Pesticides are stressors that have received considerable attention, and among these no single class has received more attention than the neonicotinoids. These insecticides are acutely toxic to honey bees, environmentally persistent and mobile in the environment (Long & Krupke, 2016).

A recent large-scale, real-world field study, published in the journal Science, evaluating neonicotinoid pesticides has been added to a growing body of evidence suggesting that these agricultural chemicals are indeed harming bee populations to a unprecedented level.

Researchers investigated three different bee species across 33 sites in the United
Kingdom, Germany and Hungary, and found that exposure to neonicotinoid-treated crops is associated with a reduced capacity of bee species to establish new populations in the year following exposure.

For honey bees, the researchers found both negative (Hungary and United Kingdom) and positive (Germany) effects during crop flowering. In Hungary, negative effects on honey bees persisted over winter and resulted in smaller colonies in the following spring (24% declines). In wild bees (Bombus terrestris and Osmia bicornis), reproduction was negatively correlated with neonicotinoid residues (Woodcock et al., 2017).

Bayer and Syngenta, makers of neonicotinoid pesticides, promptly disputed the researchers’ conclusions—even though they partially funded the study (Gardner, 2017).

The amount of research pertaining to the effects of neonicotinoids on bees is overwhelming. Here are some of the results gathered from various studies conducted evaluating the effects of neonicotinoids on bees:

• Small bodied species show greater sensitivity to neonicotinoids.
• Dosed bees were significantly less likely to return to the nest than control bees.
• Bees in the two neonicotinoid treatments grew significantly more slowly and had an 85% reduction in the number of new queens produced when compared to control colonies.
• Concentration of thiamethoxam (a neonicotinoid) in pollen significantly negatively predicted both colony weight gain and production of new queens.
  
• Field-realistic doses of neonicotinoids (<3.5 ng/g) resulted in sublethal impacts on their ability to successfully build nests and provision offspring.
• Field studies using bumblebees demonstrate that exposure to neonicotinoid-treated flowering crops can have significant impacts on colony growth and reproductive output depending on the levels exposed to.

Given the vast farmlands devoted to crops and concerns about worldwide pollinator decline, researchers set out to to determine how (that is, plant species) and when (that is, time in season), pollen-foraging honey bees are exposed to a range of pesticides in agricultural landscapes, with an eye towards clarifying potential high-risk compounds and identifying common combinations of pesticides encountered in field environments.

The most common pesticide types detected in pollen samples across all sites were fungicides and herbicides. Honey bees visited a diverse assemblage of flowering plants, collecting pollen from up to 30 plant families during the 16-week sampling period (Long & Krupke, 2016).

It is evident that bees and other non-target organisms inhabiting farmland are routinely exposed to far more complex cocktails of pesticides than any experimental protocol has yet attempted to examine. Since researchers typically study the effects of only one chemical at a time, a major challenge for scientists and regulators is to attempt to understand how chronic exposure to complex mixtures of neonicotinoids and other chemicals affects wildlife, including humans.

The results from this research are particularly important because many crops globally are insect pollinated and without pollinators we would struggle to produce many foods. Across crops, years and biogeographical regions, crop-visiting wild bee communities are dominated by a small number of common species, and threatened species are rarely observed on crops. Researchers have observed that a small number of species dominate the contribution of crop production. Across 90 studies, the researchers observed that 2% of bee species account for almost 80% of all crop visits (Kleijn et al., 2017).

Do you support the use of these pesticides? If you are purchasing products that are contaminated with these neonicotinoids, you are contributing to this problem. If you refuse to buy foods contaminated with pesticides, the companies taking these short cuts will stop producing these products. These companies function on a corporate, patent-driven agricultural model that involves monoculture crops dependent on high chemical inputs. This creates a positive feedback loop where pest plants and insects become resistant to herbicides and pesticides, prompting companies to make other, more toxic chemicals. This ever-growing dependence on chemicals, which threatens natural ecosystems and human health, is highly profitable to companies like Bayer, Syngeta and Monsanto.

It is up to everyone of us to source foods that we know how they are grown and produced - easier said than done when shopping at a supermarket. Try shopping at your local farmer's markets, where you can meet the farmers in person and know how they are growing the food you purchase. You should know what is in your food. Collectively, we have the power to choose what we as consumers want.

The ideal solution to this problem is to grow your own food in an organic garden! Both flower and vegetable gardens provide good honeybee habitats. It's also recommended to keep a small basin of fresh water in your garden or backyard, as bees actually do get thirsty. Be very mindful of pesticide use, and think twice whether such chemicals are really necessary before you spray them (this goes for flea repellents, mosquito sprays and more). You can take bee preservation a step further by trying your hand at amateur beekeeping. Maintaining a hive in your garden requires minimal time, benefits your local ecosystem, and you get to enjoy your own homegrown honey.

As for pesticides in your body, your best bet for minimizing health risks from herbicide and pesticide exposure — including both the active and "inactive" ingredients — is to avoid them in the first place by eating organic as much as possible.

Groups of cells, collectively known as tumor microenvironment of metastasis (TMEM), can serve as gateways for tumor cells entering the blood vessels. The researchers observed that several types of chemotherapy can increase the amounts of TMEM complexes and circulating tumor cells in the bloodstream (Karagiannis et al., 2017).

