Natalie+Dixon+Log

October 1, 2009

Potential topic for final research paper: Synthesis of water soluble Tris(triazolyl)borate ligands which will be used for enzymatic modeling, specifically phosphotriesterase.

October 8, 2009

The past week involved intense literature search on topic. Is it true that we can not use a more narrowed focus of our literature review topic for our research paper topic? **[that is my understanding JCB]**

October 15, 2009

New topic: Identification of the unknown element in the nitrogenase Fe-Mo cofactor.

October 16, 2009

Completed Assignment 1b:

How do gold and green open access strategies work?

Open access is defined by the free availability of academic, electronic journal articles. There are two types in which open accessed is used, green and gold, which is defined by this site [] as the following: - Green access is when an author can provide a free copy of their article on the internet, at the time of publication. The article can be an internal non-peer-reviewed article, a peer-reviewed journal article, a peer-reviewed conference paper or a monograph. - Gold access is when the author pays the publisher at the time of publication and then the publisher makes the material available free to the public.

October 20, 2009

I'm really struggling to narrow down my paper topic. I want to do something that is beneficial to my literature review paper. I want to focus on organophoshates that are found in pesticides and discuss their hazards to the environment and how it is remediated by hydrolysis. Does this seem like a good topic???

A discussion on the effects of organophosphate poisoning and possible modes of prevention is found in this article:

[]

is this a good start?????
 * [I can't access the article from the link you provided - the DOI link will be on the publisher's website, never on SciFinder JCB]**

October 21, 2009

I'm sticking wtih the topic and I've started research.

[]

Organophosphate Pesticides: Biochemistry and Clinical Toxicology, Therapeutic Drug Monitoring, 24: 144–149

October 22, 2009

Discussion on biomonitoring organophosphate pesticides and their effects on children: []

Discussion on degradation of organophosphates in pesticides:

[|**Chemosphere**] [|Volume 76, Issue 9], August 2009, Pages 1308-1314

[]

October 23, 2009

Updated answer to assignment 2:

Do you need more detail for question 14?
 * According to [] an author is able to self-archive if they meet certain requirements that are OAI complacent. Self-archiving is beneficial to a researcher because it advertises the impact their work has on their field. All significant stages of a researcher's work should be self-archived.
 * [] is a website that publishers' freely offer journals on many different subjects.
 * [Yes I made comments on the FAQ page JCB]**

October 24, 2009

Update on assignment 2:

According to [] an author is able to self-archive an article before pre-refereeing and after peer-review. The work is not considered published if not peer-reviewed. If it is peer-reviewed and fulfills the requirements **[Be specific - use ACS as an example - what are their requirements? JCB]** of the journal's referees, then it is deemed publishable. **[Please provide a link to Drexel'l official repository for chemistry and how many articles are there? JCB**]

References for research paper:

O' Mally M. Clinical Evaluation of pesticide exposure and poisoning. //Lancet// 1997; 349: 1161-1166

October 25, 2009

Update on assignment 2:

According to [] an author is able to self-archive an article before pre-refereeing and after peer-review. The work is not considered published if not peer-reviewed. If it is peer-reviewed and fulfills the requirements of a specific journal. The American Chemical Society offers information with regards to the publishing procedure. If you want to publish an article, you must upload it onto the ACS Paragon Plus Environment, where it will be released to a group of registered referees. The guidelines for each article depend on the journal of interest. You can select a specific journal, for example the Journal of the American Chemical Society, and information regarding guidelines for publishing can be found. Such requirements include, but not limited to; formatting, referencing, copyright and dedications. If the requirements are met and is satisfactory according to the journal's referees, then it is deemed publishable. This information is located at [JCB|**http://pubs.acs.org/page/jacsat/submission/recentchanges.html ]][JCB|**[Please provide a link to Drexel'l official repository for chemistry and how many articles are there? JCB**]]]

October 28, 2009

Update on assignment 2:**

According to [|**http://www.eprints.org/openaccess/self-faq**/] an author is able to self-archive an article before pre-refereeing and after peer-review. The work is not considered published if not peer-reviewed. If it is peer-reviewed and fulfills the requirements of a specific journal. The American Chemical Society offers information with regards to the publishing procedure. If you want to publish an article, you must upload it onto the ACS Paragon Plus Environment, where it will be released to a group of registered referees. The guidelines for each article depend on the journal of interest. You can select a specific journal, for example the Journal of the American Chemical Society, and information regarding guidelines for publishing can be found. Such requirements include, but not limited to; formatting, referencing, copyright and dedications. If the requirements are met and is satisfactory according to the journal's referees, then it is deemed publishable. This information is located at [|****http://pubs.acs.org/page/jacsat/submission/recentchanges.html****]. **Drexel offers a variety of databases that are related to chemistry, including SciFinder, CHEMnetBASE and Beilstein. [] is the link that brings you to the chemistry databases provided by Drexel. [] is the link on the Drexel Library website that directs you to the 6503 chemistry scholarly publications offered by drexel.

