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Tree Injections?
Nearly all commercial avocado trees in NZ are regularly injected with a systemic fungicide in an ultimately useless attempt to maintain tree health.

Injection is standard practice
Although residue standards have been established for organic orchards, we don’t now, or ever have, used this suspect method to keep our trees healthy. As a result rather than having low residue our fruit is pronounced by many to be exceptionally tasty possibly because it has no residue at all. Naturally there is no need for this injection in the first place. Trees in good health are able to easily able to cope with this disease much like a people who have an immune system in good order. Trees cant hide from fungi spores which have a universal presence, but they can easily get on top of them in a healthy situation.
This time wasting practice is bad for trees and fruit quality





Published below for those interested is an example of the slimy machinations of the powers that be,  


    Pat Clark,                         Horticultural Consultant,                         P.O.Box 126, Whangarei     


1.    Introduction

In September 1998, Dr. Jonathan Cutting, the current Chief Executive Officer of the New Zealand Avocado Industry Council, submitted an application to BioGro NZ, on behalf of the New Zealand Avocado Growers Association, to have treatment with the substance phosphorous acid accepted as a restricted activity for control of Phytophthora cinnamomi.

The report, referred to here as “the Cutting report”, contains inaccuracies, unqualified opinion and quotes references to a scientific article incorrectly, and out of context. It is also unclear who within the New Zealand Avocado Growers Association approved the application, or paid for it to be prepared.

I am aware the Cutting report was circulated in the organic fruit industry. My report is to substantiate concerns I have raised with many people about the misleading tone of the Cutting report; I identify key points and include relevant quotes from other sources. Where possible photocopies of journal articles are attached.
2.     The definition of phosphorous acid
The Cutting report refers to “phosphorous acid”, which is the term
Avocado growers in New Zealand and Australia regularly use to describe the product di-potassium phosphite. This term is misleading, as the actual product is two stages removed from phosphorous acid. The Cutting report p.3 describes phosphorous acid flake as (H3PO3). In comparison I quote from (Guest & Grant, 1991):

‘Although in both Australia and the United States, the term phosphorous acid has been widely applied to phosphonic acid, the term phosphorous acid should by IUPAC rules, be restricted to the anhydrous solid, (OH)3P, prepared by the controlled hydrolysis of phosphorous trichloride with ice cold water. When anhydrous phosphorous acid dissolves in water, the phosphorous atom changes from the trivalent to the pentavalent form, forming phosphonic acid. It is this compound which then forms phosphonates with bases, or esters with alcohols…”
Guest & Grant, (1991). The complex action of phosphonates as antifungal agents. Biological Reviews 66. p.160-161.

Thus the compound (H3PO3) described by the Cutting report as phosphorous acid, is in fact phosphonic acid. This is important because when phosphonic acid is neutralized with a base, such as potassium hydroxide (KOH), it forms the phosphonate salt potassium dihydrogen phosphite (KH2PO3)  (Lovatt, 1990). This is also referred to as potassium phosphonate (Whiley et al, 1995). In comparison, phosphoric acid (H3PO4) when neutralized with potassium hydroxide forms the phosphate salt potassium dihydrogen phosphate (KH2PO4) (Lovatt, 1990).

The key difference is the substance phosphite, as opposed to phosphate. Plants use phosphate, however the salts of phosphonic acid, referred to here as phosphonates or phosphites, are not known to occur in living organisms and are not easily metabolised in plants (Guest & Grant, 1990). The environmental fate of phosphite is discussed later.
3.    Background levels of phosphonate residue
The Cutting report Ch.6 p9 para. 3 states:
“Provided that the correct season and physiological condition of the tree is considered then residues of phosphonate in the fruit can be limited to very low levels. Research in Australia has shown that background stable levels are about 17 mg/kg fruit (Whiley et al, 1995). It is therefore intended that fruit cannot be marketed as BioGro for a period of 6 months after treatment by trunk injection. Trunk injection should be limited to the period May to August for New Zealand.”

