IELTS Academic Reading Practice Test 360

For most of the history of medicine, a drug could be given in only a few ways: swallowed, rubbed into the skin, or breathed in as a vapour. Getting a substance directly into the bloodstream was possible in principle, and surgeons had long used hollow tubes to drain wounds, but nobody possessed a reliable means of pushing a measured quantity of fluid through the skin. The instrument that solved the problem, the hypodermic syringe, appeared in the middle of the nineteenth century, and within a few decades it had transformed the treatment of pain.

The first serious experiments in injection were made in Oxford in the late 1650s. Christopher Wren, later the architect of St Paul's Cathedral, worked with the chemist Robert Boyle on a method of introducing fluids into the veins of dogs. Wren used a hollow quill attached to a small bladder, squeezing the fluid through the quill into the vein. The experiments, later reported to the Royal Society, showed that a substance could reach the blood directly and act within seconds. Similar attempts were made on human patients in Germany and England during the 1660s, with unpredictable results, and the practice was then largely abandoned.

There were good reasons for that retreat. A quill or a crude metal tube could carry infection deep into the body at a time when the causes of infection were entirely unknown. The veins of a thin or elderly patient were difficult to find, and there was no way of controlling how much fluid entered, because the equipment could not deliver small volumes accurately. Only when two other developments arrived, a fine sharp needle and a precise means of measuring the dose, could injection become a practical technique.

In 1844 Francis Rynd, a surgeon at the Meath Hospital in Dublin, described an instrument that came close. Rynd was treating patients with severe facial pain, and he introduced a solution of morphine along a needle inserted through the skin over the painful nerve. His device was simple: a short needle fixed to a small tube, with the liquid flowing in under gravity rather than being pushed. Because the fluid ran slowly, he could deliver it to a particular spot, and he recorded that his patients' pain stopped almost at once. His account, published in 1845, is the first clear description of a hypodermic injection, although his instrument had no plunger.

The modern form of the syringe appeared in 1853, when two men working independently combined a fine needle with a barrel and a plunger. Charles Pravaz, a surgeon in Lyon, wanted to treat aneurysms, the dangerous swellings of blood vessels, by injecting a chemical that would make the blood clot. His syringe was made of metal and was driven by a screw. Alexander Wood, a physician in Edinburgh, wanted to place morphine exactly where it hurt, and his syringe had a glass barrel so that the contents could be seen. It is Wood's design that most closely resembles the instrument in use today.

The technique took its name from Greek, in which hypo meant under and derma meant skin, and the adjective hypodermic soon appeared in British medical writing. The advantage of the new method was speed. Morphine taken by mouth acts slowly, because much of the dose is broken down before it reaches the blood; injected beneath the skin, it produced relief within minutes. The drug was used extensively to treat wounded soldiers during the American Civil War, and many men are said to have returned home dependent on it, although historians doubt that the addiction was widely called the soldier's disease at the time.

That outcome was the first of the syringe's complications. Because the effect of an injection was so immediate and so reliable, doctors tended to regard morphine given in this way as safer than opium taken by mouth. Addiction became a recognised hazard of medical treatment, and the hypodermic syringe had created a new route to it.

Infection was the second complication. Reused needles carried bacteria from one patient to another, producing abscesses, and in the days before sterilisation they also transmitted disease. Once doctors understood that micro-organisms caused infection, they began to boil their instruments between patients. By the end of the nineteenth century, glass syringes with metal fittings for the needle were standard hospital equipment.

For the first half of the twentieth century, injection remained a procedure that required preparation. Syringes were made of glass and metal. They were expensive, and each one had to be cleaned and boiled before use. In busy hospitals, failures of sterilisation spread hepatitis and other infections. The solution was the disposable syringe. An American inventor, Arthur E. Smith, took out patents for disposable medical syringes in 1949 and 1950. During the 1950s and 1960s, manufacturers began producing plastic syringes in quantity, so that each could be used once and thrown away.

