Annotated Bibliography-Nicotine Toxicity

Annotated bibliography

  1. Hukkanen, J., Jacob, P. & Benowitz, N. L. Metabolism and Disposition Kinetics of Nicotine. Pharmacol Rev 57, 79–115 (2005). Doi:10.1124/pr.57.1.3
    1. This article presents a highly descriptive analysis of the kinetics regarding nicotine toxicity within both systemic and localized systems following multiple routes of ingestion, and effectively demonstrates the mechanism of action and pertinent metabolites following nicotine ingestion.
  2. Celie, P. H. N. et al. Nicotine and Carbamylcholine Binding to Nicotinic Acetylcholine Receptors as Studied in Achbp Crystal Structures. Neuron 41, 907–null (2004). PMID: 15046723
    1. This crystal structure illustrating the bound nicotine within an acetylcholine receptor provides for a more nuanced view of the primary mechanism of action which is involved with metabolic toxicity of nicotine.
  3. Arredondo, J. et al. Receptor-Mediated Tobacco Toxicity. Am J Pathol 166, 597–613 (2005). PMID: 15681842
    1. This paper serves to isolate and examine a specific binding site (nAChR), its subunits, and the genetic factors that support it when exposed to nicotine. The quantitative data therein allows for analysis of the specific mechanisms of interaction applied to a major interaction site.
  4. Zevin, S., Gourlay, S. G. & Benowitz, N. L. Clinical pharmacology of nicotine. Clin. Dermatol. 16, 557–564 (1998). PMID: 9787965
    1. This paper serves to present a higher-order view of the systemic effects following nicotine ingestion, with some of the chemical transformations evidenced as well. The focus on systematic effects of chronic and acute nicotine toxicity presents a good base on which to judge ultimate effects.
  5. Schep, L. J., Slaughter, R. J. & Beasley, D. M. G. Nicotinic plant poisoning. Clinical Toxicology 47, 771–781 (2009). Doi: 1080/15563650903252186
    1. This review article focuses upon the naturally occurring alkaloid variants of the nicotine compound, and delves into the variances regarding physiological effects, as well as some information regarding the toxicological effects of these alkaloid products upon other species (specifically insects). This helps to present a more nuanced view, by way of examining the effects upon a more simplistic system.
  6. Liu, Z., Zhang, J. & Berg, D. K. Role of endogenous nicotinic signaling in guiding neuronal development. Biochem. Pharmacol. 74, 1112–1119 (2007). doi:10.1016/j.bcp.2007.05.022
    1. This paper presents a novel viewpoint, focusing upon the analysis of nicotinic-like compounds and similar effects present within the formation of CNS systems in a sample (chicken) neural cell population.
  7. Dani, J. A. & De Biasi, M. Cellular mechanisms of nicotine addiction. Pharmacology Biochemistry and Behavior 70, 439–446 (2001). Doi: 1016/S0091-3057(01)00652-9
    1. This paper provides some crucial background information relating to chronic nicotine use and its lasting effects, exploring a more commonly-encountered form of nicotine toxicity and hinting (in parallel with other papers utilized) at effects beyond neuronal systems.
  8. Bassett, R. A., Osterhoudt, K. & Brabazon, T. Nicotine poisoning in an infant. N. Engl. J. Med. 370, 2249–2250 (2014). Doi: 1056/NEJMc1403843
    1. This case study presents some top-level epidemiological information regarding acute nicotine toxicity, both broadly in the overall population and specifically within youth. The blood serum data cited herein also provides a glimpse of the most readily identifiable external effects suffered as a result of acute nicotine toxicity.
  9. Fassa, A. G. et al. Green tobacco sickness among tobacco farmers in southern Brazil. Am. J. Ind. Med. 57, 726–735 (2014). Doi:1002/ajim.22307
    1. This epidemiological-centered article provides a lens through which to examine the effects of nicotine-containing alkaloid species that occur in nature upon human biology. This provides a different model (aside from the classical cigarette/tobacco model) through which to examine the metabolic effects nicotine has, absent of usual competing factors which might also play synergistic roles in nicotine toxicity. Specifically, it provides insight as to the degree to which other stimulants packaged in nicotine delivery systems work to aggravate the same response.
  10. Tonstad, S., Gustavsson, G., Kruse, E., Walmsley, J. M. & Westin, Å. Symptoms of Nicotine Toxicity in Subjects Achieving High Cotinine Levels During Nicotine Replacement Therapy. Nicotine Tob Res ntu076 (2014). doi:10.1093/ntr/ntu076
    1. This paper examines alternate pathways through which nicotine toxicity (and mores specifically its effects) can be discerned, with the additional benefit of being able to examine the role of alternate agonists (Conitine) on the same biological system.
  11. Goniewicz, M. L., Hajek, P. & McRobbie, H. Nicotine content of electronic cigarettes, its release in vapour and its consistency across batches: regulatory implications. Addiction 109, 500–507 (2014). Doi: 1111/add.12410
    1. This pharmacological review regarding transmission of nicotine through a novel and constantly evolving mechanism presents important background information which codifies a specific mechanism of high nicotine exposure. By way of understanding the intricacies of this delivery system, and specifically the concentrations of nicotine typically involved, physiological responses can be better compared to discrete abundances.
