Course:
OET Reading Course
Text 1: Eye Damages in Divers
An investigation of the circulation of blood in the eyes of divers has produced the strongest evidence yet that tissue damage is caused by diving is more common and more severe than previously thought. Researchers from Moorefield’s Eye Hospital in London and Maurice Cross of the Diving Diseases Research Centre in Plymouth examined the retinas of 80 divers of varying experience. The researchers found evidence of damage in nearly half the divers. Although the damage tended to increase with diving experience some of the divers developed it within two years of diving. The study is the first evidence of damage to the eye tissue in amateur divers and it suggests for the first time that a career in diving almost inevitably leads to damage. Of the 26 professional divers studied all had abnormal retinas. None of the divers taking part in the study had visual problems as a result of their damaged retinas but Bird said that he “would not be surprised to find divers whose damage has progressed far enough to affect their vision”.
Evidence has mounted during recent years to show that exposure to pressure during diving subtly damages the central nervous system. Doctors believe that the damage is due to obstruction in the flow of blood through the tissues. People who take up diving as a sport know they are at risk of getting “the bends” or an air embolism, but if they follow the correct procedures the risk is very low. All professional divers know they also run the risk of bone necrosis. About 5 per cent of them develop small dead patches in their bones. Active professional divers have the bones of their thighs and upper arms x-rayed as part of their annual medical examination. Doctors have been concerned that if diving caused dead patches to appear on bones, other tissues may be suffering a similar fate.
Their concern increased in the early 2000s, when detailed neurological examinations and tests of the memory and reactions of experienced professional divers suggested that some of them might have slight damage to the brain and spinal cord.
Then, in 2006, nuclear magnetic resonance imaging revealed small areas of damage in the brains of apparently healthy North Sea divers. The following year Ian Calder, a pathologist at the London Hospital in the city’s East End, published the results of a post-mortem study of eleven professional divers. Seven of them had areas of damage in the spinal cord that had not been detected while the divers were alive. The samples were too small for researchers in the studies to draw conclusions as to how common such damage might be. The fact that few divers are currently complaining of neurological symptoms does not mean that they will not experience problems later in life. There is a great deal of extra capacity in the nervous system of young people that begins to diminish in middle age. Most people who have dived deeper than 50 metres are still relatively young. Deeper diving did not become common until the mid-1970s when drilling for offshore oil began in the deeper water of the North Sea. Over the same period recreational diving became more popular and the amateur divers began to go deeper.
In order to determine the size of the problem, the researchers needed a method of looking for the damage in a large sample of divers that did not involve surgery. The damage which occurs in the tissue of both the bones and the nerves of divers is similar. Minute areas of tissue had died, probably because they had been starved of blood, suggesting that capillaries that supplied blood to the areas had been blocked. The bone necrosis of divers closely resembles that seen in victims of sickle-cell anemia whose capillaries are temporarily blocked during a sickle-cell “crisis” when their red blood cells become too rigid to pass through. Sickle-cell disease damages the retina which doctors can see using the technique known as retinal angiography. The process involves injecting Fluorescein dye into the blood stream and photographing the back of the eye through the pupil. The technique can provide a detailed photograph of the two vascular systems supplying blood to their retina without causing too much discomfort to the patient.
The researchers used retinal angiography to assess the tissue damage in divers. The abnormalities that they detected in the angiograms of divers were very similar to those seen in sickle-cell disease. There was clear evidence of obstruction to the capillaries. The researchers suggested three mechanisms to explain how diving causes this obstruction. When divers come back to the surface air bubbles sometimes form in their veins and their lungs. If bubbles also form in the arteries, they would block the capillaries. Bubbles forming in the lungs trigger changes in the body’s clotting mechanism which could result in minute clots becoming trapped in the capillaries.
The third suggestion is that the mechanism might also be similar to that of sickle-cell disease. The pressure that divers experience at 30 meters causes their white blood cells to become rigid just as red blood cells do during a sickle-cell crisis. The researchers hope that clues to the cause of the obstruction will come from investigations into the individual differences between divers. Some of the divers studied had relatively little damage even though they had been diving for many years and done a great deal of deep diving. On the other hand, a few inexperienced divers had quite extensive damage.