Disposables transformed both safety and waste, but they did not remove every risk. Injuries from needles were common among nurses, and in the 1980s the spread of HIV made a needlestick injury a source of genuine fear. The response was engineering rather than instruction: sharps containers in every ward, and later needles that retract or lock after use. In the United States, legislation in 2000 required hospitals to provide such safety devices. The syringe has come a long way from Wren's feather, yet its basic principle, a hollow needle and a measured dose, has scarcely changed.

Stress is one of the most widely used words in discussions of health, and one of the least precise. In physiology it refers not to an event but to a set of internal changes that an organism makes when the demands placed on it exceed what it can easily manage. A deadline, a sudden noise and a serious illness all provoke such changes, and the changes themselves are neither good nor bad: they are what allows a person to run faster, concentrate harder and stay awake when necessary. The distinction that matters for health is between an episode that ends and a response that continues for months or years.

The first of the two systems that produce these changes acts within seconds. When the brain registers a threat, signals travel down the spinal cord to the adrenal glands, which sit above the kidneys, and these release the hormone adrenaline, also known as epinephrine, into the blood. Adrenaline speeds the heart, raises blood pressure, opens the airways and releases glucose from the liver. Blood vessels in the skin and digestive organs narrow while those supplying the muscles widen, so that the body's resources are redirected to where they may be needed. The American physiologist Walter Cannon, who studied these reactions in the early twentieth century, called the pattern the fight-or-flight response.

The second system is slower and its effects last longer. The hypothalamus, a small region at the base of the brain, releases a hormone that instructs the pituitary gland to send a chemical signal, adrenocorticotropic hormone, through the blood to the adrenal cortex, the outer layer of the adrenal glands. There the signal stimulates the production of cortisol, a steroid hormone that raises blood glucose, increases the availability of energy to muscles and tempers some of the body's inflammatory reactions. Cortisol reaches its peak in the blood some twenty to thirty minutes after the initial trigger, and its influence on cells can persist for hours.

In a healthy person, cortisol is not released evenly. Its concentration follows a strong daily rhythm, rising sharply in the first hour after waking and then declining through the day to reach its lowest point in the middle of the night. This pattern is controlled by the brain's internal clock rather than by events, which is why people who work night shifts or fly across several time zones often feel unwell for days. Researchers studying long-term stress therefore try to avoid taking a single blood sample in the afternoon, because at that hour the level says little about the person's overall state.

The idea that different pressures produce the same bodily response was set out by Hans Selye, a Hungarian-born researcher working in Montreal. In the 1930s he noticed that rats exposed to a variety of harmful conditions — cold, infection, injury, exhausting exercise — all developed the same trio of changes: enlarged adrenal glands, shrinkage of certain immune organs and bleeding ulcers in the stomach. Selye called this pattern the general adaptation syndrome and described it as passing through three stages, which he termed alarm, resistance and exhaustion. His model dominated the field for decades, and later critics argued that it underplayed how much the response varies with the type of challenge and with the individual.

The harm attributed to stress arises mostly when the response fails to switch off. Blood pressure that stays raised puts a continuous load on the heart and arteries; cortisol that remains high encourages the liver to release glucose and makes muscle and fat cells less responsive to insulin, which over years can contribute to type 2 diabetes. Persistent inflammation, normally kept in check by cortisol, may itself become chronic. The brain is affected too: the hippocampus, a structure essential for memory, contains large numbers of receptors for cortisol, and prolonged exposure appears to alter its activity. A framework developed by the American neuroscientist Bruce McEwen, known as allostatic load, describes the cumulative wear produced by systems that are constantly adjusting and never fully resting.

Yet the picture is far from settled, largely because long-term stress is so hard to measure. A blood or saliva sample captures a single moment; cortisol in hair, which accumulates over months, is promising but has not been standardised. Nor does everyone respond in the same way. Studies of people who endured severe hardship in childhood suggest that early experience can recalibrate the stress system, sometimes making it react more strongly and sometimes blunting it altogether. Researchers also disagree about whether these differences reflect a lasting vulnerability or an adaptation that is useful in the circumstances that produced it.

