commitment, and especially his sense of humour. Keep well in the future, John.

Dr John Clearwater has a PhD from the University of Alberta, Edmonton, Canada, and a BSc and MSc from Massey University, Palmerston North, New Zealand. He is the principal scientist at Clearwater Research and Consulting.

From 1975 to 1979, Dr Clearwater carried out ecological research on the sorghum shoot fly at the International Centre of Insect Physiology and Ecology in Nairobi, Kenya.

In 1979, he returned to New Zealand and joined the DSIR, transferring in 1992 to Hort Research.

During his career, Dr Clearwater developed a method of controlling codling moth with pheromones and in 1992 produced the first New Zealand export crop of organic apples with Tony Belcher of Waihi. After failing to convince his managers of the value of this achievement, he resigned and set up a programme of organic apple growing in the Hawkes Bay. This followed the invitation of a local grower, John Bostock, and John Mangan of Freshco. By 2001, this programme had grown to include over 50 growers and five percent of New Zealand’s apple growers. By the 2000/2001 season, the best return was $80/carton of organic Royal gala apples on the US market, compared to $8.25 (loss of $1/carton) for conventional apples. The biological insecticide Bacillus Thuringiensis is a key tool in this activity.

Dr Clearwater provided the pheromone-based monitoring system for the successful programme that eradicated the White-Spotted Tussock Moth from the suburbs of Auckland. The monitoring allowed accurate placement of the biological insecticide B. thuringiensis.

Number of referred publications: 29.

Dr A Neil Macgregor

Sadly, Neil died on 16 September 2009. He had been active in PSRG/PSGR since its inception. Neil brought a wealth of experience to the work he did, dedication, and a great sense of humour. He will be sadly missed.

Neil Macgregor was a biological scientist with primary expertise in soil biology and biochemistry, soil microbial ecology, and microbial genetics. He graduated BSc and MSc from the University of Otago (NZ) in 1961, and PhD from Cornell University (USA) in 1968.

Dr Macgregor held both teaching and/or research positions at Cornell University, the University of Arizona in Tucson, the University of Wisconsin in Madison, the International Atomic Energy Agency (IAEA) in Vienna, the Institut National de la Recherche Agronomique (INRA) in Montpellier, Makerere University in Kampala, Uganda, and Massey University, Palmerston North (Tiritea Campus), New Zealand. From 1991-99 he was an academic member of the University Council of Massey University, and was national Vice President and President of the Association of University Teachers in New Zealand (AUTNZ) from 1985-1989.

Dr Macgregor had relevant research experiences in soil biological processes and land-use systems including biological nitrogen fixation and transformations in both terrestrial and aquatic natural environments, land disposal of rural and urban waste streams, soil and water quality, and the experimental use of reporter genes in soil microbial ecology studies.

Specific research interests included the biological decomposition of herbicides, the role and soil persistence of microbial inoculants in biological nitrogen fixation and sulphur oxidation, biochemical transformations of nitrogen and carbon in soil and aquatic environments, and the use of reporter genes in soil microbial ecology. He had ongoing major interests in soil biology and ecotoxicology, microbial ecology of land-use systems, as well as in the animal health industry, anthropogenic stresses of soil biological activity, and sustainability of land-use systems.

Dr Macgregor authored/co-authored over 70 refereed publications and conference papers. He contributed the chapter ‘Footprints of Genetic Engineering in Agriculture’ to Designer Genes and frequently addressed community groups on the effects of transgenic crops on soil biology, and on further soil research in the organic and vermiculture industries.

He was a Trustee of Physicians and Scientists for Responsible Genetics and Co-Editor of the digital publication, Journal of Organic Systems.

Neil Macgregor was a founder of the Journal for Organic Systems and a tribute to him and his work can be found on http://www.organic-systems.org/journal/Vol_4(1)/pdf/01-03_Neil_Macgregor_Appreciation_Hill.pdf.

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PSGR was established at around the same time the Human Genome Project (HGP) mapped the human genome. HGP data showed us that genetic heredity played a much smaller role in driving health and disease than previously presumed and that often dozens if not hundreds of genes might play a role in disease aetiology.

More frequently, poor nutrition or environmental stressors could provide a greater 'tipping point' into disease or syndrome states via toxic exposures; the alteration for example, of microbiome function; and/or alteration of gene expression.

Despite the insight that was gained from the HGP - genetic and molecular research for medicine or for industrial or agricultural applications trumps research exploring the complex drivers of disease - in humans or in agriculture. Research exploring the environmental drivers of health and disease remains low priority, even as technologies that could shed light on environmental and genetic drivers of disease have advanced.