Assignment 1: Summary of Journal Article

Natalie Dixon Chem Info Retrieval Assignment 1 Due: 10/28/2009

Journal Article: O’Malley, M. Clinical Evaluation of Pesticide Exposure and Poisoning, //Lancet// 1997; 349: 1161-1166.

__ 10.1016/S0140-6736(96)07222-4 __ [Full Marks JCB]

1.) The article is a review of the toxicity of different pesticides and the symptoms that the patient exhibit when over exposed. 2.) Regulations are enforced to prevent pesticide poisoning, such as providing composition and appropriate use on the label. However, failure of complying with these regulations or misuse of the product leads to pesticide poisoning. This is often more common in under-developed countries. 3.) Pesticide poisoning can occur through inhalation, ingestion, or topically. It is important to address the different types of exposure, because the symptoms vary for each and also could show no systemic symptoms. Nearly 50% of the cases in California involved skin, eye or inhalation that showed no systemic symptoms. 4.) Most poisoning cases are addressed by a specialist rather than a general physician. 5.) Organophosphates and carbamates are the components in pesticides that lead to poisoning. The degree of poisoning is dependent on the nature of exposure. 6.) Organophosphates break down acetylcholinesterase, a neurotransmitter responsible for recycling acetylcholine in the nervous system. Degradation of acetylcholinesterase leads to a build-up of acetylcholine, which leads to undesired side-effects on the nervous system. 7.) N-methyl-carbamate behaves similarly as organophosphates, however, the interaction between the carbamate and acetylcholinesterase is not as strong, and therefore is reversible. It is less toxic and harder to detect than organophosphates. 8.) Irritation of the skin and upper respiratory tract are associated with over-exposure to organophosphates. This is due to the presence of mercaptan and sulphides odour-producing agents. 9.) Delayed neuropathy can occur 1-2 weeks after exposure to organophosphates and is considered one of the most serious non-cholinesterase side-effect. However, the compounds that lead to this are no longer used. 10.) The intermediate syndrome can be detected after recovery. 11.) There is an ongoing debate about the persistence of neurobehavioral side-effects after recovery from organophosphate poisoning. Some studies suggest there are, while others report negative results. 12.) Identification of active ingredients in pesticides is essential when addressing a poison case. The label or MSDS associated with the chemical lists the active ingredients present. 13.) It is important to be aware of the inactive ingredients listed; they could be harmful to humans. 14.) Diagnostics of organophosphate poisoning include several blood tests that monitor red blood cells and plasma cholinesterase that are compared to a baseline value. The regeneration of acetylcholinesterase can be tested. 15.) Different tests are done to establish the degree of poisoning. For example, nerve conduction tests are done to determine delay neuropathy. 16.) Not all patients are required to report to the hospital. In this case, decontamination of skin is required and zero exposure is enforced until the organophosphates are completely removed from their system. 17.) For patients who seek hospital care, an antidote is administered. The antidote is determined by the symptoms experienced. For example, atropine is used to reverse muscarinic symptoms. 18.) Severe cases, ingestion of organophosphates (rather than exposure), requires immediate attention. Oxygen, removal of secretions, ventilation and antidotes are required. 19.) Pyrethrum is the active ingredient in most insecticides. Pyrethrum is rapidly hydrolysed in mammalian liver and destroys the nervous system. Its draw back is allergic rhinitis. 20.) Synthetic pyrethroids are developed to improve stability of pyrethrin and are used as a substitute in pesticides. Reports claim poisoning due to over exposure, for example, 10 mg/kg ingested orally can lead to seizures. 21.) Treatment requires prevention of exposure. Topical treatments can be used to remediate symptoms. Acute poisoning requires additional treatment. 22.) DDT is an organochloride that is found in insecticides. They are less toxic than organophosphates but have a slower degradation and remain in the environment much longer. Endrin is one type of organochloride that does degrade quicker, however, has a higher toxicity than other organochlorides. 23.) Exposure to organochlorides results in chronic neurotoxic effects. Reports of exposure to low-levels of chlordane resulted in poisoning. 24.) Studies on the symptoms that result from organochlorides showed a production of liver tumours in rodents. Cases have been reported that exposure to children can result in neuroblastoma and blood dyscrasias. It’s unclear if exposure leads to cancer. 25.) Fumigants and nematocides are prepared from reaction aluminium phosphide with oxygen or water to create phosphine. Phosphine is poisonous to cells such that it interacts with cytochrome oxidase. It’s dangerous because exposure under 0.3 ppm could go undetected, yet is toxic enough to cause defects. 26.) Symptoms that result from exposure to phosphines include gastrointestinal, cardiorespiratory and CNS. No lab abnormalities have been detected. Serum aluminium is used to detect exposure if ingested, however, it does not detect if phosphine is inhaled. 27.) Phosphine exposure can result in breakage of specific chromosome bands and excess non-Hodgkin lymphoma is indicated. 28.) Methyl bromide is another type of fumigant. It results in acute CNS symptoms, pulmonary, hepatic and renal injuries occur. A blood bromide concentration of 1mmol/L can lead to fatality. 29.) There is not a specific antidote that treats methyl bromide poisoning. 30.) 2, 4-dichlorphenoxy acetic acid acts as a herbicides. If mildly exposed, acute skin and respiratory irritation can result. Ingestion leads to more harmful side-effects such as myotonia, vomiting, diarrhoea, and peripheral neuropathy. 31.) 2, 4-dichlorphenoxy acetic acid has not shown to be carcinogenic, but can lead to non-Hodgkin lymphoma. 32.) If exposed to dipyridyl paraquat, topical irritation may occur, along with discoloration of fingernails, sore throat and coughing. Ingestions results in vomiting and diarrhoea. If not treated promptly, pulmonary fibrosis may occur. 33.) Some scientists believe that exposure to paraquat may lead to Parkinson’s disease due to structure analogy between paraquat and 1-methyl-4-phenylpyridinium. 34.) Bentonite and fuller’s earth is used to treat dipyridyl poisoning.

