Banishing Glyphosate

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Banishing Glyphosate
Glyphosate alone has also
been shown in numerous
studies to cause kidney
toxicity. Nile tilapia exposed
to glyphosate show
changes in proximal tubular
cells. Exposed juvenile
African catfish develop
haematopoietic cell death
and kidney histopathological
changes including dilatation
of Bowman’s space (a region
of the kidney involved in
the first filtration of the
blood to form urine) as well
as degenerated tubules.
Mammalian studies found
increased serum creatinine,
blood urea and reduced
kidney weight of rats fed
with glyphosate exposed
maize. Oral exposure
increases blood urea
levels and leads to renal
dysfunction in rats and dairy
cows
hard water, showing that hard water alone is not sufficient to cause CKDu. The
authors used these observations to describe the expected properties of compound
X listed below:
(a) A compound made of recently (2–3 decades) introduced chemicals to the
CKDu endemic area
(b) Ability to form stable complexes with hard water
(c) Ability to capture and retain arsenic and nephrotoxic metals and act as a “carrier”
in delivering these toxins to the kidney
(d) Possible multiple routes of exposure: ingestion, dermal and respiratory
absorption.
(e) Not having a significant first pass effect when complexed with hard water (a
phenomenon of drug metabolism, usually by the liver, whereby the concentration
of a drug is greatly reduced before it reaches the systemic circulation)
(f) Presenting difficulties in identification when using conventional analytical
methods.
Glyphosate is further implicated by the fact that it is by far the most commonly
used herbicide in Sri Lanka, with quantities of glyphosate use exceeding all
other pesticides combined.
Glyphosate forms metal complexes that bioaccumulate in the body
Glyphosate was first used as a descaling agent to clean out calcium and other
mineral deposits from pipes and boilers, aided by the chemical’s high water solubility.
Descaling agents bind to metals, making them water soluble and removable.
Its stability in water depends on a number of factors, including phosphate
which competes with glyphosate for soil absorption. Further, its binding to metals
can result in strong complexes that affect its biodegradability, with glyphosate
degradation time increasing to 7-22 years depending on pH. In water above
pH 6.5, glyphosate turns into a dianion (an anion with a -2 negative charge), suggesting
it forms metal complexes in alkaline conditions, increasing its solubility
and thus leaching deep into soils [14, 15]. Alkaline conditions are known to reduce
the weed killing capacity of glyphosate, as glyphosate-metal complexes are
stable in basic but not acidic conditions. The effects of pH are also important in
understanding the stability of the lattice structure in the acidic conditions of the
kidney, as will be explained below.
Studies using nuclear magnetic resonance (NMR) techniques shows that
glyphosate interacts with calcium, magnesium and other metals, and that the
resulting complexes become more stable with time [16, 17]. Further, the paddy
farming soil in regions endemic for CKDu are rich in metals including calcium,
magnesium, iron, nickel, chromium and cobalt. Ferric irons alter soil absorption
of glyphosate and its metabolite, AMPA (α-Amino-3-hydroxy-5-methyl-4-
isoxazolepropionic acid). This problem is confounded by the application of triple
phosphate (TSP) fertiliser to paddy fields, which have been found contaminated
with certain metal ions as well as high levels of arsenic. This leaves people highly
vulnerable from exposure to stable, toxic glyphosate-metal complexes in drinking
water. Glyphosate exposure also occurs through the skin; farmers are found
to have glyphosate in urine following spraying. Glyphosate can mix with sweat
in hot and humid climates before being absorbed through the skin. Further, Sri
Lankan farmers do not often wear protective gear to prevent respiratory exposure. Arsenic and cadmium also commonly contaminate
rice, vegetables and tobacco leaves which are often chewed along with betel leaves by Sri Lankans. This transdermal
and respiratory exposure therefore provides an additional opportunity for glyphosate to bind to nephrotoxic metals consumed in
foods and bioaccumulate in the body.
Based on previously published studies on how glyphosate forms metal complexes and matrices [14-17], the authors propose
the formation of stable glyphosate metal lattices, which can explain how glyphosate, hard water, arsenic and other nephrotoxic
metals cause kidney disease in Sri Lanka. This proposed glyphosate metal lattice, depicted in Figure 2, is based on previous NMR
studies showing the ability of hard water ions to bind to both the phosphonate and carboxyl functional groups of the glyphosate
molecule to form complexes.
It is worth noting that glyphosate’s causative role in CKDu has previously eluded researchers due to its chemical properties
including its ionic character, high polarity, high solubility in water, low volatility, insolubility in organic solvents and strong complexion
behaviour, which make it very difficult to detect in the lab.
Mechanism of glyphosate’s role in kidney disease
The glyphosate metal lattice hypothesis is supported by the observation that people who drink natural spring water do not suffer
the disease, with these waters being devoid of magnesium and calcium, making the water unable to retain glyphosate. It also
explains why regions with hard water but low levels of herbicide and chemical fertilizer are free of CKDu. Further, CKDu patients
show accumulation of metals (As and Cd) in the hair and nail samples, but low levels of urinary excretion of metals (compared
Rice at Market in Sri Lanka, photo 4Neus, Flickr
Institute of Science in Society