Iron deficiency

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Characteristics and occurrence

Iron (Fe) deficiency is frequently encountered on calcareous soils. In these soils, the availability of iron to plants is reduced through precipitation of iron at high pH, or by high concentrations of phosphorus. Under such conditions, iron deficiency may often be associated with deficiencies of other micronutrients, such as manganese, copper and zinc, whose availability is also pH-dependent. Heavy applications of lime or phosphorus fertilisers can likewise induce iron deficiency. Iron deficiency may also be expected on sandy soils, organic soils or acid soils having excessively high levels of manganese.

A number of other disorders which impair root function, including toxicities of manganese, aluminium or zinc, or calcium deficiency, can inhibit iron uptake and induce symptoms of iron deficiency in the leaves. In all cases of iron deficiency, care should be taken to determine the conditions responsible for the disorder.

Iron deficiency is one disorder where visible symptoms are obvious when crop growth is only mildly affected, a feature which probably contributes to the frequent observation of iron deficiency in sweetpotato crops.


The distinctive symptom of iron deficiency is chlorosis of the youngest leaves. As the chlorosis is a result of photobleaching, leaves in bright sunlight will be more affected than those in shade. Initially, a yellow interveinal chlorosis develops, which is characterised by a sharply contrasting green network of veins. However, as the condition becomes more severe, the chlorosis becomes white and the veins may lose their green colour. If young leaves are normally purple, they become pink as a result of iron deficiency. While all the leaves of the plant may become affected, youngest leaves generally show the greatest intensity. However, if iron supply has been restored, new leaves become bright green and chlorotic leaves may be found below them.

Severely affected leaf blades become necrotic, the necrosis usually spreading from the tip and margins into interveinal zones. Eventually, the growing points may die, both at the terminal apex and in axillary shoots.  Necrotic tissue on expanded leaf blades is generally light brown and soft, but may be dark and brittle on the shoot tips.

Possible confusion with other symptoms

Boron deficiency may also cause death of growing points and chlorosis of young leaves, but the chlorosis is not distinctly interveinal. In particular, the minor veins are not sharply defined, as is seen in iron deficiency. Also, thickening and deformation of young leaves is not observed in iron deficiency.

Iron deficiency may be induced by a number of disorders which adversely affect root function. These include calcium deficiency and toxicities of manganese, zinc or copper. Correction depends on identifying the primary cause in these cases.

Diagnostic soil and plant tissue tests

A critical concentration of 33 mg iron/kg in the 7th to 9th youngest leaf blades was estimated in solution culture studies using the cultivar Wanmun. In healthy plants, concentrations were generally between 45 and 500 mg iron/kg. This is consistent with the findings of Spence and Ahmad (1967) who reported 35 mg iron/kg dry weight in young shoots of plants which showed mild symptoms of iron deficiency without growth reduction, and 28 mg iron/kg from plants showing severe chlorosis.

Due to the large number of factors which affect the availability of soil iron to plants, soil measurements are not generally reliable for diagnosing iron deficiency.

Diagnosis can be confirmed by painting a chlorotic leaf with a 1% solution of ammonium ferric sulfate, which will cause regreening after a few days. It is important to clearly label the painted leaf so that it can be identified on later inspection. By painting only one half of the leaf, the other half may be used for comparison of the response (Plate 15g). Including a small amount of an agricultural wetting agent or mild detergent in the solution may aid the uniform wetting of the leaf surface, but it is not essential for sweetpotato leaves, which wet relatively easily.


On soils of high pH, application of iron compounds as a fertiliser to the soil is likely to give a poor response, as the added iron will be precipitated and become unavailable to plants. Treatment of an iron deficient crop is best achieved by a foliar spray of chelated iron or 1-2% ammonium ferric sulfate solution. Burying small pieces of scrap iron, such as nails and steel food cans, in the mound at planting, can also be effective in reducing iron deficiency. Soaking cans in sea water before burying accelerates rusting and has been successful in increasing their effectiveness as an iron supplement on calcareous atoll soils.

If iron deficiency occurs on an acid soil, it may be a secondary effect of another nutritional disorder, such as manganese toxicity or calcium deficiency. In this case, liming may alleviate the iron deficiency by eliminating the underlying problem.


Bourke, R.M. 1983. Crop micronutrient deficiencies in Papua New Guinea. Technical Report 83/3, Department of Primary Industry, Papua New Guinea.

Cable, W.J. 1992. Common nutrient deficiency symptoms of crops of Tokelau and other coral soils and their correction. Journal of South Pacific Agriculture, 1(2), 43-52.

O’Sullivan, J.N., Asher, C.J. and Blamey, F.P.C. 1997. Nutrient Disorders of Sweet Potato. ACIAR Monograph No. 48, Australian Centre for International Agricultural Research, Canberra, 136 p.

Spence, J.A. and Ahmad, N. 1967. Plant nutrient deficiencies and related tissue composition of the sweet potato. Agronomy Journal 59, 59-62.



Contributed by: Jane O'Sullivan

Characteristics and occurrence


Confusion with other symptoms

Diagnostic tests



Yellowing of younger leaves on iron deficient plant (J. O'Sullivan).

Typical  yellowing between veins with veins sharply contrasting (J. O'Sullivan).

Very pale chlorosis on young leaves (J. O'Sullivan).

Normally purple tips become pink (J. O'Sullivan).

Necrosis of pale young leaves and death of vine tip and axillary buds (J. O'Sullivan).