November 5, 2009

Assignment 1:

Open access is defined by the free availability of academic, electronic journal articles. There are two types in which open accessed is used, green and gold, which is defined by this site [] as the following:** . **Drexel offers a variety of databases that are related to chemistry, including SciFinder, CHEMnetBASE and Beilstein.** [|**http://www.library.drexel.edu/databases/chemistry**] **is the link that brings you to the chemistry databases provided by Drexel.** [|**http://innoserv.library.drexel.edu/search/X?SEARCH=chemistry&searchscope=9&SORT=D**] **is the link on the Drexel Library website that directs you to the 6503 chemistry scholar publications offered by drexel. This is the link to Drexel's Green repository for the chemistry department:** [|**http://idea.library.drexel.edu/simple-search?query=chemistry**]**.**
 * Green access is when an author can provide a free copy of their article on the internet, at the time of publication. The article can be an internal non-peer-reviewed article, a peer-reviewed journal article, a peer-reviewed conference paper or a monograph. According to [] an author is able to self-archive an article before pre-refereeing and after peer-review. The work is not considered published if not peer-reviewed. If it is peer-reviewed and fulfills the requirements of a specific journal. The American Chemical Society offers information with regards to the publishing procedure. If you want to publish an article, you must upload it onto the ACS Paragon Plus Environment, where it will be released to a group of registered referees. The guidelines for each article depend on the journal of interest. You can select a specific journal, for example the Journal of the American Chemical Society, and information regarding guidelines for publishing can be found. Such requirements include, but not limited to; formatting, referencing, copyright and dedications. If the requirements are met and is satisfactory according to the journal's referees, then it is deemed publishable. As far as green access is concerned with ACS, "As the ACS policy is currently worded, it only charges the fee for self-archiving the published edition of an article. Hence it leaves the door open for no-fee self-archiving of the final version of their peer-reviewed manuscript, rather than the published edition." This quote is taken from: []. This information is located at [|**http://pubs.acs.org/page/jacsat/submission/recentchanges.html**]
 * **Gold access is when the author pays the publisher at the time of publication and then the publisher makes the material available free to the public.** [|**http://www.doaj.org/**] **is a website that publishers' freely offer journals on many different subjects.**

> **Assignment 3 - Have you graded?**
 * **[8/10 3 of your links to not go to the articles JCB]**

> **CAS # [|107539-20-8] ** > **5 properties** >
 * Yttrium Barium Copper Oxide (YBCO), YBa2Cu3O7**