Dr. Karagiannis, the lead author of the study, found the number of doorways was increased in 20 patients receiving two common chemotherapy drugs. It should be noted such a small sample size constitutes a major limitation of this study, the results and implications of this research are very significant.

While prevention is by far the best cure for chronic disease, not everyone has this luxury. A number of modifiable risk factors are responsible for many premature or preventable diseases and deaths. Modifiable risk factors fall into three main groups (Danaei et al., 2011):

• Lifestyle risk factors, such as tobacco smoking, physical activity, and alcohol use.
• Dietary risk factors, such as a high salt intake or a low intake of fruits and vegetables.
• Metabolic risk factors, such having high blood pressure or blood cholesterol and being overweight or obese.

In regards to dietary interventions, numerous studies have substantiated the chemopreventative effect of increasing cruciferous vegetable intake against cancer. As a chemoprevention agent, sulforaphane, the active molecule in cruciferous vegetables, possesses many advantages, such as high bioavailability and low toxicity (Li et al., 2010).

Increasing the consumption of cruciferous vegetables is only one of the many preventive measures that can be taken when taking control of your health. Remember, the health of your environment reflects the health of your body; you are the product of your environment.

The environment teems with microbes, which includes microscopic living organisms such as bacteria, protists, many fungi, as well as viruses. Most microbes live in the water or soil. Most of the ones that live in animal bodies do no harm and may even be beneficial. Some microbes, however, are pathogens, which may result in disease (Audesirk, Audesirk & Byers, 2011).

A growing body of evidence suggests that the immune effects of early-life microbial exposure are long-lasting and continue into later life, since these immune effects have been associated with the prevention of diseases such as inflammatory bowel disease (IBD) and asthma (Olszak et al., 2012).

Vertebrates have evolved three major forms of protection against disease:

• nonspecific external barriers - these barriers, such as skin and secretions, cover the external surfaces of the body and line the body cavities that come in contact with the external environment
• nonspecific internal barriers - if the external barriers fail, collectively, a variety of nonspecific internal defenses called the innate immune response, begin to initiate. White blood cells may destroy infected cells, chemicals and proteins released by cells may trigger inflammation and fever.
• specific internal defenses - this final adaptive immune response, in which immune cells selectively destroy the invading microbe and "remember" the invader, permits a speedy faster recovery if it were to appear in the future.

Invading microbes that penetrate the skin or mucous membranes will encounter an array of internal defense mechanisms developed by humans which involve a large number of different cell types, including neutrophils, dendritic cells, macrophages, natural killer cells, mast cells, B cells and T cells. Innate immune responses are nonspecific, in that they attack many different types of microbes rather than a specific invader. White blood cells, also known as leukocytes, are specialized to attack and destroy invading cells. The body contains various types of leukocytes, collectively known as phagocytes, which literally ingest foreign invaders and cellular debris by phagocytosis. Natural killers cells are another type of leukocyte, which act primarily at the body's own cells that have become invaded by microbes. Such cells recognize the proteins of the major histocompatability complex (MHC). The MHC proteins identify the body's cells as "self" (Audesirk, Audesirk & Byers, 2011). 

Natural killer T (NKT) cells have been observed to play an important role in the development of ulcerative colitis, a major form of IBD, and in asthma. Therefore, the researchers investigated the regulation of NKT cells by the use of microbes in mouse models. First, the researchers examined NKT cells in the tissues of 8-week-old germ-free and specific pathogen-free mice. Here, relative and absolute numbers of NKT cells were measured and observed to be at an increased level in germ-free mice within the mucous membranes, resulting in increased morbidity in models of IBD and asthma. The differences in NKT cell numbers between the germ-free mice and the specific pathogen-free mice were detectable, suggesting early and persistent effects of the microbes.

Upon establishing relevance of the findings, the researchers examined whether reintroducing microbes in adult germ-free mice would normalize NKT cell levels in the mucous membranes. To a surprise, exposure of germ-free mice to microbes did not restore NKT cells to the levels observed in the specific pathogen-free mice, nor did it reverse mortality. Afterwards, the researchers wondered whether normalized NKT cell levels and function were dependent on the age at which the microbial contact occurred. Indeed, when the researchers exposed microbes to pregnant germ-free female mice just before delivery, therefore exposing neonatal germ-free mice to the specific pathogen-free mice conditions on their first day of life, a complete normalized NKT cell level was observed and persisted even two months afterwards.

Colonization of neonatal - but not adult - germ-free mice with conventional microbes protected the animals from mucosal NKT accumulation and related pathology. These results suggest that an age-sensitive contact with symbiotic microbes is critical for establishing mucosal NKT cell tolerance to later environmental exposures. Therefore, these observations are in accordance with research known as the "hygiene hypothesis", which proposes that early-life exposure to specific microbe-enriched environments decreases susceptibility to diseases, such as IBD and asthma. Early-life microbial exposure elicits long-lasting effects on NKT cells, and in their absence, later-life exposure to factors that stimulate these cells may induce an autoinflammatory response. Given the extensive similarities between mice and human cell systems, these findings are predicted to extrapolate to humans.