The Influence of Lethal and Sub-Lethal Pesticide Exposure on Apis Mellifera

Populations of Apis mellifera (the honey bee) have declined over the past eight years. This has resulted in a strong interest to research and solve the problem. “In 2006 the widespread appearance of this phenomenon in the United States was noted and referred to as Colony Collapse Disorder (CCD) by researchers, beekeepers, and the media” (Lawrence & Sheppard, 2013, p.1). The commercial value of honey bees is significant. Domesticated honey bees are used as the pollinators of virtually every commercial crop, of great importance to humans. Additionally, honey bees create honey, a valuable crop in and of itself. Unfortunately, the environment that honey bees exist in is exposed to a multitude of issues most notably pesticides. “Entomologists suspect that a number of other factors also contribute to the CCD, including climate change, habitat destructing (sic) and handling practices that expose bees to foreign pathogens. But the effect of agricultural chemicals is particularly alarming” (Brown, 2013, p 1). Research suggests that honey bee exposure to various pesticides has contributed substantially to the decrease in the honey bee population. To provide some scope of the potential disaster that CCD could create; consider California’s almond industry. “Bees are declining at such a fast rate that one bad winter could trigger an agricultural disaster… CCD is a major threat to this $4 billion industry” (Brown 2013, p.1). Oldroyd, (2007) provides some additional financial scope; “Honey bees are essential pollinators: in 2000, the value of American crops pollinated by bees was estimated to be $14.6 billion” (p.1). With this in mind, pesticide exposure is a problem affecting honey bees in two ways: lethally and sub-lethally.

Lethal exposure to pesticides is created when levels of a given pesticide are significant enough to cause almost immediate death. Toxicity levels can be affected by: “the measures taken during its application, the dosage applied, the adsorption on soil colloids, the weather conditions prevailing after application, and how long the pesticide persists in the environment” (Damalas & Eleftherohorinos, 2011, p. 1404). Most of these conditions are regulated or managed successfully. However, when any of these conditions exceeds safe levels, honey bees are at risk of death through direct contact. As foragers, honey bees travel throughout large fields and orchards in search of pollen. During the course of a single foraging expedition, honey bees can be exposed to many pesticides. Andree, Lichtenberg, Pettis, Rose, Stitzinger and VanEngelsdorp (2013) noted; “Our pollen samples contained an average of nine different pesticides, ranging as high as 21 pesticides in one cranberry field” (p.1). Direct contact with concentrated pesticides is likely to cause a lethal effect. Many pesticides were “most toxic when directly sprayed on the bees” (Araujo et al., 2014, p.1). Lethal effects of pesticides are almost instantaneous and can be devastating to a single colony if sprayed. However, this does not normally occur in an endemic fashion and is inconsequential in relation to CCD. The sub-lethal effects of pesticides play a more important role in the CCD phenomenon.

The effects of sub-lethal pesticide exposure are wide-ranging and are contributing factors of CCD. “Sub-lethal effects have been described as effects on physiology and behavior of an individual that has been exposed to a pesticide without directly causing death” (Fuchs, Grünewald, Schneider, & Tautz, 2013, p.1). Some “sub-lethal effects… include impaired learning behavior, short- and long-term memory loss, reduced fecundity (fertility and reproduction), and altered foraging behavior and motor activity of the bees” (Lawrence & Sheppard, 2013, p.3). Additionally, pesticides have been implicated “in either depressing bees’ immune systems or increasing their susceptibility to biological infections” (Lawrence & Sheppard, 2013, p.3). While not immediately lethal, various combinations of these symptoms are deadly in the long run.

Neonicotinoids are a group of pesticides that can elicit all of the sub-lethal effects of exposure previously named. Ironically, their recent popularity lies in the perception that they are a “safer pesticide” (Lawrence & Sheppard, 2013, p. 4). This particular pesticide group is very dangerous for honey bees because of the way that it moves throughout the structure of a plant. “Neonicotinoids are systemic insecticides that are taken up by a plant through either its roots or leaves and move through the plant just like water and nutrients do. It can also be found in the nectar and pollen of the flowers” (Lawrence & Sheppard, 2013, p.4). “When considering oral ingestion, honeybees can be exposed in different ways including nectar, pollen, and guttation water. Guttation water, an excretion of xylem water at the leaf margins, was recently discovered to hold high residues of neonicotinoid substances” (Fuchs, Grünewald, Schneider, & Tautz, 2013, p.1). Honey bees can be exposed to neonicotinoids in more than one way from the same plant, with serious consequences. The sub-lethal symptoms of neonicotinoid exposure are diverse. Two of the most significant symptoms are the impact on the honey bee immune system and the impact on foraging and time spent in the hive.