**-Physica. C., 468, 2008, 1567: doi []****: 2.65 MA/cm2 -IEEE Transactions on Applied Superconductivity, 15, 2005, 3050: 1.2 MA/cm2: doi: [] -Supercond. Sci. Technol., 18, 2005 1271 : 3 MA/cm2, doi: [] - IEEE Transactions on Applied Superconductivity, 19, 2009, 3270: > 1 MA/cm2 for plain YBCO, doi: []
 * 1.)** **Critical Current Density (Jc)**
 * - Supercond. Sci. Technol., 15, 2002, 907. : 1.1 x 10^4 MA/cm2: doi: []**

2.)** **Critical Temperature (Tc)** -IEEE Transactions on Applied Superconductivity, 15, 2005, 3050: 90 K doi:** [|**http://dx.doi.org/10.1109/TASC.2005.848733**]
 * - Supercond. Sci. Technol., 15, 2002, 907. : 92 K, doi:** [|**http://dx.doi.org/10.1088/0953-2048/15/6/312**]
 * -Physica. C., 468, 2008, 1567: doi** [|**http://dx.doi.org/10.1016/j.physc.2008.05.068**] **: 90 K
 * -Supercond. Sci. Technol., 18, 2005 1271 : 91 K, doi:** [|**http://dx.doi.org/10.1088/0953-2048/18/10/004**]
 * - Wikipedia.org/YBCO: 95 K** [|**http://en.wikipedia.org/wiki/YBCO**]

-Physica C: Superconductivity, 282-287 Part 2, 1997, 571, doi: [|http://dx.doi.org/10.1016/S0921-4534(97)00371-7]: perovskite** -**Supercond. Sci. Technol., 10, 1997, 862, doi: []** :**perovskite**
 * 3.)** **Crystal Structure**
 * - Supercond. Sci. Technol., 15, 2002, 907. : perovskite, doi:** [|**http://dx.doi.org/10.1088/0953-2048/15/6/312**]
 * -Wikipedia.org/YBCO: perovskite,** [|**http://en.wikipedia.org/wiki/YBCO**]
 * -Physica B: Condensed Matter, 387, 2007, 143, doi:** [|**http://dx.doi.org/10.1016/j.physb.2006.03.096**] **: perovskite

- density = 4.453 g/cm3, Journal of Superconductivity, 18, 361, doi : [] - density= 5.24 g/cm3, J. Materials Science, 28, 4744, doi: [] -density= 5.7 g/cm3, Czech. J. Physics, 46, 1405, doi: [] -density= 6.593 g/cm3, Physica C. Superconductivity, 468, 1350, doi: []
 * 4.)** Density
 * - density= 4.4 - 5.3 g/cm3, []

5.)** **Peritectic Point** **- J. Phys. Condens. Matter, 15, 2003, 7149, doi: []: 1010oC - J. Cryst Growth, 234, 611: []: 1010oC - Q. Rao et al./Scripta Materialia, 57, 2007, 663, []: 1010oC - J. Mater Res., 11, 1996, 786, doi: []: 1015oC**
 * J. Superconductivity, 11, 1998, 575, doi:[]: 1010oC**

November 27, 2009

Uploaded chem info paper rough draft. Edited FAQ question:

Open access is defined by the free availability of academic, electronic journal articles. There are two types in which open accessed is used, green and gold, which is defined by this site [] as the following:
 * Green access is when an author can provide a free copy of their article on the internet, at the time of publication. The article can be an internal non-peer-reviewed article, a peer-reviewed journal article, a peer-reviewed conference paper or a monograph. According to [] an author is able to self-archive an article before pre-refereeing and after peer-review. The work is not considered published if not peer-reviewed. The American Chemical Society offers journal articles for free. For example, Drexel offers a variety of databases that are related to chemistry, including SciFinder, CHEMnetBASE and Beilstein, where you can find ACS articles for free. [] is the link that brings you to the chemistry databases provided by Drexel. [] is the link on the Drexel Library website that directs you to the 6503 chemistry scholar publications offered by drexel. This is the link to Drexel's Green repository for the chemistry department: []. The NIH provides a website the indicates levels of access permitted by each publisher: [], such as advertising green access offered by Elsevier.
 * Gold access is when the author pays the publisher at the time of publication and then the publisher makes the material available free to the public. [] is a website that publishers' freely offer journals on many different subjects.

