The European Commission imposed a 2-year ban on certain neonicotinoids (clothianidin, imidacloprid, thiamethoxam) in 2013. Their use remains restricted in the European Union until a review of this policy’s effects is completed in January 2017. As of January 2016, the US Fish and Wildlife Service banned neonicotinoid use in wildlife refuges. Neonicotinoids are suspected to contribute to colony collapse disorder because they suppress immunity against bee pathogens including the mite (Varroa destructor) that also serves as a vector for viruses and the Nosema species of fungi that parasitize the gut of bees. Research to ascertain the effect of neonicotinoids on pollinators such as bees and butterflies requires carefully controlled conditions. Neonicotinoid residues have a long half-life (5 months to 3 years) in the soil, and because they are systemic and enter the plant stem, leaves, and flowers, they can present a long-lasting hazard to pollinators. The Australian government’s report on neonicotinoids and honey bees recounts that Australia is one of a few countries that lack Varroa, which therefore provides an opportunity to test neonicotinoids in the absence of compounds used to treat this mite that contributes to bee pathology.
1. Acute toxicity—The fatal dose of nicotine is approximately 40 mg, or 1 drop of the pure liquid. This is the amount of nicotine in two regular cigarettes. Fortunately, most of the nicotine in cigarettes is destroyed by burning or escapes via the “sidestream” smoke. Ingestion of nicotine insecticides or of tobacco by infants and children is usually followed by vomiting, limiting the amount of the alkaloid absorbed.
The toxic effects of a large dose of nicotine are simple extensions of the effects described previously. The most dangerous are (1) central stimulant actions, which cause convulsions and may progress to coma and respiratory arrest; (2) skeletal muscle end plate depolarization, which may lead to depolarization blockade and respiratory paralysis; and (3) hypertension and cardiac arrhythmias.
Treatment of acute nicotine poisoning is largely symptom-directed. Muscarinic excess resulting from parasympathetic ganglion stimulation can be controlled with atropine. Central stimulation is usually treated with parenteral anticonvulsants such as diazepam. Neuromuscular blockade is not responsive to pharmacologic treatment and may require mechanical ventilation.
Fortunately, nicotine is metabolized and excreted relatively rapidly. Patients who survive the first 4 hours usually recover completely if hypoxia and brain damage have not occurred.
2. Chronic nicotine toxicity—The health costs of tobacco smoking to the smoker and its socioeconomic costs to the general public are still incompletely understood. However, the 1979 Surgeon General’s Report on Health Promotion and Disease Prevention stated that “cigarette smoking is clearly the largest single preventable cause of illness and premature death in the United States.” This statement has been supported by numerous subsequent studies. Unfortunately, the fact that the most important of the tobacco-associated diseases are delayed in onset reduces the health incentive to stop smoking.
Clearly, the addictive power of cigarettes is directly related to their nicotine content. It is not known to what extent nicotine per se contributes to the other well-documented adverse effects of chronic tobacco use. It is highly probable that nicotine contributes to the increased risk of vascular disease and sudden coronary death associated with smoking. In addition, nicotine probably contributes to the high incidence of ulcer recurrences in smokers with peptic ulcer. These effects of smoking are not avoided by the use of electronic cigarettes (“vaping”) since only the nonnicotine components (“tars”) of tobacco are eliminated.