Arrested ear development (AED), sometimes called, “hollow husk” is a rather understudied and somewhat unexplained phenomenon that has been observed occasionally in Delaware corn and has been found in other corn growing regions in the United States. Symptoms of AED vary from tiny ears of corn similar to those you may consume in Asian food to stout cobs sometimes referred to as, “beer can” cobs (Figure 1). Overall, ears are shorter, contain fewer kernels, and have dried tips. Husks tend to be slender and pointed at the tip as a result of smaller ears. Often silk emergence is reduced and leaves may develop a red or purple color. AED is sometimes associated with multiple ears at a node and its occurrence can be rare and sporadic within a field. Several other disorders can resemble AED. For example, injury from a period of drought stress at the wrong stage of development can result in short, blunt ears similar to AED. Poor, incomplete kernel set due to poor pollination or asynchronous pollen shed and silking, insect feeding and silk clipping, as well as a number of other related causes differ from AED in that the cob grows to nearly its full length but kernel set is either scattered, concentrated at the butt or tip end, or is limited at the tip end. Another syndrome called “banana” ears or “zipper” ears is often associated with extreme environmental conditions or defoliation injury and possibly even excessive silk growth.
Although the literature on AED is limited, the disorder has been associated with several factors including sudden drops in temperature and application of pesticides during early ear development (V8-V16). Although the exact mechanism is unknown (some speculate ethylene is involved -e.g. Schmitz et al. 2011. DOI: 10.2134/agronj2011.0048) we do know that AED is not the result of disease.
A brief cold shock of even a few hours can result in AED during the early stages of ear formation. In 2005, we identified a case of AED on a farm in Sussex County where the flow of the land allowed cold air to flow down field contours. Examination of temperature records for the nearest weather station confirmed a short period of two or three days of cool/cold temperatures in mid-June. Even on the relatively flat ground in southern Delaware, we have found that cold air can flow and accumulate in pockets which may lead to the development of AED on scattered plants. Since the effect appears so infrequently, little research is available to identify why arrested ears show up on one plant next to a plant with a normal ear. Whether a small difference in air temperature or a small difference of one or two leaves in growth stage can impact which ears are affected is just not known.
In 2007 AED was found in several parts of the Midwest. Researchers at Purdue University determined that problem fields had pesticides and or spray additives applied prior to tasseling and conducted trials to examine the role of pesticides and pesticide additives in the development of AED. In their preliminary work, pesticides were applied after ear size was complete and silks were beginning to emerge from the ends of cobs (V14). Fungicides were applied alone or in various combinations with NIS, COC, AMS, insecticide, glyphosphate, and 2,4-D (Figure 2). Results from this study indicated that the addition of COC or NIS to fungicides alone or in fungicide + insecticide combinations increased the frequency of AED compared to controls by 3-35%. Cob length was also reduced by 6-48%, which resulted in fewer kernels per ear. Although fungicides applied alone did not result in AED, these products did cause a reduction in kernels per ear (http://www.agry.purdue.edu/ext/corn/news/articles.08/arrestedears-1209.html).
Figure 2. Treatments used in preliminary work on Arrested Ear Development syndrome at Purdue University. This figure was obtained on September 26 2013 from http://www.agry.purdue.edu/ext/corn/news/articles.08/arrestedears-1209.html.
Subsequent research conducted at Purdue University indicated that the use of NIS prior to tasseling (VT), particularly between V12 and V14, can increase the severity of AED. Researchers at BASF arrived at a similar conclusion. In their work, which was published in Agronomy Journal in 2011, pyraclostrobin (the active ingredient in Headline®) applied alone did not promote AED. The group concluded that the cause of malformed corn ears was APE, a common component of NIS which is routinely added to fungicide applications in corn. APE-containing NIS applied to corn at V12 and again at V16 caused 36 and 21% AED, compared to untreated controls or when three different pyraclostrobin formulations were applied without additives. In addition, pyraclostrobin plus APE-containing NIS caused maximum AED (10–62%) when applied at the V10 to V14 growth stages. Pyraclostrobin applied alone at any corn growth stage or pyraclostrobin plus NIS applied at V8, V18, VT, R1, or R2 did not cause AE development.
The mechanisms behind AED are still unclear and complex and research on the subject continues. The bottom line is that environmental influences may be beyond the control of the grower. However, because pesticides may play a role in AED, careful attention should be paid to pesticide labels and the growth stage of corn to avoid adjuvant or pesticide-induced AED. Additional information on AED can be found on Purdue Extension Factsheet BP-85-W (http://www.extension.purdue.edu/extmedia/BP/BP-85-W.pdf) as well as the Corny Network, authored by Dr. Bob Nielson (http://www.agry.purdue.edu/ext/corn/news/archive.html).