User:Peter Damian/investigation

Elementary mistakes

The (II) in Nitrogen (II) oxide means the oxidation state of the nitrogen in the compound. For two-element compounds, each oxidation state times the number of that atom present cancels to zero. Since the oxidation state of oxygen is always -II in compounds, nitrogen(II) oxide will be NO as a +2 nitrogen will cancel a -2 oxygen. For nitrogen(IV) oxide, we have a +4 nitrogen and so need two -2 oxygens to balance the charge, and so nitrogen(IV) oxide is NO₂.

Wikicology also made the mistake of thinking carbon(I) oxide was CO when it would actually be C₂O - which doesn't exist! Carbon monoxide is CO, and would be carbon(II) oxide under this naming system.This is a beginner mistake: it is taught at High School in Australia.

His classification of beryllium poisoning as an example of gas poisonings was also a surprise, as any chemist should know that beryllium is a solid at room temperature. Further, beryllium poisoning is characterised by granulomas ("an inflammation found in many diseases. It is a collection of immune cells known as histiocytes. Granulomas form when the immune system attempts to wall off substances it perceives as foreign but is unable to eliminate.") formed by the body to deal with solid particles of beryllium. Gas poisonings aren't like this, and while some symptoms might be superficially similar, a biochemist wouild understand the process and the differences.

Another example is the statement from the biochemical effects part of the article: "It also causes a decrease in Glucose-6-phosphate dehydrogenase which may results in Glucose-6-phosphate dehydrogenase deficiency known as favism, a condition that predisposes to hemolysis (spontaneous destruction of red blood cells).[47]" Ref 47 is another rat study on NO₂, which is a questionable basis for such a broad statement. More disturbingly, the abstract states that "The activities of glucose-6-phosphate dehydrogenase and glutathione reductase were significantly higher than those in the control group for the 9-month exposure. In the 18-month exposure, however, they showed a tendency to return to control level." Any scientist should know that the control group is the one not exposed to the test and so the abstract actually says that the levels of this enzyme were higher in the treatment group but the article says the levels decreased. These examples suggest limited understanding of the chemistry, poor choice of sources, and mistaken interpretation of those sources, in addition to sources being incorrect.

Yet another example from the lead of the article is:

Known sources of Nitrogen gas poisoning includes automobile exhaust, Power stations, The toxicity may also results from non-combustible sources such as the one released from anaerobic fermentation of food grains and Anaerobic digestion of Biodegradable waste.

However:

• Nitrogen gas poisoning is the bends and has nothing to do with nitrogen dioxide poisoning.
• "Anaerobic fermentation" is wikilinked to lactic acid fermentation, which doesn't involve nitrogen (it is a major source of methane from sugars).
• The linked anaerobic digestion page show that nitrogen in these cases ends up mostly as ammonia. The reference does mention nitrogen and its oxides, but a biochemist should know that significant NO₂ production requires oxygen (ie. aerobic not anaerobic conditions) and that the anaerobic product of metabolising nitrogen is overwhelmingly ammonia. In other words, interpreting the reference appropriately requires recognition that one of the products listed is vastly more significant in terms of quantity than are the others.

The description of nitrogen dioxide in the lead is incomplete, in that it is a red-brown gas but exists in equilibrium as colourless dinitrogen tetroxide (N₂O₄) and at low temperatures this second form is the dominant form. It does not become colourless though the colour intensity may fade to be not noticeable as concentration decreases, in addition to reacting to form N₂O₄.

The impression is that Wikicology is enthusiastic about science but has knowledge gaps that one would hope not to see in a graduate in the field.