Text 2: Plumbism
Plumbism is the technical term for lead poisoning, which represent a diseased condition, produced by the absorption of lead, common among workers in this metal or in its compounds, as among painters, typesetters, etc.
Lead is a metal which is toxic to humans when ingested or inhaled. When lead enters the bloodstream, whether the route of entry is the lungs or the gastrointestinal tract, it is distributed to the tissues and organs of the body, including the brain, liver and kidneys. In the long term, lead is stored in the teeth and bones. Although it is excreted gradually (mostly in the urine, but also in faeces, sweat, hair and nails), repeated exposure and absorption results in an accumulation of lead in the body. Cumulative doses of lead over time can result in chronic lead poisoning, while acute lead toxicity may be observed in cases of short-term, high-dose exposures.
A naturally occurring element, lead may be dispersed by natural processes such as erosion, volcanic eruptions and forest fires. Overwhelmingly, however, hazardous human exposure to lead is due to its release into the environment through industrial processes, and to the widespread use of lead-containing products, most notoriously petrol, paints, and plumbing and building materials. Many everyday household items including adhesives, batteries, ceramics, glassware and children’s toys may also contain lead, particularly if manufactured in the twentieth century. Other items that have traditionally contained lead include bullets and radiation shields.
Industrial sources of lead contamination of soil, water and air include mining and smelting of lead and lead containing ore, car manufacture and combustion of large quantities of fuels such as coal in the generation of electricity. The leading cause of lead poisoning among adults is occupational exposure, particularly for those working in the industries previously mentioned.
To alleviate the incidence of environmental exposure due to contact with building materials and other products containing lead, industry guidelines and government legislation have been introduced in many countries: drinking water is no longer prone to lead contamination where alternatives to lead pipes and lead-soldered fittings, roofs and water tanks are required in new houses; maximum allowable lead content in domestic paint is now specified in a growing number of jurisdictions; and the last two decades or so have seen leaded petrol banned in most countries around the world. However, exposure to lead particles is still a significant health risk due to the lingering contamination of soil and dust from past fuel emissions, from continuing industrial exposure, and from contact with older lead-based products still in use.
Even small quantities of lead taken into the body are considered hazardous to human health. Adverse systemic effects can extend to the neurological, cardiovascular, gastrointestinal and renal. Damage caused by lead poisoning is known to be irreversible in some cases, such as severe neuro-behavioural impairment resulting from acute intoxication. However, health outcomes are influenced by the timing, duration and amount of exposure (or dosage), and by how much accumulation has occurred. Among the available biological markers of lead dose, blood lead levels provide a more accurate measure if there has been recent exposure to lead, while levels of lead in bone, measuring stored lead, are more accurate indicators of accumulation.
Among the most vulnerable to lead exposure and its effects are children under the age of six. Where lead is present in soil, dust, paint or toys, young children are at an increased risk of ingesting lead, as they may touch lead-based or contaminated materials with their fingers and mouths. A child’s body is also more susceptible to lead absorption -it has been estimated that a child’s body can absorb 50% of lead particles on exposure compared with only 10% for an adult’s. The likely health effects for young children are even more dire considering the vulnerability of the developing brain to permanent disadvantage as a result of the neurotoxicity of lead. Intelligence quota (IQ) deficit has been linked to neuro-toxic effects in children with lead blood levels as low as five micrograms per decilitre (5μg/dL). Less research has been conducted on the effects of lead exposure during prenatal development but, because lead is able to cross the blood brain barrier and the placenta, the risk of significant harm to the brain and to the developing fetus is a key concern. One study in Mexico led researchers to conclude that fetal neurodevelopment is adversely affected by lead exposure and particularly so during the first trimester of pregnancy.
Studies suggest that chronic lead toxicity in individuals could change behavior and cognitive function and even trigger psychosocial disturbances that contribute to aggressive behavior. One study observed a significant decline in rates of violent crime throughout the 1990s in the United States, a country where the use of leaded petrol was phased out during the 1970s. The researchers hypothesized that this change in crime rate is attributable to a reduction of childhood exposure to lead in the decades prior to the 1990s. Studies like this one, which documents an association between childhood lead exposure and criminal behavior in adults, are supported by findings that some adolescent criminals have blood lead levels quadrupling the average among teenagers. Despite these alarming health effects, the World Health Organization has described lead poisoning as a completely preventable disease.
