Wheeling Creek is the subject of a case study, as a tributary of the Ohio River. Since Wheeling had been first settled in 1769, the Creek had undergone many changes until the present day. It had been a highly industrialized urban center, including river and rail transportation facilities, as well as bridges carrying roads across the Ohio River. In the Wheeling Creek watershed, agriculture is dominated by cattle and dairy operations. There have been many hypothetical asunptions as to why the Creek had become the way it is today. However, after some detailed and meticulous research of Wheeling Creek's background information, I may have evidence to support my theories as to what I believe the causes may be. The two pollutants that are responsible for the pollution of this stream is due to the old process of dredging and surrounding sewage and runoff.
As I said before, the first source of pollution of the creek would be of agriculture and sewage. This also includes the factor of acid mine drainage. Evidence in support of this assumption is that the creek had been located in an area where mines had been located as well. The high concentrations of sulfuric acid had been drained into the creek. this may account for the fact that closer to the Ohio River there is less oxygen because it had been dissolved until saturation. It may have had a higher temperature as well. It also has a higher alkilinity which shows that it has a higher buffering capacity. This is shown by the relative average in pH of the stream, that never reaches below 6. The creek also has conductivity.Because industries have popped up around the creek, there has been runoff and sewage problems of pollution. Combined sewage outflows carry both sewage and stormwater runoff away as the excess is released into rivers and streams. They are major sources of pollution in watersheds, too. Finally, agriculture had also sprouted up around the creek. It enters the streams in the form of runoff from pesticides, fertilizers and as chemical toxins. When I mentioned that it's an area run by cattle and dairy operations, other examples of pollutants include animal waste from feedlots, siltation from plowing near streams and stream bank erosion caused by cattle.
Another source of pollutant that causes the contamination of the creek is the previous work of dredging. Dredging of the stream bed has occured throughout history in many stream beds. The shape of the creek has been noticed currently with all of its meanders and the order of all the different streams. Dredging involves the deliberate removing of large rocks and cobble. In this particular watershed, sides of rocks were dredged in order to provide fill material for roads and building activities. However, more recently it has occured due to frequent flooding along the lower area. Because of the machines that were used in order to perform this process, disruption of the stream bed occurs and short-term siltation can cause harm to downstream communities. It alos takes habitats away from plants and animals. This has alluded to the fact that rocks have been dispersed throughout the stream. The closer area to the Ohio River have more uniform rock size and are much smaller, that allow for a greater velocity and water depth. Also, on a negative side, it overturned sediment that therefore polluted the water.
These are two of the many problems that may have caused the problems in the stream. Combined with sewage and runoff, and dredging, this creek has become yet another victim to pollution of today. There are so many factors today that may cause this. However, in this particular case these two causes are relevant from the beginning of its origin to today. It has been changed drastically and mainly by human interaction and impact. Agricultural industries and factories should become aware or should be reported for such incidents of leaking chemical toxins as pollutants as runoff into streams like this. Streams that have existed since origin, that have provided habitat for many organisms and supplied the natural resource of water for its various services should be maintained and protected. No more dredging should occur either so that the stream could flow naturally. Humans should become aware of how different activities can affect mother nature and how to mitigate these situations from prior actions. The Lower Wheeling Creek is a subject of pollution under intensive case study and its causes are pretty severe.
Tuesday, February 15, 2011
Case Study 1: Lower Wheeling Creek
Make a list of all of the things that could have caused changes with stream water quality. Which of these could change the water quality in lower Wheeling Creek?
A second-order stream joins a fourth-order stream. Does the fourth-order stream double in size with the addition of a second-order stream?
A fourth-order stream does not double in size with the addition of a second-order stream. In order for this to occur, a fourth-order stream would have to join two separate second-order streams or a third-order stream. Simply the addition of a second-order stream to a fourth-order stream does not double its size.
A third-order stream. How does the stream's width and forest canopy compare with those of the first-order stream and the sixth-order stream?
A third-order stream's width and forest canopy greatly compare with those of the first-order stream and the sixth-order stream. The first-order stream is very small in width and has the greatest forest canopy surrounding it on either side. A sixth-order stream has a rather larger width than both the first- and third-order streams, and also with lesser forest canopy due to its width.
Aerial view of a third-order stream entering a fourth-order stream. Does stream order change when this tributary enters the larger stream?