Gibbs's thermodynamic surface

Wikipedia	Virginia tech
In 1873, Josiah Willard Gibbs, an American Scientist published the theory associated with thermodynamic state by designing a graphical method of expression of the relationship between energy, entropy, volume, temperature, and pressure.	Objective: To show the independence and sufficiency of a general graphical method coextensive in its' application, that when applied to the thermodynamic theory of state demonstrates the relationship between state variables of energy, entropy, volume, temperature, and pressure
	with and without analytic expressions, where the emphasis will be not to use analytic experssions as recommended by Gibbs and endorsed by Maxwell.
This historical publication was divided into part 1 and part 2. The part 1 involves a graphical methods in the thermodynamics of fluids while Part 2, deals with a method of geometrical representation of the thermodynamic properties of substances by means of surfaces.	J. Willard Gibbs created the theory associated with thermodynamic state by development of a graphical method in his two historic publications, Part 1, "Graphical Methods in the Thermodynamics of Fluids" and Part 2,"A Method of Geometrical Representation of the Thermodynamic Properties of Substances by Means of Surfaces", Ref.[1].
The graphical methods in the thermodynamics of fluids published by Gibbs provided an intuitive understanding of the thermodynamic property relationships governed by the 1st and second laws of thermodynamics.	In the first publication, Part 1, as the title implies, Gibbs developed a general graphical method that provided insight into thermodynamic property relationships governed by the first and second laws of thermodynamics.
The first paragraph of Gibbs's part 1 publication reads “Although geometrical representations of propositions in the thermodynamics of fluids are in general use, and have done good service in disseminating clear notions in this science, yet they have by no means received the extension in respect to variety and generality of which they are capable. So far as regards a general graphical method, which can exhibit at once all the thermodynamic properties of a fluid concerned in reversible processes, and serve alike for the demonstration of general theorems and the numerical solution of particular problems, it is the general if not the universal practice to use diagrams in which the rectilinear co-ordinates represent volume and pressure. The object of this article is to call attention to certain diagrams of different construction, which afford graphical methods coextensive in their applications with that in ordinary use, and preferable to it in many cases in respect of distinctness or of convenience.”	In the first paragraph Gibbs explains, "Although geometrical representations of propositions in the thermodynamics of fluids are in general use, and have done good service in disseminating clear notions in this science, yet they have by no means received the extension in respect to variety and generality of which they are capable. So far as regards a general graphical method, which can exhibit at once all the thermodynamic properties of a fluid concerned in reversible processes, and serve alike for the demonstration of general theorems and the numerical solution of particular problems, it is the general if not the universal practice to use diagrams in which the rectilinear co-ordinates represent volume and pressure. The object of this article is to call attention to certain diagrams of different construction, which afford graphical methods coextensive in their applications with that in ordinary use, and preferable to it in many cases in respect of distinctness or of convenience."