What follows from all this for ordinary life is more modest than the headlines suggest. The measures with the best evidence behind them are unglamorous: regular sleep, physical activity and close relationships with other people, all of which appear to reduce the frequency and intensity of the response. Psychological treatments that teach people to interpret a racing heart as preparation rather than collapse have shown some benefit in small trials. It is also worth remembering that the system exists for a reason. A life entirely without stress would be one in which nothing was worth making an effort for.

At half past eight on a weekday morning, the street outside many primary schools becomes a narrow channel between parked cars, idling engines and children. Some parents stop on the yellow lines, others turn in the road while a stream of five-year-olds crosses behind them. Since the late 2010s a growing number of local authorities in Britain and elsewhere in Europe have responded with a simple measure: for half an hour at the start and end of the school day, the road is closed to motor vehicles. These school streets, as they are usually called, are cheap, quick to introduce and popular with head teachers. Whether they improve children's health, however, is a question that demands more than enthusiasm.

The case for closing the street begins with injury. Road traffic is among the leading causes of death for children over the age of five in many countries, and a high proportion of those collisions happen on the short journeys to and from school. It continues with air. Children breathe more rapidly than adults and take in more air in proportion to their body weight, and their lungs are still developing, so the nitrogen dioxide and fine particles produced by diesel engines do them proportionately more harm. Pollution is not spread evenly across a neighbourhood: concentrations are highest at the kerb, in the queue of cars waiting at the school gate, which is precisely where children walk.

The evidence gathered so far is encouraging but limited. Monitoring by councils has generally shown that a closure removes most moving vehicles from the street during the periods concerned, and surveys of parents report that the walk to the gate feels safer. A few schemes have recorded small increases in the number of children cycling or walking. What almost no evaluation can show is whether these local changes alter children's overall health, because exposure during the school run is only one part of a day that also includes the journey home, the playground and the house they live in. Health studies of air pollution usually estimate exposure across a whole day, and on that measure the difference made by one closed street is likely to be small.

The objections deserve more attention than they usually receive. The first is displacement. A road that is closed does not remove the vehicles that used it; they reappear on the parallel streets, which are often residential and whose residents were not consulted. The second is enforcement. A closure that depends on a camera and a fine is a closure paid for by a small number of drivers, and those drivers are not always the wealthiest. The third is access. Some parents live ten kilometres away and pass three other schools on the way; some are disabled; some are collecting a second child from a different gate. A rule that treats all of them as irresponsible is unlikely to be obeyed.

Transport researchers have observed that closing a road does not always shift the whole of its traffic onto neighbouring streets. In some documented cases a proportion of journeys is simply not made, or is combined with another, a phenomenon sometimes called traffic evaporation. The effect is not guaranteed and appears to depend on how many alternative routes exist and how easily drivers can change their habits. It is, nonetheless, a reason for scepticism about the claim that a closure must move a problem rather than solve it.

There is also a question of fairness between places. A school street makes sense where most families live within a short walk, where pavements are wide and where an alternative route exists for through traffic. In a scattered suburb or a village on a main road, the same measure may simply inconvenience everyone without changing anything. And the schools that most need protection, those on busy arterial roads in poorer districts, tend to be the hardest to close, because their catchment areas are larger and their parents have less flexibility about working hours.

None of this means the idea should be abandoned. The most persuasive argument for school streets is not the pollution reading at the gate but the loop they interrupt. Fear of traffic is one of the main reasons parents drive their children to school; each car adds to the danger that frightens the next family into doing the same. A closure, if it is well designed, breaks that loop locally, and the effect on children's independence may outlast the bollards. Where schemes have worked, they have usually been accompanied by exemptions for residents and disabled drivers, by clear signs, and by a genuine attempt to consult the families affected.

My own view is that closing the street at the school gate is justified as a public-health measure, but only as one element of a wider plan and only where its costs are honestly counted. It should come with monitoring of the neighbouring streets, exemptions that are simple to obtain, and investment in the routes children use for the rest of their journey. A council that closes a road, installs a camera and considers the matter settled has not made a school safe; it has moved a problem and claimed a victory. The question is not whether cars should be banned outside schools, but which streets, for how long, and with what else.