Humans are exposed to an unprecedented array of exposures from conception. We have a far greater body-burden than our ancestors (apart from those for example, that historically worked in or lived near toxic industrial sites). The blood brain barrier often does not protect the brain from exposures, and the developing foetus often shares many of the same exposures as the mother. Pre-conception exposures can damage subsequent generations.

Almost daily, scientists are demonstrating that DNA as genetic instructions of cellular biology, are only the tip of the iceberg when discussing human (and environmental) biology, from evolution to disease development. It is now understood that a liver cell is initially the same as a fingernail cell. The development and function of all living things are not solely dependent on our genetic instructions, but on epigenetic influences that arise from environmental exposures.

(Paper 'When is a gene not DNA?' by Professor Jack Heineman)

Genes are driven by a vast array of physiological drivers – epigenetic processes, which act to modify gene expression and phenotype (physiological characteristics), turning genes on and off - and influencing how they work. The DNA or gene sequence remains unchanged. Epigenetics loosely translated, means ‘above the gene.’ Humans have one genome, and hundreds of epigenomes (Ficz 2915).

Epigenetics has been referred to as the ‘missing link between genetics, the environment, and endocrine functions’ (Zhang 2011). When a tadpole changes into a frog, the tadpole produces a surge of thyroid hormone which, as Dr Barbara Demeneix explains, turns into a series of epigenetic switches.

‘The epigenetic changes do not alter any DNA sequence, but they turn off certain genes and turn on others’ (Demeneix 2017, p.120).

In the long debate of nature versus nurture, scientists considered that our phenotype – who we are as a result of our genes and environment, was predominantly due to the influence of genes - genetic inheritance (recognised as Darwinian natural selection or Mendelian inheritance). Yet the relatively new field of epigenetics is clearly challenging this, and evidence that epigenetic traits can be inherited (without changing the gene) further muddies the (gene) pool. It is complicated, for example genetic sequences can influence subsequent developmental epigenetic events (Ficz 2015).

With this relatively new field of science, humanity doesn’t just need to know what is happening within the cell, we also need to understand what is going on in and between cells – rather than cellular biology – it’s molecular biology. Instead of acting as a closed loop within a neat biological system, our bodies constantly respond and interact to both our internal biological environment and the external environment.

The vast majority of environmental factors and toxicants do not have the ability to alter DNA sequence or promote genetic mutations. In contrast, the environment can dramatically influence epigenetic processes to alter gene expression and development. Therefore, epigenetics provides a molecular mechanism for the environment to directly alter the biology of an organism (Skinner 2014).

New mechanisms of epigenetic modifications are likely to emerge, however the

‘key mechanisms underlying epigenetic modifications include: chromatin remodeling, methylation of cytosinein CpG dinucleotides (often referred to as DNA methylation), histone tail N-terminal modification, and post-translational modification of genes regulation by non-coding/small RNA (ncRNA/sRNA). Collectively, these processes and the components upon which they act constitute the epigenome. Individually or in concert, they play a key role in turning gene expression on or off, thus facilitating or inhibiting the production of specific proteins'. (Norouzitallab et al 2019).

Of these mechanisms, methylation, which plays a key role in cellular memory, is the most studied.

The developmental origins of health and disease (DOAD)

There are specific periods (or windows) of vulnerability in developmental life stages where the foetus, and the developing child, but also teenagers, are more susceptible to toxic environmental exposures. (WHO 2008) In the first trimester of pregnancy, the foetus is most vulnerable (Demeneix 2017). The impact of environmental chemicals on fertility is also recognised (Trasande 2019).

The chemical body-burden of the mother is absorbed by the foetus. Infants and young children will frequently consume more than adults relative to their body-weight. As a result, they are exposed to higher doses (Grandjean et al 2007). Chemicals can also persist and bioaccumulate in the body (WHO UNEP 2013).

Risk from electromagnetic field (EMF) may more adversely harm the developing foetus, babies and children than adults, adversely altering growth and development. Increased brain risk may arise from babies and children having smaller skulls, thinner bone density in the skull and more embryonic stem cells. EMF exposure can decrease DNA repair, while increasing DNA damage and EMF exposure. The relationship between these effects and increased cell division in young children, suggest exposed children may be at heightened risk for cancer (Environmental Health Trust, European Parliamentary Research Service (2021)).

Prenatal and postnatal chemical exposures can alter the way genes are expressed and predispose the individual to disease in later life. The 2012 Faroes Statement advised

‘These epigenetic changes can cause lasting functional changes in specific organs and tissues and increased susceptibility to disease that may even affect successive generations’ (Grandjean et al 2012).

One of the earliest demonstrations of epigenetic influence was where mice parents’ (dams) diets were supplemented with B12, folic acid, choline and betaine. The phenotype was altered as a result, and the obese, yellow parent gave birth to brown offspring (Waterland and Jirtle 2003).