This indicates that there is a residual level of 17 mg/kg of phosphonate that could be reasonably expected in avocado trees. However the paper quoted in the Cutting report actually states:
“Prior to trunk injection, low levels of H3PO3 (<3.0g g-1fw) were detected in all parts of the tree, although there was no previous history of the use of phosphonate fungicides on the experimental trees in the orchard. It is unlikely that these pre-treatment concentrations of H3PO3 were derived from natural sources. Weeds were regularly controlled in the orchard by using glyphosate [N- (phosphono-methyl) glycine], an ambimobile phosphonate based herbicide. Glyphosate is completely degraded to CO2 by microorganisms in the soil, with the main intermediary metabolite being aminomethylphosphonic acid. It is likely that H3PO3 is a metabolite from the degradation of aminomethylphosphonic acid, in which case it may have been taken up by the tree, thereby accounting for its presence in tissues before treatments were applied.”
Whiley et al (1995) Changing Sink Strengths Influence Translocation of Phosphonate in Avocado (Persea americana Mill.) Trees. Australian Journal of Agricultural Research. 46: p.1082.

This shows that no phosphonate residue can naturally be expected in an avocado tree, and the initial level found in the trial was probably attributable to the use of glyphosate herbicide. Even then, the level found was only 3 mg/kg, not 17 mg/kg as described by the Cutting report. This is misuse of the term “background stable level”.

The actual reference to 17 mg/kg comes later in Whiley (1995):
“Concentrations of H3PO3 in young fruit increased sharply following trunk injection, reaching 60.8 g g-1fw eight days after treatment. Thereafter concentrations declined until stabilizing (at 17.0 g g-1fw) 64 days after injection.”
Whiley et al (1995) p.1083

This reference, apart from being misquoted in the Cutting report, is a trial in Australian conditions. A major difference between Australian and New Zealand is that local fruit remains on the tree for 12 months and more. There is risk in applying the research directly to New Zealand conditions. Later trials conducted here by HortResearch (Ward & Spiers, 1999) have shown residues of 54 mg/kg, 3 months after treatment, more residual than the Australian research revealed. Ward & Spiers (1999) found no residues in an untreated tree.

It is clear there are no natural background levels of phosphite in avocados, and residues from one application last for many months, possibly indefinitely. The 6-month estimate from injection to meet organic standards is speculative rather than scientific. The compounding effect of further phosphonate applications in addition to existing residues has not been researched, and is discussed later in this report.

4.    Environmental fate of potassium phosphonate
The Cutting report describes the phosphonate anion as being ”readily oxidised to phosphate by soil microbes”, at p.3 para. 3, Ch.3 p.4, and Ch.4 p.4. This is misleading, because it implies a similar fate within the plant. I quote from Guest & Grant (1991):
“Plants absorb and translocate, but do not appear to be able to metabolise phosphonate…”
Guest & Grant (1991) p.172 para. 2.

Guest & Grant (1991) continues that some plants, such as Allium sp. may be able to metabolise phosphonate under some conditions. However the general view appears most plants, including avocado, cannot metabolise phosphite easily. This raises the question of what happens to the phosphite, and how it affects the plant. I quote from Guest & Grant (1991):

“Phosphate and phosphonate mutually compete for transporter binding sites in all concentrations.”
Guest & Grant (1991) p.172 para 1.

This indicates that phosphite is not neutral within the plant. Guest & Grant (1991) suggest early experimentation with phosphonates, during World War II, showed phosphonate to be less effective at stimulating plant growth than conventional sources of phosphorous.

Australian research (Sukarno et al, 1998) found a relationship between restricted growth of onion plants and high internal concentrations of phosphonate. They attributed this to competition within the plant for uptake of phosphonate and phosphate.

There has been no research, in New Zealand conditions, on the effect of continued use of phosphonate when earlier residues are still present. Although the effects of this practice are unknown, they are probably detrimental to the tree, and the fruit.  Potassium phosphite is regularly injected in New Zealand avocado orchards; sometimes three injections per year, although it would appear most trees are injected only once.