Stream order does not change when this tributary enters the larger stream. A tributary stream is a smaller stream that joins the main stream at different angles and such. They usually bring sediment or waste from sources of higher elevations, yet do not have any effect on the stream order.
Wheeling Creek nearing the Ohio River. How does this stream differ from those above?
This stream differs from any stream above because of its order. It is a larger order than any other listed above. One could easily observe this by considering the width of the stream and its forest canopy. Because it is a larger stream with a wider width, it is different than the others with lesser forest canopy and more open space.
- Urbanization
- Climatic changes
- Drainage basin
- Stormwater runoff
- Chemical toxins from industrious wastes
- Streambed sediment
- Fertilizer runoff
A second-order stream joins a fourth-order stream. Does the fourth-order stream double in size with the addition of a second-order stream?
A fourth-order stream does not double in size with the addition of a second-order stream. In order for this to occur, a fourth-order stream would have to join two separate second-order streams or a third-order stream. Simply the addition of a second-order stream to a fourth-order stream does not double its size.
A third-order stream. How does the stream's width and forest canopy compare with those of the first-order stream and the sixth-order stream?
A third-order stream's width and forest canopy greatly compare with those of the first-order stream and the sixth-order stream. The first-order stream is very small in width and has the greatest forest canopy surrounding it on either side. A sixth-order stream has a rather larger width than both the first- and third-order streams, and also with lesser forest canopy due to its width.
Aerial view of a third-order stream entering a fourth-order stream. Does stream order change when this tributary enters the larger stream?
Stream order does not change when this tributary enters the larger stream. A tributary stream is a smaller stream that joins the main stream at different angles and such. They usually bring sediment or waste from sources of higher elevations, yet do not have any effect on the stream order.
Wheeling Creek nearing the Ohio River. How does this stream differ from those above?
This stream differs from any stream above because of its order. It is a larger order than any other listed above. One could easily observe this by considering the width of the stream and its forest canopy. Because it is a larger stream with a wider width, it is different than the others with lesser forest canopy and more open space.
Thursday, January 20, 2011
My Perspective on Toxicology
When you hear the word toxicology, what do you think? What even comes to your mind? Give up yet? HA! I had the same reaction. I hadn't a clue what it meant whatsoever. It confused me to the max. Yet, I became rather curious to find out what it really entailed. To have known that it involves is a branch of biology, chemistry, and medicine concerned with the study of the adverse effects of chemicals on living organisms, would never have entered my mind. It is the study of symptoms, mechanisms, treatments and detection of poisoning, especially the poisoning of people.
Mrs. Winkler initiated this chapter of environmental science with a current event. This event included 100,000 fish and 5,000 birds mysteriously suddenly dying in Beebee, Arkansas on New Years Day. This project included detailed research and reports on different aspects of the case. We were involved in rigorous research in trying to come up with a scientific-based hypothesis for why these happenings occured. This would just be a small job compared to what an actual toxicologist does.
Before this project I didn't have a good idea of what toxicology entailed. But I now have a better understanding. It requires meticulous detail to explain symptoms and treatments of different chemicals and diseases. So I hope this gives all a great understanding of what toxicology is and how it affects us in our daily affairs in life.
Mrs. Winkler initiated this chapter of environmental science with a current event. This event included 100,000 fish and 5,000 birds mysteriously suddenly dying in Beebee, Arkansas on New Years Day. This project included detailed research and reports on different aspects of the case. We were involved in rigorous research in trying to come up with a scientific-based hypothesis for why these happenings occured. This would just be a small job compared to what an actual toxicologist does.
Before this project I didn't have a good idea of what toxicology entailed. But I now have a better understanding. It requires meticulous detail to explain symptoms and treatments of different chemicals and diseases. So I hope this gives all a great understanding of what toxicology is and how it affects us in our daily affairs in life.
Wednesday, January 19, 2011
Methemoglobinemia
Methemoglobinemia is a disorder characterized by the presence of a higher than normal level of methemoglobin in the blood. Methemoglobin is an oxidized form of hemoglobin that has almost no affinity for oxygen, resulting in almost no oxygen delivery to the tissues. When its concentration is elevated in red blood cells, tissue hypoxia can occur.