Immune system suppression is extremely significant because it provides an opportunity for a colony to become compromised by a wide variety of diseases and parasites. According to Brown (2013) studies have “found that the pesticides hindered the bees’ abilities to resist the infection, thus contributing to their deaths. The fungicide chlorothalonil and chlorothalonil DF were particularly destructive, tripling the risks of parasitic infection” (p.1). Chlorothalonil and chlorothalonil DF are two commonly used neonicotinoids. Increased occurrence of frequency and severity of two types of parasitic infections affecting honey bees has been noted in relation to neonicotinoid exposure: the gut pathogen Nosema ceranae and Varroa (a parasitic mite of the honey bee). “These increases may be linked to insecticide-induced alterations to immune system pathways, which have been found for several insects, including honey bees” (Andree et al. 2013, p. 1). Combined exposure to neonicotinoids and parasites can increase the risk of infection.

Nosema ceranae has been linked to CCD largely in its influence on overwintering colonies. Honey bee colonies are vulnerable in this state and during the following spring become weaker and more susceptible to CCD. “The endoparasitic fungal infections of N. apis and N. ceranae adversely affect honey bee colony health, and can result in complete colony collapse” (Andree et al., 2013, p.1). Honey bees in an overwintering state are living in the densest possible concentration. These conditions are necessary in order to harness their metabolic activity, which regulates hive temperature throughout the winter. Nosema attacks the lining or epithelium of the midgut. Proliferation in the host occurs. “In 3-7 days spores are shed into the digestive tract and are eliminated in the feces” (Moeller, 1978, p.2). In these abnormally close quarters, the honey bees are exposed to higher concentrations of fecal matter. The likelihood of large scale infection is dramatically increased in the overwintering state. This combined with a depressed immune system caused by neonicotinoids can result in an epidemic of Nosema. “Nosema prevalence in bees fed pollen containing those chemicals was more than double the Nosema prevalence in bees that did not consume these chemicals” (Andree et al., 2013, p.1).

If infected with Nosema CCD can occur because of a combination of factors. Nosema is especially insidious because; “when a hive becomes infected with Nosema the symptoms are often subtle enough to go unnoticed until the hive has collapsed” (Moeller, 1978, p.2). Effects include: “50% shorter worker bee lifespan, reduction in brood size (affecting the amount of honey produced), retarded development of package bees and most importantly supersedure of the queen (which occurs 2-6 weeks after infection)” (Moeller, 1978, p.3). All of these leave a hive vulnerable to a vicious cycle of low productivity, ultimately resulting in collapse.

Honey bees are also being exposed to neonicotinoids by beekeepers interested in their use to control mites; most commonly varroa. “Miticides used by beekeepers to control varroa infestation had a pronounced effect on bees’ ability to withstand parasite infection” (Andree et al., 2013, p.1). The results of exposure are the same as if the exposure occurred in a field or orchard. Sub-lethal symptoms develop and can contribute to CCD. However, tactics exist which can eliminate this use of neonicotinoids. “An increasingly popular practice, rotating combs out of hives to remove accumulated pesticides, is expected to reduce miticide levels in hives, and will hopefully decrease spread of these chemicals to the environment” (Andree et al., 2013, p.1). Berry, Delaplane, Hood, Parkman, and Skinner (2005) describe another technique that addresses mite infestation without the use of pesticides. Use of screens as hive floors tended to reduce colony mite levels (24-h sticky sheet counts), sometimes significantly. Increased government regulation could also play a part in the introduction of less toxic pesticides which could replace neonicotinoids (p.160). “Regulation encourages firms to develop less toxic pesticides” (Ollinger & Fernandez-Cornejo, 1995, p.3). While neonicotinoids weaken hives by deteriorating the honey bees’ immune system, they also contribute to CCD by affecting honey bees’ ability to forage.