  12. Tomizawa, Motohiro, and John E. Casida. “Selective toxicity of neonicotinoids attributable to specificity of insect and mammalian nicotinic receptors.” Annual review of entomology 48.1 (2003): 339-364.
    1. This paper explained much of the mechanistic details present in the use of neonicotinoid pesticides.
  13. Mayer, B. How much nicotine kills a human? Tracing back the generally accepted lethal dose to dubious self-experiments in the nineteenth century. Arch Toxicol 88, 5–7 (2013). Doi: 1007/s00204-013-1127-0
    1. This article presents an interesting retrospective analysis, as well as a necessary frame of reference for any papers of sufficient age (before 1990), as there are some flawed foundations which manifest themselves as cited sources, and can chip away at otherwise stellar research. It further provides experimentally derived data for novel conclusions in regards to LD50 and other toxicity markers.
  14. Mazei-Robison, M. S. et al. Self-Administration of Ethanol, Cocaine, or Nicotine Does Not Decrease the Soma Size of Ventral Tegmental Area Dopamine Neurons. PLoS ONE 9, e95962 (2014). Doi: 1371/journal.pone.0095962
    1. This paper underlines the specific physiological effects that increased nicotine levels (and resultantly conitine) have upon neuronal complexes. The lack of detrimental activity upon the dopamine sensitive neurons implies limited effects of chronic nicotine use, the specifics of which are just as important as the more immediate negative effects.
  15. Riah, O. et al. Evidence that nicotine acetylcholine receptors are not the main targets of cotinine toxicity. Toxicology Letters 109, 21–29 (1999). Doi:10.1016/S0378-4274(99)00070-3
    1. This interrogation into the specific target for nicotine and related compounds provides a necessary foundation for identifying the specific mechanism of action.
  16. Montalto, N., Brackett, C. C. & Sobol, T. Use Of Transdermal Nicotine Systems In A Possible Suicide Attempt. J Am Board Fam Pract 7, 417–420 (1994). Doi:10.3122/jabfm.7.5.417
    1. This case study examines another route of ingestion regarding nicotine toxicity, and also interrogates the LD50 as it pertains to adolescent females.
  17.  True WR, Xian H, Scherrer JF, et al. Common Genetic Vulnerability for Nicotine and Alcohol Dependence in Men. Arch Gen Psychiatry. 1999;56(7):655-661.
    1. This research on the genetics behind long term dependence within the bounds of nicotine helps elucidate the effects of chronic exposure of nicotine upon nAChR’s within the body, and corresponding population data.
  18. Saccone, Scott F., et al. “Cholinergic nicotinic receptor genes implicated in a nicotine dependence association study targeting 348 candidate genes with 3713 SNPs.” Human molecular genetics 16.1 (2007): 36-49.
    1. The examination of gene-mediated binding affinities here further exposed the role of nAChR’s and ion channels as being of prime importance in facilitating the effects of nicotine usage.
  19. Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Neuroscience. 2nd edition. Sunderland (MA): Sinauer Associates; 2001. Excitatory and Inhibitory Postsynaptic Potentials.
    1. The information regarding the neurochemistry and physiology of nicotine and acetylcholine mediated potentials within the brain is of crucial importance when describing the functional components of any toxic system, especially one with such strong dependency-promoting effects.
  20. Ding, Fei, and Wei Peng. “Biological assessment of neonicotinoids imidacloprid and its major metabolites for potentially human health using globular proteins as a model.” Journal of Photochemistry and Photobiology B: Biology 147 (2015): 24-36.
    1. The experimental analysis of pesticide-introduced metabolites that can bind to and activate neonicotinoid receptors presents both context as to the mechanism of binding to nAChR as well as suggests the rise of a public health problem based upon nicotine toxicity.
  21. Schep, Leo J., Robin J. Slaughter, and D. Michael G. Beasley. “Nicotinic plant poisoning.” Clinical toxicology 47.8 (2009): 771-781.
    1. This paper was instrumental in examining both the acute effects of nicotine toxicity as well as determining the medical interventions necessary.
  22. Griffiths, Roland R., JACK E. Henningfield, and GEORGE E. Bigelow. “Human cigarette smoking: manipulation of number of puffs per bout, interbout interval and nicotine dose.” Journal of Pharmacology and Experimental Therapeutics220.2 (1982): 256-265.
    1. This older research paper gave valuable explanations on the nature of how nicotine can act in two disparate ways upon the body and nervous system depending on quantity ingested.
  23. Schroeder, Megan J., and Allison C. Hoffman. “Electronic cigarettes and nicotine clinical pharmacology.” Tobacco control 23.suppl 2 (2014): ii30-ii35.
    1. This paper further examined the quantities of nicotine absorbed between classical and electronic cigarettes, and highlighted the standard nicotine concentration for classical cigarettes.
  24. Feyerabend, C., and M. A. H. Russell. “A rapid gas‐liquid chromatographic method for the determination of cotinine and nicotine in biological fluids.”Journal of Pharmacy and Pharmacology 42.6 (1990): 450-452.
    1. This paper provided the clinical trials best utilized in diagnosing acute nicotine toxicity.