TYPES
Congenital methemoglobinemia
Due to a deficiency of the enzyme diaphorase I (NADH methemoglobin reductase), methemoglobin levels rise and the blood of met-Hb patients has reduced oxygen-carrying capacity. Instead of being red in color, the arterial blood of met-Hb patients is brown. This results in the skin of Caucasian patients gaining a bluish hue. Hereditary met-Hb is caused by a recessive gene. If only one parent has this gene, offspring will have normal-hued skin, but if both parents carry the gene there is a chance the offspring will have blue-hued skin.
Another cause of congenital methemoglobinemia is seen in patients with abnormal hemoglobin variants such as hemoglobin M (HbM), or hemoglobin H (HbH), which are not amenable to reduction despite intact enzyme systems. Methemoglobinemia can also arise in patients with pyruvate kinase deficiency due to impaired production of NADH – the essential cofactor for diaphorase I. Similarly, patients with Glucose-6-phosphate dehydrogenase (G6PD) deficiency may have impaired production of another co-factor, NADPH.
Acquired methemoglobinemia
Methemoglobinemia can also be acquired.The protective enzyme systems normally present in red blood cells maintain methemoglobin levels at less than one percent of the total hemoglobin in healthy people. Exposure to exogenous oxidizing drugs and their metabolites may accelerate the rate of formation of methemoglobin up to one-thousandfold, overwhelming the protective enzyme systems and acutely increasing methemoglobin levels. Other classical drug causes of methemoglobinaemia include antibiotics, local anaesthetics, and others such as aniline dyes, metoclopramide, chlorates and bromates. Ingestion of compounds containing nitrates can also cause methemoglobinemia. Infants under 6 months of age are particularly susceptible to methemoglobinemia caused by nitrates ingested in drinking water (called blue-baby syndrome), dehydration usually caused by gastroenteritis with diarrhea, sepsis, and topical anesthetics containing benzocaine or prilocaine. Nitrates used in agricultural fertilizers may leak into the ground and may contaminate well water. The current EPA standard of 10 ppm nitrate-nitrogen for drinking water is specifically designed to protect infants.
TREATMENT
Methemoglobinemia can be treated with supplemental oxygen and methylene blue 1% solution 1 to 2 mg/kg administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state.
This is achieved by providing an artificial electron acceptor (such as methylene blue, or flavin) for NADPH methemoglobin reductase (RBCs usually don't have one; the presence of methylene blue allows the enzyme to function at 5x normal levels) The NADPH is generated via the hexose monophosphate shunt.
Diaphorase II normally contributes only a small percentage of the red blood cells reducing capacity but is pharmacologically activated by exogenous cofactors, such as methylene blue, to 5 times its normal level of activity. Genetically induced chronic low-level methemoglobinemia may be treated with oral methylene blue daily. Also, vitamin C can occasionally reduce cyanosis associated with chronic methemoglobinemia but has no role in treatment of acute acquired methemoglobinemia.
SYMPTOMS
Signs and symptoms of methemoglobinemia (methemoglobin >1%) include shortness of breath, cyanosis, mental status changes (~50%), headache, fatigue, exercise intolerance, dizziness and loss of consciousness. Arterial blood with elevated methemoglobin levels has a characteristic chocolate-brown color as compared to normal bright red oxygen containing arterial blood. Severe methemoglobinemia (methemoglobin >50%) patients have dysrhythmias, seizures, coma and death (>70%). Healthy people may not have many symptoms with methemoglobin levels < 15%, however patients with co-morbidities such as anemia, cardiovascular disease, lung disease, sepsis, or presence of other abnormal hemoglobin species (e.g. carboxyhemoglobin, sulfehemoglobin or sickle hemoglobin) may experience moderate to severe symptoms at much lower levels (as low as 5-8%).
TYPES
Congenital methemoglobinemia
Another cause of congenital methemoglobinemia is seen in patients with abnormal hemoglobin variants such as hemoglobin M (HbM), or hemoglobin H (HbH), which are not amenable to reduction despite intact enzyme systems. Methemoglobinemia can also arise in patients with pyruvate kinase deficiency due to impaired production of NADH – the essential cofactor for diaphorase I. Similarly, patients with Glucose-6-phosphate dehydrogenase (G6PD) deficiency may have impaired production of another co-factor, NADPH.