Foraging is the hunting and gathering activities of worker bees. This is the means by which the raw materials are provided to the hive that are used to produce honey and wax. When this ability is affected, hives become weaker and susceptible to CCD. Neonicotinoid exposure can affect foraging. Fuchs, Grünewald, Schneider and Tautz (2013) observed that exposure “reduced the number of foraging flights and prolonged the duration of homing flights for up to three days” (p.1). This decrease in productivity can lead to lower honey production. Additionally, Fuchs et al.’s (2013) study showed that “in the trials conducted among the bees treated with 3 ng and 6 ng imidacloprid (a member of the neonicotinoid group) that were not directly flying to the hive, we observed reduced mobility, followed by a phase of motionlessness with occasional trembling and cleaning movements”(p.1). They also noted; “administration of 3 ng imidacloprid led to a significantly prolonged first stay inside of the hive. Bees that were treated with 1 ng and 2 ng clothianidin (a member of the neonicotinoid group) had longer first in-hive stays compared to the controls” (Fuchs et al., 2013, p.1). Efficient foraging is critical to hive health and species proliferation. In “maximizing delivery per unit of expenditure they (workers) may, in fact, be maximizing the total amount of nectar delivered during the life of each worker. This results in more drones and more queens produced in a season” (Kacelnik, Houston, & Schmid-Hempel, 1986, p.21). Longer stays in the hive means less time foraging and a higher risk of CCD. This can be caused by neonicotinoid intoxication.

CCD is a significant problem facing any industry that relies on bees as pollinators. It has the potential to be an expensive problem. Fortunately, many of the causes of CCD can be linked to the use of pesticides. The challenge for the agricultural industry going forward will be in how they address the use of pesticides. In light of this, organic growing methods may be promoted. According to Douds, Hanson, Hepperly, Pimentel, and Seidel (2005); “Conventional agriculture can be made more sustainable and ecologically sound by adopting some traditional organic farming technologies” (p.579). Unfortunately, the expense of organic farming is greater than that of its conventional counterparts. It seems likely that consumers will face higher fresh produce prices in the future as a result of lower supplies and more expensive growing methods if the CCD problem is not solved.

References

Andree, M, Lichtenberg, E.M., Pettis, J.S., Rose, R., Stitzinger, J., VanEngelsdorp, D. (July 24, 2013). Crop Pollination Exposes Honey Bees to Pesticides Which Alters Their Susceptibility to the Gut Pathogen Nosema ceranae. Plosone.org. Retrieved March 6, 2014 from http://www.plosone.org

Araujo E.L., Bezerra C. E., Costa E.M., Maia A.P., Silva F.E.L., Silva J.G. (January 2014) Toxicity of insecticides used in the Brazilian melon crop to the honey bee Apis mellifera under laboratory conditions. Apidologie , 45, 34-44.

Berry J., Delaplane K., Hood M., Parkman J., & Skinner J., (2005). Integrated pest management against Varroa destructor reduces colony mite levels and delays treatment threshold. Journal of Apicultural Research, 44(4), 157–162.

Brown, Steve (August 13, 2013) Scientist’s Confirm: 2 Common Pesticides Killing American Honey Bees. Reuters.com. Retrieved March 5, 2014 from www.reuters.com

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Kacelnik A., Houston A. & Schmid-Hempel P. (June 1986). Central-place foraging in honey bees: the effect of travel time and nectar flow on crop filling. Behavioral Ecology and Sociobiology, 19, 19-24.

Lawrence, Timothy, Sheppard, Walter (November 6, 2013). Neonicotinoid Pesticides and Honey Bees. Washington State University Extension Fact Sheet, FS122E, 1-7.

Moeller F. E., (1978). Nosema Disease: Its Control in Honey Bee Colonies. Madison, Wisconsin. United States Department of Agriculture.

Oldroyd B.P.,( June 12, 2007 ). What's Killing American Honey Bees? Plosone.org. Retrieved March 9, 2014 from http://www.plosone.org

Ollinger M.& Fernandez-Cornejo (December 1995). Innovation and Regulation in the Pesticide Industry. Washington, DC. United States Census.