December 4, 2009 Final Paper

**[Your final paper must be on its own page and remove all this formatting that is making the text hard to read and forcing me to scroll left and right constantly JCB]** ** Toxic Behavior of Organophosphate Pesticides and Analytical Techniques Utilized in Detecting Organophosphates Found in Environmental Samples ** Organophosphate is the term used to define esters of phosphorous acids and is typically used to represent the phosphor-carbon bond in these molecules.(1) Effective organophosphates contain a phosphoryl group, two lipophilic groups attached to the phosphorous atom, and a leaving group, commonly a halide, also bound to the phosphorous atom.(1) The side-chains are diverse and lead to different reactive behaviors which correspond to the different levels of poisoning caused by organophosphates.(2) In 1932, a German chemist, Gerard Schrader, studied the effects of organophosphates on insects after Willy Lange discovered the toxic effects of organophosphates on the parts of the nervous system that are related to acetylcholinesterase.(1) Organophosphates are effective inhibitors of acetylcholinesterase, which is essential to nerve function in insects, animals, and humans. Organophosphates’ toxic behavior and increased hydrolytic rates when exposed to sunlight, soil and air, (1) make them an ideal replacement for the former active ingredient in pesticides, organochlorides. However, organophosphates have shown to be more toxic in humans than organochlorides. Pesticides are inherently toxic since they are composed of more than 200 organophosphates, with the active ingredient found on the label or MSDS.(2) Structures of common organophosphates found in pesticides can be seen in Figure-1.3
 * Natalie Dixon **
 * University **** of Drexel **
 * Submitted: December 5, 2009 **



(a.) Parathion Ethyl (b.) Malathion (c.) Fenthion

** Figure-1: Structures of common organophosphate pesticides, including parathion, malathion and fenthion. ** The utilization of organophosphates as components in pesticides has become increasingly common in the global agriculture sector. Globally, production and consumption of pesticides increased 10-fold between 1955 and 1985 and is currently in high demand.(4) As the global population increases, there is a greater demand on the industrial and agricultural sectors for the production of food. This demand requires preservation of crops that can be destroyed by natural disasters or pests. To address the issue imposed by insects, pesticides are employed. To meet the higher demand for food, the use of pesticides is increased which in turn increases pollution on the environment.(5) Organophosphate contaminants are generally found in freshwater reserves and soil.(5) The presence of organophosphates in soil and water is a result of water run-off caused by rain or flooding. Another common form of organophosphate contamination is caused by inhalation which can result from the distribution of pesticides among the crops or by chemical fires that occur at warehouses where pesticides are stored.(6) Agriculture workers are the most common victims of organophosphate exposure; however, the contamination of fresh-water by organophosphates endangers society, animal-life and the environment. Organophosphate poisonings are also found as the cause for many suicides due to the relative ease in obtaining organophosphate containing pesticides. Organophosphate poisonings commonly occur in under-developed nations, such as Sri-Lanka, however, even the most regulated countries struggle to prevent the impairment or death of citizens that were exposed to organophosphates.(7)

Toxic exposure of organophosphates on agriculture workers leads to more than 3 million poisonings and 200,000 deaths per year, globally.(2) Most of the poisonings occur in deprived nations, such as Taiwan (7), however, in the United States, 13,348 toxic organophosphates exposures were reported.(8) Organophosphate exposure occurs through respiratory, gastrointestinal, ocular and dermal absorption of pesticides. Symptoms occur more rapidly from the inhalation of the organophosphate odor.(2) The organophosphates from the pesticides accumulate in fat, liver and kidneys. Patients begin to exhibit symptoms as quickly as 12 hours. The symptoms are a result of inhibition of the enzyme, acetylcholinesterase.

Acetylcholinesterase is an important biological enzyme found in the central nervous system of insects, animals and humans. Acetylcholinesterase is found in the central nervous system at neuromuscular junctions and synapses, as well as, the membranes of red blood cells. It is an enzyme that rapidly hydrolyzes the neurotransmitter, acetylcholine. Acetylcholine binds to the hydroxyl group on the serine residue 203 in acetylcholinesterase, which forms an intermediate that is broken down by the hydrolysis of acetylcholine and then regeneration of acetylcholinesterase.(2) The choline that is produced from the hydrolysis of acetylcholine is recycled back into the nerve terminals where it is used to produce new acetylcholine molecules.(9) Acetylcholinesterase breaks-down 5,000 molecules of acetylcholine every second.(9) The presence of cholinesterase inhibitors prevents the acetylcholinesterase from functioning. Without the activated acetylcholinesterase, the acetylcholine receptors are over stimulated and eventually breakdown due to the accumulation of acetylcholine.(2) The accumulation of acetylcholine results in neuromuscular paralysis across the entire body which results in death by asphyxiation.(9)