Nitrogen dioxide poisoning

Nitrogen dioxide (NO2) is an irritant of the mucous membrane and is linked with other air pollutants that cause pulmonary diseases such as obstructive lung disease (OLD), asthma, chronic obstructive pulmonary disease (COPD), and sometimes acute exacerbation of COPD and in fatal cases, death.[2]	http://emedicine.medscape.com/article/302133-overview NO2 is a mucous membrane irritant commonly associated with other toxic products of combustion. Symptoms most commonly range from mild cough and mucous membrane irritation to severe exacerbations of underlying pulmonary diseases like COPD or asthma and, in extreme cases, death.
Nitrogen gas poisoning only causes severe damage to the pulmonary artery and respiratory tract. Nitrogen (II) oxide poisoning is not harmful to all forms of life just like "Chlorine gas poisoning" and Carbon (I) oxide. It is easily absorbed through the lungs and its inhalation result in heart failure and sometimes death in severe and fatal cases.[9]	'Search has expired' Chlorine gas poisoning "Chlorine gas poisoning only causes severe damage to the respiratory tract and is therefore not harmful to all forms of life like carbon monoxide poisoning". " It is easily absorbed through the lungs and its inhalation result in CNS damage and death."
Individual and races may differ in Nitrogen (II)oxide tolerance level and individual tolerance level for the gas may be altered by several factors, such as metabolic rate, barometric pressure and hematological disorders but significant exposure may result in fatal conditions that could lead to shorter life span due to heart failure.[10]	10 is http://www.ncbi.nlm.nih.gov/pubmed/8768665 "Indoor pollution from heating" Chlorine gas poisoning states that ' Different people and races may have different chlorine gas tolerance levels. Chlorine gas exposure may lead to a significantly shorter life span due to heart damage. Individual tolerance level for chlorine gas may be altered by several factors, such as metabolic rate, hematological disorders and barometric pressure'.
Exposure to high level of Nitrogen (II) oxide may lead to inflammation of the mucous membrane and the lower and upper respiratory tracts.[11]	"Determinants of nitrogen dioxide concentrations in indoor ice skating rinks. American Journal of Public Health" [link – not given in article]
The symptoms also resembles that of pneumonia or viral infection and other inhalational injuries but common symptoms includes Rhinitis wheezing or coughing, conjunctivitis, headache, throat irritation and dyspnea which may progress to nasal fissures, ulcerations, or perforation.[12]	http://www.ncbi.nlm.nih.gov/pubmed/18717983 "Is a quantitative risk assessment of air quality in underground parking garages possible?" Appears to bear little relation to the claim. Beryllium poisoning states that 'Nasopharyngitis can progress to formation of nasal fissures, ulcerations, or perforation'.
The patient is usually ill-appearing, and presents with hypoxemia coupled with shallow rapid breathing. Therapy is supportive and includes removal from further Nitrogen (II) oxide exposure Systemic symptoms include fever and anorexia. Electrocardiography and Chest radiography can help in revealing diffuse, bilateral alveolar infiltrates. The Chest radiography may be used in diagnosis and the baseline could be established with a Pulmonary function testing.[13][14]	13 is http://www.ncbi.nlm.nih.gov/pubmed/9645595 " Indoor environment of residential homes in Hong Kong--relevance to asthma and allergic disease" 14 is http://www.ncbi.nlm.nih.gov/pubmed/8831283 "Measurements of indoor and outdoor nitrogen dioxide concentrations using a diffusive sampler"
There is no specific laboratory diagnostic test for acute Nitrogen dioxide poisoning but analysis of arterial blood gas level, Methemoglobin level, Complete blood count, Glucose test, Lactate threshold measurement and r peripheral blood smear may be helpful in the diagnosis of Nitrogen (II) oxide poisoning.[15]	15 is http://www.ncbi.nlm.nih.gov/pubmed/9949739 "Impact of residential nitrogen dioxide exposure on personal exposure: an international study "
The determination of Nitrogen (II)oxide in urine or tissue does not establish the diagnosis, and there are technical and interpretive problems with these tests.[16]	16 is http://www.ncbi.nlm.nih.gov/pubmed/8240759 " Nitrogen dioxide and respiratory illness in children. Part II: Assessment of exposure to nitrogen dioxide."
Prolong exposure to a very high level of Nitrogen (II) oxide in micro meter-size range, may have an inflammatory effect that principally targets the respiratory tracts leading to chronic Nitrogen dioxide poisoning which can occur within a days or weeks after the threshold limit value is excessively exceeded.[17]	17 is http://www.ncbi.nlm.nih.gov/pubmed/12194158 " The Po River Delta (north Italy) indoor epidemiological study: effects of pollutant exposure on acute respiratory symptoms and respiratory function in adults."