Therefore the sustainability of phosphonate use in New Zealand avocado is questionable. Some New Zealand avocado growers were experimenting with potassium phosphite about 1990, but the widespread use began about 1994 with the arrival of Dr. Cutting from South Africa, with a different and more efficient injection technique than growers had used previously. The significant increase in planted area, and crop production, began about two years later so the full effects of compounded phosphonate use are yet to be seen.

The Cutting report, Ch.6 p.9 para.2, suggests that under research conditions root levels of 20 to 35 mg/kg are effective in controlling P.cinnamomi. I understand many of Dr. Cutting’s orchard clients are now using higher injection rates than before, and in excess of label rates. It also appears to me that some orchards, using phosphonates, are no longer getting responses to doses that were previously effective. If this is so, and residues are increasing within the tree, it is possible the effectiveness of those parameters, 20 to 35 mg/kg, is unsustainable. The result could be that some growers will eventually increase their injection rates to a level where there is no further response.

Thus even if the Cutting report were correct in the argument of 17 mg/kg background levels, it is likely that the applications necessary to achieve those levels would be inadequate to control further P.cinnamomi infection, causing an organic grower to face the dilemma of increasing application rates and losing certification, or retaining certification with arguably a less healthy orchard than before the phosphonate was applied.
5.    Marketing issues
Considering that avocados need a premium price, and relevant reputation, fruit quality is paramount to the conventional industry; let alone the organic. Yet phosphonate residues are already a quality issue overseas. A recent report on phosphonate residues in wine, from the reputable Swiss Research Institute of Organic Agriculture states:

“In conclusion, potassium phosphonate is an effective fungicide for the control of downy mildew, but the application of potassium phosphonate inevitably leads to phosphonate residues in the wine. It is suggested that phosphonate residues are not compatible with the reputation of organic wine among consumers.”
Speiser, et al. (1999) Control of downy mildew of grapevine with
potassium phosphonate: effectivity and phosphonate residues in wine.
Biological Agriculture & Horticulture. 17: 4, 305-312.

The keeping quality of New Zealand avocados is arguably decreasing. An Avocado Industry Council scientist, Dr. Henry Pak, has publicly expressed concern over ethylene production in the fruit affecting storage quality. In the opinion of Dr. Adrian Spiers of HortResearch, high phosphite levels in fruit increase ethylene production; he has found this in other crops, such as apples. Dr. Spiers has told Dr. Cutting, and Dr. Pak, personally of his view. Although the Avocado Industry Council is doing extensive research into causes of fruit rots, including fungicide trials, the industry will not research the link between phosphite and ethylene production. This suggests they are sensitive to phosphonates being a cause of reduced fruit quality and would rather ignore the risks.

It is already recognised that P.cinnamomi affected trees produce poorer quality fruit; so if phosphite residues are also a factor, the combination could be responsible for reducing tree health and fruit quality, but not necessarily production. This indicates unsustainable practice at the expense of short-term profit.

It is arguable that the New Zealand Avocado Growers Association is unwise in ignoring the risks of phosphite residues and in doing is so risking the future and good name of the entire New Zealand avocado industry for years to come.

6.    Alternatives for control of P.cinnamomi
Dr. Adrian Spiers, and Brian Ward, of HortResearch have researched and identified natural compounds, that leave no detectable residue, for control of P.cinnamomi.

I do not know if Dr. Cutting knew of these when he wrote his report of September 1998, but he did by the following year. The Avocado Growers Association has done nothing to advance research into these alternatives, and arguably have acted to stall the research.

Orchard management, especially crop loading, is a key factor in control of P.cinnamomi. Once the disease is stabilised by injection, either by a natural compound or potassium phosphite, good management is necessary to restore the tree to proper health. The difference between potassium phosphite and the natural compounds is that the phosphonate activity can stimulate the tree to produce fruit, and appear healthy, without any change in management practice in the medium term.  It is an easy, but unsustainable, option for growers to rely on the medium-term effects of potassium phosphite rather than manage the tree for true health, and fruit quality.