Organophosphates are one example of a common inhibitor of acetylcholinesterase. When organophosphate is present, phosphorylation occurs at the serine residue 203, forming an organophosphorous intermediate that is stabilized, slowing the rate of hydrolysis or even preventing regeneration of acetylcholinesterase, depending on the phosphorylated group bound to acetylcholineserase.(2) Figure-2 is a general schematic of acetylcholinesterase inhibition caused by organophosphate pesticides.(2)

The side-chains bound to the organophosphate determine its affinity to acetylcholinesterase, rate of hydrolysis, regeneration of acetylcholinesterase, and toxicity.(2) For example, acetylcholinesterase ages if the phosphorylated enzyme loses an alkyl group before it is regenerated. An aged enzyme is permanently phosphorylated and cannot be regenerated.(2) These effects are enhanced in insects, ultimately leading to their death, which makes the use of organophosphates in pesticides ideal. Research has been done on the effects of organophosphates present in humans. The studies have shown that organophosphates have neurological and detrimental effects on humans and will be discussed further. Interestingly enough, organophosphates are still used as pesticides. Due to their high toxicity on humans, strict regulations must be employed on the use of organophosphates as pesticides to prevent over-exposure.
 * Figure-2: General scheme of acetylcholinesterase inhibition caused by organophosphates. **

Despite regulations and instructions associated with the use of pesticides, misuse and environmental contamination leads to exposure of the skin and respiratory tract and ultimately acute toxic effects, especially in agricultural workers.(10) Organophosphate poisoning is most common amongst agriculture workers in underdeveloped countries, but can also be found as the cause for many suicides.(10) The following studies discussed further focus on undesired exposure to organophosphate pesticides. Pesticides lead to 1 million accidental poisonings and 2 million suicide attempts world-wide, with 13,000 poisoned patients and 1,000 deaths occurring in Sri Lanka and 100,000 cases occurring in China.(10) The main ingredient in each pesticide varies depending on the major organophosphate present. A study was done in California between 1982 and 1990 to determine the type of organophosphate that led to poisoning amongst non-agricultural workers and agricultural workers. People who were not agricultural workers were poisoned by organophosphates of moderate toxicity including malathion, chlorpyrifos, dichlorovos, dimethoate, and propetamphos. Poisonings amongst agricultural workers were associated with high-toxicity organophosphates including mevinphos, methomyl, methamidophos, oxydemeton, and parathion, as well as moderately toxic organophosphates including dimethoate and phosalone.(10) The level of toxicity determines the systemic effects observed in victims of organophosphate poisoning.

Organophosphate poisoning can occur through consumption of contaminated water or inhalation of the odours. Pesticides found in the soil pose a threat to ground water, water reserves and wells due to surface run-off caused by rain.(11) A case study involving contaminated waters was done in Somalia’s North-West Zone. A pesticide store was damaged after a bombing, which led to the theft of chemical drums in which some contained organophosphate pesticides. The looters dumped the chemical drums, contaminating 3,700 square miles of soil with up to 3,728 ppm of pesticides. The high concentration of pesticides found in the soil and water led to the death of humans, lizards, and frogs, as well as many cases of organophosphate poisonings amongst the citizens of Somaliland. (11) Organophosphate poisoning does not only occur through consumption, but can also be a result of inhalation. The inhalation of organophosphates can result from the spraying of crops with pesticides. An example of exposure through inhalation involves an oil-company employee that noticed the odor of malathion, an organophosphate pesticide, coming from a helicopter. The employee reported symptoms including a sore-throat, headache, and burning skin. The cholinesterase activity was measured and was reported as normal. In this case, malathion is a less toxic pesticide. The odor is a result of mercaptans and sulphides present in organophosphates which can provoke symptoms such as a headache and nausea, which are symptoms independent from acetylcholinesterase inhibition. Atypical symptoms of organophosphate poisoning that arise from inhalation include tightness of the chest, wheezing, and bronchoconstriction and require careful attention.(10) Inhalation of organophosphates can also result from the burning of pesticides. One of the most common hazards of plants that store pesticides is a chemical fire. The decomposition of pesticides and their by-product result in hazardous consequences on the environment.(6) The level of toxicity is hard to measure due to the complex combinations of different chemical reactions that ensue.