Image: James, P; Silver, M; Prentice, A (2018) Epigenetics, Nutrition, and Infant Health. In: The Biology of the First 1,000 Days. CRC Press, Boca Raton, FL, USA, p.341. ISBN 9781498756792

Epigenetic processes impact all cellular functions; however many scientists are focussing on neurodevelopmental exposures which can result in neurological damage and IQ loss. Early life epigenetic changes can influence later gene expression in the brain (Roth 2012). Neurodevelopmental damage frequently arises via endocrinologic processes. Harm from endocrine disruption from environmental chemicals including delay and IQ loss, has been estimated at as much of 2% of global GDP. (Attina et al 2016)

The environmental aetiology of disease - how environmental stressors (see Figure 22.3) shape and contribute to disease is poorly understood, and research in this area, in contrast to studies funding for the genetic causes of disease, is poorly funded (Demeneix 2017).

‘The root causes of the present global pandemic of neurodevelopmental disorders are only partly understood. Although genetic factors have a role, they cannot explain recent increases in reported prevalence, and none of the genes discovered so far seem to be responsible for more than a small proportion of cases' (Grandjean and Landrigan 2014).

Intergenerational Effect

Science is very clear that a wide range of chemicals not only exert epigenetic influences on the generation exposed to the particular chemical, but that these epigenetic influences can be carried through, in a process described as transgenerational epigenetic inheritance, to subsequent generations. For example, exposing a parent rat to the endocrine disrupting fungicide vinclozolin resulted in higher disease incidence in the great and great-great grand offspring (F3 and F4 generation) who were never exposed to the chemical. The transgenerational inheritance was paternally transmitted via sperm, altering non-coding RNA (Schester et al 2016) (Skinner 2014).

As such, with full awareness of the potential intergenerational consequences of harmful exposures, it is becoming rather critical to understand the ‘exposome’ - our cumulative environmental exposures over a lifetime. Epigenetic mechanisms don’t only push one way, many epigenetic modifications may be reversible.

Governments and regulators in the areas of toxicity and risk assessment are yet to address epigenetics and the potential for chemical mixtures in food and environment to adversely affect biological function.

Dedicated public funding is required to address the environmental drivers of disease, the toxic exposures and stressors (among other things) that directly influence not only the development of mutations to the DNA in our cells, but also the way chemical mixtures drive harm, damaging developmental and driving disease pathways.

This knowledge has the potential to change how civil society and governance approach non-communicable disease and how governments address health policy. It is already driving pharmaceutical enterprise, there is a burgeoning field of epigenetic medicine and therapy.

This new molecular spotlight naturally draws attention to the role nourishing food plays, complete with essential minerals and vitamins - which we can now observe acting epigenetically. However, this also explains the toll on bodies of a bad diet, stress, chemicals and toxins.

Complex chemical mixtures such as personal care products and pesticides consumed in daily lives undergo very little regulation. They are not assessed for potential to influence delicate molecular level epigenetic functioning, particularly in relation to the endocrine system (Kortencamp and Faust 2018).

Paper: When is the gene not DNA?
Professor Jack Heinemann
Lecturer in Genetics
University of Canterbury, New Zealand

When is the gene not DNA?

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References

Attina et al 2016. Exposure to endocrine-disrupting chemicals in the USA: a population-based disease burden and cost analysis. Lancet Diabetes Endocrinol 2016; 4: 996–1003

ERMA (2004) Transfer Notice. Hazardous Substances (pesticides) Transfer Notice 2004. Issue No. 72. P.1645-1718 https://www.epa.govt.nz/assets/Uploads/Documents/Hazardous-Substances/Policies/Hazardous-Substances-Pesticides-Transfer-Notice-2004.pdf

Ficz, G. (2015) New insights into mechanisms that regulate DNA methylation patterning. Journal of Experimental Biology 2015 218: 14-20; doi: 10.1242/jeb.107961

Grandjean et al 2008. The Faroes Statement: Human Health Effects of Developmental

Exposure to Chemicals in Our Environment. Basic & Clinical Pharmacology & Toxicology. 102(2):73-5. doi: 10.1111/j.1742-7843.2007.00114.x.

Grandjean, P., Landrigan, P.J. (2014) Neurobehavioural effects of developmental toxicity. Lancet Neurol. 2014:13, 330–338.