Acquired methemoglobinemia
Methemoglobinemia can also be acquired.The protective enzyme systems normally present in red blood cells maintain methemoglobin levels at less than one percent of the total hemoglobin in healthy people. Exposure to exogenous oxidizing drugs and their metabolites may accelerate the rate of formation of methemoglobin up to one-thousandfold, overwhelming the protective enzyme systems and acutely increasing methemoglobin levels. Other classical drug causes of methemoglobinaemia include antibiotics, local anaesthetics, and others such as aniline dyes, metoclopramide, chlorates and bromates. Ingestion of compounds containing nitrates can also cause methemoglobinemia. Infants under 6 months of age are particularly susceptible to methemoglobinemia caused by nitrates ingested in drinking water (called blue-baby syndrome), dehydration usually caused by gastroenteritis with diarrhea, sepsis, and topical anesthetics containing benzocaine or prilocaine. Nitrates used in agricultural fertilizers may leak into the ground and may contaminate well water. The current EPA standard of 10 ppm nitrate-nitrogen for drinking water is specifically designed to protect infants.
TREATMENT
Methemoglobinemia can be treated with supplemental oxygen and methylene blue 1% solution 1 to 2 mg/kg administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state.
This is achieved by providing an artificial electron acceptor (such as methylene blue, or flavin) for NADPH methemoglobin reductase (RBCs usually don't have one; the presence of methylene blue allows the enzyme to function at 5x normal levels) The NADPH is generated via the hexose monophosphate shunt.
Diaphorase II normally contributes only a small percentage of the red blood cells reducing capacity but is pharmacologically activated by exogenous cofactors, such as methylene blue, to 5 times its normal level of activity. Genetically induced chronic low-level methemoglobinemia may be treated with oral methylene blue daily. Also, vitamin C can occasionally reduce cyanosis associated with chronic methemoglobinemia but has no role in treatment of acute acquired methemoglobinemia.
SYMPTOMS
Signs and symptoms of methemoglobinemia (methemoglobin >1%) include shortness of breath, cyanosis, mental status changes (~50%), headache, fatigue, exercise intolerance, dizziness and loss of consciousness. Arterial blood with elevated methemoglobin levels has a characteristic chocolate-brown color as compared to normal bright red oxygen containing arterial blood. Severe methemoglobinemia (methemoglobin >50%) patients have dysrhythmias, seizures, coma and death (>70%). Healthy people may not have many symptoms with methemoglobin levels < 15%, however patients with co-morbidities such as anemia, cardiovascular disease, lung disease, sepsis, or presence of other abnormal hemoglobin species (e.g. carboxyhemoglobin, sulfehemoglobin or sickle hemoglobin) may experience moderate to severe symptoms at much lower levels (as low as 5-8%).
Life in Infinite Shades of Being
We all bleed red – except, perhaps, for the famed 19th century Fugate clan of the Appalachian Mountains. Blue Caucasians popped up in the hills as late as 1975, but the sprawling family never granted an interview and it took a scientist years to track down a member.
Blueish skin is caused by a rare disease known as hereditary methemoglobinemia, or met-H. This disease results in espresso colored blood, which in turn makes the skin appear blue. Since it is a recessive gene, it can only occur if both parents happen to carry it. In the case of the Fugates, they were blue due to intermarrying with another met-H clan, the Smiths. (Of all the luck.) Subsequent decades of many marriages between close cousins – let’s restrain ourselves here, people – created a very blue group. Fortunately, in the 1960s, a scientist persuaded one Fugate to accept enzyme treatment, and within minutes of the dose, said Fugate turned into a regular old whitey.
Toxicology
Toxicology is a branch of biology, chemistry, and medicine concerned with the study of the adverse effects of chemicals on living organisms. It is the study of symptoms, mechanisms, treatments and detection of poisoning, especially the poisoning of people.
The responsibility of the toxicologist is to:
The responsibility of the toxicologist is to:
1) develop new and better ways to determine the potential harmful effects of chemical and physical agents and the amount (dosage) that will cause these effects. An essential part of this is to learn more about the basic molecular, biochemical and cellular processes responsible for diseases caused by exposure to chemical or physical substances;
2) design and carry out carefully controlled studies of specific chemicals of social and economic importance to determine the conditions under which they can be used safely (that is, conditions that have little or no negative impact on human health, other organisms, or the environment);3) assess the probability, or likelihood, that particular chemicals, processes or situations present a significant risk to human health and/or the environment, and assist in the establishment of rules and regulations aimed at protecting and preserving human health and the environment.
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