The acute systemic effects vary according to individual pesticides and are the determining factor of organophosphate poisoning.(10) However, exposure to eye, skin or lungs causes topical reactions without systemic illness. In 1994, 1,332 possible pesticide poisoning cases reported had involved 48.9 % with only topical symptoms, 34.1% with systemic systems and topical systems, and 16.7% with only systemic symptoms.(10) The initial symptoms that occur are a result of overstimulation of the receptors in the nervous system that interact with acetylcholine. The degree of the inhibition of the acetylcholinesterase is impossible to determine. Therefore, the rate of acetylcholinesterase inhibition is related to the onset of symptoms.(10) The main symptoms of organophosphate poisoning include miosis, urination, diarrhoea, diaphoresis, lacrimation and excitation of the nervous system.(10) Organophosphate poisoning cannot be treated by general physicians. Treatment from a specialist is required in which many patients are typically administered to hospitals for remediation.(10) A patient exposed to organophosphates is diagnosed with organophosphate poisoning once their blood test of red-cell and plasma cholinesterase is reported as being positive.(10) The tests include observing the rate of regeneration of the acetylcholinesterase enzyme after treatment of the same blood sample with the cholinesterase antidote pralidoxime. The results are compared to a baseline value. Patients are treated with an antidote, usually atropine, which reverses the muscarinic symptoms caused by organophosphate poisoning. The prescription required depends on the amount of exposure. Pralidoxime is another antidote that remediates symptoms in exposed patients. Pralidoxime treats nicotinic and muscarinic symptoms. For patients with the most serious case of poisoning, oxygen ventilation, clearance of secretions and treatment with an antidote is required. For patients that don’t require hospitalization, washing of the skin is required and future exposure to pesticides is not recommended.(10) Long-term neurological effects have been found in patients with high exposure to organophosphates over a long period of time. The fate of victims who are highly exposed to toxic organophosphates over a short period of time result in death.

Organophosphate poisonings that do not end in mortality have a likely chance of initiating long-term neurological and nervous system effects due to inhibition of the acetylcholinesterase enzyme resulting in over accumulation of acetylcholine. Multiple studies have been done on assessing the effects of organophosphate poisoning on neurological and nervous systems. One such report involved studying agricultural workers from Nicaragua who had high exposure to organophosphates between July 1, 1986 and July 1, 1988 and compared the behaviour of their central nervous system to that of men who were not exposed to such organophosphates.(4) The group that was deemed poisoned was exposed to pesticides two years prior to the study. The two groups participated in six subtests developed by the World Health Organization that are the overall composition of a neuropsychological test. The poisoned groups’ performance on five of the six tests was much worse. The two groups also completed additional tests that assessed verbal and visual attention, visual memory, visuomotor speed, problem solving, motor steadiness and dexterity. The poisoned group’s performance was unsatisfactory on three of the six tests. The study found that there was a decrease in neuropsychological performance amongst the group that was poisoned by organophosphates. From this study, it was observed that exposure to organophosphate pesticides resulted in a decline in neurological performance. Another neurological study was extended beyond underprivileged nations to that of a more regulated country. The results were strikingly similar.

The same results were found in a study that was done a few years later that involved determining the chronic neurological effects of organophosphate poisoning. The study was done on 128 men that were poisoned by organophosphate pesticides in California from 1982 to 1990. The men underwent neurological physical examination, five nerve conductions tests, two vibrotactile sensitivity test, ten neurobehavioral tests and one postural sway test. The study found that the poisoned men performed worse on two neurobehavioral tests. When the study focused on comparing men who were severely poisoned as opposed to the men who were less exposed, the more highly-exposed group showed worse vibrotactile sensitivity.(12) Though the size of the study is limited, this study coupled with the previous study confirms the harmful effects organophosphate exposure has on humans. They also reinforce the notion that exposure of organphosphate pesticides must be eliminated. Detection of organophosphate pesticides in the environment is critical in prevention against organophosphate poisoning.