Gross L, Birnbaum LS (2017) Regulating toxic chemicals for public and environmental health. PLoS Biol 15(12): e2004814. https://doi.org/10.1371/journal.pbio.2004814

Kortenkamp and Faust 2018 Regulate to reduce chemical mixture risk. Science. Vol 361 Issue 6399. p.224-226

Norouzitallab et al 2019. Can epigenetics translate environmental cues into phenotypes? Science of the Total Environment. 647:1281-1293

Roth TL. (2012) Epigenetics of neurobiology and behavior during development and adulthood. Dev Psychobiol 2012; 54: 590–97.

Schuster A., Skinner M., and Yan W. (2016) Ancestral vinclozolin exposure alters the epigenetic transgenerational inheritance of sperm small noncoding RNAs. Environmental Epigenetics. 2016; 2(1): dvw001.

Skinner. M. (2014) Endocrine Disruptor Induction of Epigenetic Transgenerational Inheritance of Disease. Mol Cell Endocrinol. 2014 Dec; 398(0): 4–12. 2014 Jul 31. doi: 10.1016/j.mce.2014.07.019 PMCID: PMC4262585

Trasande et al 2015. Estimating Burden and Disease Costs of Exposure to Endocrine-Disrupting Chemicals in the European Union. J Clin Endocrinol Metab, April 2015, 100(4):1245–1255doi: 10.1210/jc.2014-4324 http://press.endocrine.org/doi/pdf/10.1210/jc.2014-4324

Trasande et al 2016. Burden of disease and costs of exposure to endocrine disrupting chemicals in the European Union: an updated analysis. Andrology. 2016 Jul;4(4):565-72. doi: 10.1111/andr.12178. Epub 2016

Trasande L. 2019 Sicker, Fatter, Poorer: The Urgent Threat of Hormone-Disrupting Chemicals to Our Health and Future . . . and What We Can Do About It. Houghton Mifflin Harcourt.

Attina T, Hauser R., Sathyanarayana S., Hunt P., Bourguignon J.P., Myers J.P. , Digangi J., Zoeller R.T., Trasande L.. Exposure to endocrine-disrupting chemicals in the USA: a population-based disease burden and cost analysis. The Lancet Diabetes & Endocrinology, 2016 DOI: 10.1016/S2213-8587(16)30275-3

UN Human Rights Council. Report of the Special Rapporteur on the implications for human rights of the environmentally sound management and disposal of hazardous substances and wastes on his mission to Germany* 14 September 2016. A/HRC/33/41/Add.2

World Health Organization, United Nations Environment Programme, Inter-Organization Programme for the Sound Management of Chemicals, Bergman, Åke, Heindel, Jerrold J. et al. (‎2013)‎. State of the science of endocrine disrupting chemicals 2012. World Health Organization.

Waterland, R.A. and Jirtle R.L. (2003) Transposable Elements: Targets for Early Nutritional Effects on Epigenetic Gene Regulation. Molecular and Cellular Biology 2003; 23(15): 5293–5300.

WHO. Children are not little adults. Children's Health & the Environment, WHO Training Package for the Health Sector World Health Organization July 2008

Zhang, X., and Ho, S.M. (2011) Epigenetics meets endocrinology. Journal of Molecular Endocrinology. 46(1): R11–R32. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4071959/pdf/nihms-601840.pdf

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For over 20 years the Physicians and Scientists for Global Responsibility New Zealand Charitable Trust (PSGR) has produced reports and submitted to government Bills and Inquiries.

We’ve been extraordinarily busy over the past 2 years with our work.

This Update aims to inform members and colleagues – and act as a go-to summary of our recent work.

2022 UPDATE - PDF

As well as our recent work All PSGR’s submissions are available to the public on our Submissions pages. In addition, we are now on LinkedIn, Twitter, Odysee & Instagram.

MEMBERSHIP

Please – without your support and membership PSGR cannot do this work. We’ve kept our fees deliberately low because your membership is important to us.

MOVING FORWARD 2022+

The PSGR recognise that the perspectives that have been expressed by the PSGR from 2020 onwards will not necessarily reflect the perspectives of all trustees and all members.

However, we sincerely hope that PSGR’s perspectives are more likely to reflect the perspectives of the majority of our membership and of collegial organisations – which represents a diverse quorum of inquiring minds.

We hope that we have demonstrated a consistency to our work, that reflects and upholds the principles reflected in 20 years of research, information communications and submissions to policy

Reports and Papers

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Dr Robert Anderson

Dr A Neil Macgregor

The developmental origins of health and disease (DOAD)

Intergenerational Effect

Paper: When is the gene not DNA?Professor Jack HeinemannLecturer in GeneticsUniversity of Canterbury, New Zealand

References

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2022 UPDATE - PDF

MEMBERSHIP

MOVING FORWARD 2022+

Reports and Papers

Royal Commission

Information

Paper: When is the gene not DNA?
Professor Jack Heinemann
Lecturer in Genetics
University of Canterbury, New Zealand