Avocados are one of the most complex and difficult of orchard trees to manage. This explains the slow growth of the industry until 1995. It is arguable that the dynamic growth of the New Zealand avocado industry since 1995 relies heavily on the easy medium-term management provided to naive growers by the use of potassium phosphite. The industry may be worth over $50 million this season, so there is much vested interest in the status quo, providing a motive to ignore alternative control options for P.cinnamomi.
7.    Summary

The Cutting Report to BioGro, of September 1998, seeking restricted use status in avocados for the fungicide product phosphorous acid, contains incorrect information, including:
•    That the product is phosphorous acid; when it is actually potassium phosphite, a substance with a metabolite that does not occur naturally in living organisms.
•     That the metabolite breaks down to phosphate; when although it does so in soil, it cannot as easily in plants and remains to an extent indefinitely.

•    That Australian research established “ background stable levels of 17 mg/kg” when in fact there are no such natural, nor stable, background levels; the Australian research found historical levels of 3 mg/kg which the authors attributed to previous use of glyphosate herbicide.

•    That fruit should be suitable for BioGro certification 6 months after injection with potassium phosphite. This assumption is speculative, and not based on proper scientific research.

The Cutting report also:
•    Ignores evidence of local growers increasing application rates of potassium phosphite to maintain tree performance.
•    Ignores evidence that phosphite residues may be detrimental to both avocado trees and fruit quality.

In other developments since the Cutting report:
•     Reputable overseas research indicates that phosphite residues in wine are incompatible with the organic reputation.

•    New Zealand research has identified organically acceptable compounds, for control of P.cinnamomi in avocado, that leave no detectable residue.

•    The New Zealand Avocado Growers Association has ignored the alternative compounds and arguably tried to stall the research.
The Cutting report to BioGro of September 1998 should be interpreted as the biased opinion of a person with a vested short-term interest in the continuing use of phosphonates in the New Zealand avocado industry; it has insufficient credibility to be considered seriously by the organic industry.

However, organic certifying agencies should be able to rely to an extent on the opinion of a scientist with the national reputation of Dr. Cutting. That he is responsible for such misleading information reflects on either his motives, or competence, and is ultimately the responsibility of the Avocado Growers Association. They now have an opportunity to address the situation.
8.    References

Guest, D. Grant, B. (1991) The complex action of phosphonates as antifungal
agents. Biological Reviews of the Cambridge Philosophical Society, Great Britain. 66:159-187.

Lovatt, C.J. (1990). A definitive test to detemine whether phosphite fertilisation
can replace phosphate fertilisation to supply P in the metabolism of “Hass” on “Duke 7”. California Avocado Society Yearbook 74: 61-64.

Speiser, B. Berner, A. Haseli, A. Tamm, L. Control of downy mildew of
grapevine with potassium phosphonate: effectivity and phosphonate residues in wine. Biological Agriculture & Horticulture. 1999. 17: 4, 305-312.

Sukarno, N. Smith, F.A. Scott, E.S. Jones, G.P. Smith, S.E. 1998. The effect
of fungicides on vesicular-arbuscular mycorrhizal symbiosis.III. The influence on phytotoxic effects following application of foestyl-aluminium and phosphonate. New Phytologist. 139: 2 321-330.

Ward, B, Spiers, A. 1999. Residues of Phosphorous Acid in Avocado – Report
submitted to the Avocado Industry Council, 8 September 1999.

Whiley, A.W, Hargreaves, P.A, Pegg, K.G, Doogan, V.J, Ruddle, L.J,
Savanah, J.B. Langdon, P.W. (1995). Changing sink strengths influence translocation of phosphonate in avocado. Australian Journal of Agricultural Research. 46:1079-90.