In order to detect the presences of pesticides in the environment and then remediate areas that have been contaminated, analytical techniques are employed to measure the concentration of the different types of organophosphates present in environmental samples.(13) Environmental contamination caused by pesticides can be studied by applying analytical methods such as gas-chromatography used in conjunction with mass-spectrometry (GC/MS), high-pressure liquid chromatography (HPLC), liquid chromatography used in conjunction with mass spectrometry (LC/MS), ultraviolet-visible absorption spectroscopy (UV-VIS), solid-phase extraction disks (SPE-disks) and solid-phase micro-extraction (SPME) followed by GC/MS, and optical sensor sol-gel techniques.(14) European Union regulations set a 0.5 µg/L limit for all pesticides present and a 0.1 µg /L limit for individual compounds present. Therefore, detection limits of organophosphates in water samples must be below a concentration of 0.1 µg /L.(3) The presence of pesticides in food is monitored by multi-residue extraction methods (MRMs), with the most common method involving solvent extraction, using acetone or ethyl acetate, followed by gas chromatography (GC).(15) GC-MS is successful in detecting the presence of pesticides because it allows for simultaneous confirmation and quantization of a large number of pesticides. However, the limitation of using GC arises from the high limits of detection, which need to be decreased to meet the European Union regulations.(15) One option in decreasing the limits of detection includes increasing the injection volume of the sample. Large column injection based on cold on-column and programmable temperature vaporizing injections that inject 1-2 µL are typically used. One study included using a split/split-less injector that injects 10 microliters.(15) This technique analyzed 110 pepper, cucumber and tomato samples and found organophosphate resides on 46% of the samples analyzed, with 23% of the samples exceeding the tolerance. GC-MS has also been used to determine the bi-products of organophosphate combustion. GC-MS has proven to more effective in confirming the presence of these products than the typical micro-scale experiments that are used for investigation.(6)

LC/MS is another technique used to determine trace levels of organophosphates.(16) Direct-electron ionization is a relatively new interfacing device that combines a nano-HPLC column with a mass spectrometer that has electron ionization capability, which is expected to optimize the introduction of the liquid into the EI source and detect the presence of organophosphates at concentration levels of a few parts per billion (ppb).(17) The direct liquid introduction previously used was limited in success due to clogging of the transport capillary, unstable source pressure and sample sputtering. It also allows micro- and nano-HPLC columns to perform well at very low flow rates. EI spectra give structural information that is easily interpreted and obtained. The coupling of HPLC with MS is a better alternative to GC/MS since organophosphates are thermally labile and chemically reactive which result in decomposition during analysis.(18) Studies using this technique have identified several organophosphate pesticides in water samples below 0.5 ppm.(17)

Another technique used to determine the presence of organophosphates in environmental samples includes the use of sol-gel based mid-infrared sensors on aqueous solutions. This is a better alternative to gas or liquid chromatographic techniques. LC/GC techniques rely heavily on sensitivity. The concentration levels of organophosphates change due to the changing environment. These techniques, LC/GC, do not account for the changing conditions. A better detection technique to account for varying environmental conditions is to use a monitoring device that measures the presence of the organophosphates while still in the environment, rather than in samples taken from contaminated sites. This type of technique would rely on developing biosensors to study the organophosphate interaction with surface-immobilized enzymes.(19) One limitation in using biosensors is that they are difficult to purify and they have low stability. Optical sensors are a better alternative such that they have “intrinsic molecular specificity, robustness, remote sensing capability, and are absent of interferences such as electromagnetic fields or surface potential.”(19) The sol-gel technique is a method used to develop ceramics by hydrolysis and polymerization of organic materials. This method allows for preparation of analyte layers with large surfaces areas, as well as, advantageous optical, dielectric, thermal and acoustic properties that are stable under severe environmental conditions and have shown to detect organophosphates at low ppm concentrations.(19) One study used this method to determine the presence of the following organophosphate pesticides: parathion, fenitrothion and paraoxon, in aqueous solution. ZnSe Attenuated Total Reflectance (ATR) crystals were coated with a sol-gel film that the organophosphates interacted. The increased surface area and porosity of sol-gel optical sensors allowed for lower limits of detection of these organophosphate containing pesticides.(5)

The techniques described above are examples of different detection methods used to determine the presence of organophosphates in environmental samples. Organophosphate compounds have been the primary components in pesticides since the 1980’s and have shown to cause acute effects on the nervous system with high-levels of exposure.(20) Corrective measures can then be taken to prevent harmful exposure to these pesticides. Currently, remedial solutions of organophosphates include avoiding use or limited use and chemical solutions. Current synthetic work involves developing catalytic mimics of the metalloenzyme, acetylcholinesterase; that can be used to increase the rate of hydrolysis of the organophosphate bond.(21) However; extensive research on effects on the environment as well as human health needs to be considered when employing these chemical solutions. Considering the neurological and detrimental side-effects from exposure to organophosphate pesticides, it is clear that an alternative solution to the utilization of organophosphate pesticides must be found.

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