
(Fluoride Damage to Scots Pine. Photograph by Davison & Weinstein.)
Visible symptoms of fluoride injury
Alan Davison,
AES, Ridley Building,
University of Newcastle,
Newcastle upon Tyne NE1 7RU
England
Leonard Weinstein,
Boyce Thompson Institute,
Tower Road, Cornell University,
Ithaca NY
(Visit Weinstein's and Davison's website
at http://www.ncl.ac.uk/airweb/ which
contains a number of photos of fluoride induced damage to vegetation.)
Examples of all of the symptoms described
will be provided. This section should be read in conjunction with
that on mimicking symptoms.
Fluoride-induced symptoms have been described in
many reviews (Weinstein and McCune 1970; Weinstein and McCune, 1971;
Thomas and Alther 1966; Brandt and Heck 1977; Treshow and Pack 1970;
Guderian et al. 1969; Hindawi 1970; Thomas 1961). The most recent
account, with illustrations is: Weinstein, Davison & Arndt,
1998 (Recognition of Air Pollution Injury to Vegetation, Ed. Richard
B Flagler). The basis for the following description is Weinstein
and McCune (1971) plus our own experience in the field in several
countries.
Gaseous fluoride enters the leaf through the stomata
(=pores) then it dissolves in the water permeating the cell walls.
The natural flow of water in a leaf is towards the sites of greatest
evaporation, which are the margins and tip. Carried by the water,
the fluoride concentrates in the margins and tip so it is these
areas that generally are the first to show visible injury. Clearly
this concentration mechanism is one reason why fluoride is so toxic
to plants but there is an important corollary; most of the leaf
may have very little fluoride present and may function normally
in terms of assimilation.
Generally, leaves are most sensitive when they
are young and still expanding. Once fully developed they may be
many times more resistant. Therefore symptoms are more often seen
in young, expanding leaves. Where fumigation is periodic, symptoms
may reflect this as only those leaves that are at the sensitive
stage of development when the fumigation occurs will develop injury.
The rate at which symptoms appear depends on the weather. There
can be a considerable lag between the time of exposure to the fluoride
and the development of the symptoms.
Exposure to a high concentration causes necrosis
of part or even the whole of the leaf. The term necrosis comes form
the Greek nekros meaning a dead body. The tissues die. The initial
stages vary with species and both the speed of development of the
symptoms and their appearance depend on the weather. In most monocotyledonous
(narrow-leaved species including grasses and lilies) plants, the
initial symptom is the development of chlorosis (= yellowing) at
the tips and margins of elongating leaves. In some the tissues take
on a "water-soaked" appearance that looks very like early
frost injury, then the tissues desiccate and change colour. In some
species the dead, necrotic areas are pale white to tan, in others
they are brown and they may be black (eg in Populus spp.) or have
reddish tinges. Characteristically, there is a dark brown margin
along the basal part of the necrotic area. This line of demarcation
is very useful in identifying multiple exposures. The necrotic area
is sharply delineated from the healthy portion of the leaf blade
by a narrow band of chlorotic tissue sometimes streaked with red
as in some varieties of Sorghum. Dead, dry pieces of leaf may become
brittle and fall off, giving the leaf a tattered appearance. This
is common in Chinese apricot and Italian prune and many Populus
varieties. When very young leaves are injured in this way the resulting
leaf may only be a fraction of the normal size and completely mis-shaped.
Pine species (Pinus) vary greatly in sensitivity.
For example, young ponderosa pine (Pinus ponderosa) needles
first exhibit a lightening in color which turns light brown to reddish-brown
at the tip and progresses basipetally along the needle. The discoloration
is often accompanied by narrow, dark banded zones, which may be
the result of intermittent exposures to fluoride spaced at different
periods. Dark bands may also occur at the interface of necrotic
and healthy tissues. Needles are born in groups (2, 3, 5 depending
on species). They tend to be marked to the same extent.
Although necrosis is the symptom most frequently
referred to in texts, often being called tip burn, other symptoms
are at least as common or, in some areas, more common. In dicotyledonous
("broad-leaved") species the initial symptom of fluoride
effects on leaves is usually chlorosis of the tip, which later extends
downward along the margins and inward toward the midrib. This chlorosis
becomes more intense and extensive with prolonged exposure until
the midrib and some veins appear as a green arborescent pattern
on a chlorotic background. Continued exposure may lead to the tip
becoming necrotic and falling off, leaving the leaf notched.
The symptoms produced in corn (Zea mays), Sorghum,
and some other grasses begin as scattered chlorotic flecks at the
tips and upper margins of middle-aged leaves. As the symptoms progress,
the flecking becomes more intense and extends downward, especially
along the margins. The amount of chlorosis diminishes from the tip
downward and from the margins toward the midrib. A greater degree
of chlorosis is usually present at the arch of the leaf and wavy
areas of the margin. At high fluoride concentrations, there is less
chlorotic flecking and a greater tendency for tip, marginal, and
interveinal necrosis, or a transverse necrotic band at the arch
of the leaf.
In young, developing leaves of broad-leaved species,
and occasionally in petals, the translocation of fluoride to the
margins and tips leads to a distorted shape. This may be accompanied
by chlorosis at the margins and/or necrosis . This occurs because
cells in the mid parts of the leaf have low fluoride and expand
normally but those on the margins are slower-growing so the leaf
buckles and distorts, becoming cupped and concave or convoluted
like a savoy cabbage.
There is little information about the effects of
fluoride on fruits but there are two important examples. Bonte &
Garrec described fluoride-induced distortion of strawberry fruits
(Fragaria). It was cuased by lack of fertilisation of some of the
seeds, wich are responsible for hormonal-induced swelling of the
fruit. Peach also shows an unusual disorder induced by fluoride
called "suture red spot" or "soft suture" of
the fruit. It is characterized by premature ripening of the flesh
on one or both sides of the suture toward the stylar (blossom) end
of the fruit (Benson 1959; MacLean et al. 1984). The ripening of
this tissue considerably precedes that of the normal fruit and is
often accompanied by splitting of the flesh along the suture. At
harvest, the affected areas are soft and often decomposing.
Finally, although the economic value of injury
to a peach crop can be claculated, it is almost impossible to calcualte
or predict the effects of injury on other plants. If fluoride kills
all of the leaves on a tree then there will, of course, be an effect
on subsequent growth. However, apart from this very rare occurrence,
there is little or no relationship between visible injury and either
growth or longevity. A plant that is visibly injured is not necessarily
dying and there have been some cases of spectacular recovery of
trees after severe injury. Many that show a significant degree of
injury (such as Populus) continue to grow at normal rates. Conversely,
just because a plant does not show visible injury it does not mean
that there is no effect of fluoride on assimilation or growth. Predicting
the effects of fluoride is not a job to be undertaken lightly!
Learn more about fluoride pollution at www.fluoridealert.org/f-pollution.htm
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