This condition causes fever, rapid breathing coupled with rapid heart rate, Fever and Severe Seizure of breath. Other effects includes: Diaphoresis, chest pain and persistent dry cough, all of which may result in weight loss, anorexia and may also lead to right-side heart enlargement and heart disease in advanced cases. Prolong exposure to relatively low levels of Nitrogen (II) oxide may cause persistent headaches and nausea.[18]	18 is http://www.ncbi.nlm.nih.gov/pubmed/14649750 "Sources and concentrations of indoor nitrogen dioxide in Barcelona, Spain" Note that the Wikipedia article on Beryllium poisoning states that Chronic beryllium disease can cause "a persistent dry cough. It can result in anorexia, weight loss, and may also lead to right-side heart enlargement and heart disease in advanced cases."
Nitrogen dioxide is sparingly soluble in water. On inhalation, it diffuses into the lung and slowly hydrolyzes to nitrous acid and nitric acid, which causes pulmonary edema and pneumonitis; this leads to inflation of the bronchioles and pulmonary alveolus via lipid peroxidation as well as oxidative stress.[21]	21 is (link) "Relationship between outdoor and indoor air quality in eight French schools"
Mucous membranes are primarily affected, along with type I pneumocytes and the respiratory epithelium. The generation of free radicals from lipid peroxidation results in irritation of the bronchioles and alveoli, causing rapid destruction of the respiratory epithelial cells. The reaction's net result is the release of fluids, leading to pulmonary edema.[22]	22 is http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1392240/ This contains none of the text whatsoever, and few references to Nitrogen Dioxide.
Nitrogen dioxide poisoning may alter macrophage activity and immune function, leading to susceptibility of the body to a wide range of infections. Overexposure to the gas may also lead to methemoglobinemia, a disorder characterized by a higher-than-normal level of methemoglobin (metHb, i.e., ferric [Fe3+] rather than ferrous [Fe2+] hemoglobin) in the blood.	https://books.google.co.uk/books?id=rVrEJltQ8fIC&pg=PA268
Methemoglobinemia prevents the binding of oxygen to hemoglobin, causing oxygen depletion which can potentially lead to severe hypoxia.[23]
If poisoning goes untreated, fibrous granulation tissue is likely to develop within the alveolar ducts, tiny ducts that connect the respiratory bronchioles to alveolar sacs, each of which contains a collection of alveoli (small mucus-lined pouches made of flattened epithelial cells). The overall reaction may cause obstructive lung disease.	Alveolar duct " tiny ducts that connect the respiratory bronchioles to alveolar sacs, each of which contains a collection of alveoli (small mucus-lined pouches made of flattened epithelial cells)."
Meanwhile, proliferative bronchiolitis is a secondary effect of nitrogen dioxide poisoning.[24]	http://www.nature.com/jes/journal/v17/n5/full/7500532a.html
Occupational exposure constitutes the highest risk of toxicity.This risk is often high for farmers, especially those dealing with food grains. It is equally high for firefighters and military personnel(especially those dealing with explosives). The risk is also high for arc welders, traffic officers, aerospace staff, and miners, as well as people whose occupation is connected with nitric acid.[25]
Silo-filler's disease is a consequence of nitrogen dioxide exposure to farmers dealing with silos. Food grains such as corn and millet, grasses such as alfalfa, and some other plant materials produce nitrogen dioxide within hours due to anaerobic fermentation.[26]
Threshold concentrations of nitrogen (II)oxide are often attained within 1 to 2 days, and begin to decline gradually after 10 to 14 days; however, if a silo is well sealed, the gas may remain there for weeks. Heavily fertilized silage, particularly if produced from immature plants, generates a higher concentration of the gas within the silo.[27]
Nitrogen dioxide is about 1.5 times heavier than air; thus during storage of silage, it may remain in the silage material. Improper ventilation may result in exposure during leveling of the silage.[28]
The EPA have some regulations and guidelines for monitoring nitrogen dioxide levels, although historically, some areas in the U.S including Chicago, the Northeast Corridor and L.A have high levels of nitrogen dioxide. In 2006, the WHO estimated that over 2 million deaths result annually from air pollution in which nitrogen dioxide constitutes one of the pollutants. While over 50% of the disease that results from these pollutants are common in developing countries, the effects in developed countries is not insignificant.[29]	29 - http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0668.2008.00555.x/abstract Magnitude of indoor NO2 from biomass fuels in rural settings of Ethiopia
An EPA survey in the U.S suggests that 16 percent of the country's housing units are sited close to airports, highway, and railroads, increasing the exposure risk of approximately 48 million Americans. A feasibility study of the ozone formed from the oxidation of nitrogen dioxide in ambient air reported by the WHO suggested that daily deaths of 1 to 2% are attributed to exposure to ozone at a concentration above 47.3 ppb and that exposure above 75.7 ppb is attributed to a 3 to 5% increase in daily mortality. Levels above 114 ppb were attributed to a 5 to 9% increase daily mortality. Silo filler's disease in particular is pervasive during the harvest seasons of food grains.[30]	http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0668.2004.00311.x/abstract Indoor/outdoor relationships of carbon monoxide and oxides of nitrogen in domestic homes with roadside, urban and rural locations in a central Indian region