IELTS Academic Reading Practice Test 316

For much of human history, malaria was explained by the places where it occurred. The illness was common in low-lying districts near marshes and stagnant water, and it was widely assumed to be produced by the foul air that such places gave off. The very name reflects this belief: it comes from the Italian mala aria, meaning bad air. In nineteenth-century Europe and India, the standard response was therefore to drain swamps and open land to the wind, measures that sometimes reduced the disease without anyone understanding why.

The first clue to a different explanation came from a microscope. In 1880 a French army doctor, Alphonse Laveran, was working in Constantine, in what is now Algeria, when he noticed small, moving, pigmented bodies in the blood of a soldier who had died of malaria. He suggested that these were parasites, and over the following years he showed that they were always present in the blood of sufferers. Many doctors, however, remained sceptical, partly because Laveran could not explain how the parasite reached a new patient. He was awarded the Nobel Prize in Physiology or Medicine in 1907.

Meanwhile, a Scottish physician, Patrick Manson, had been working in China. He was interested in filariasis, a disease caused by a worm that lodges in the lymphatic vessels, and he had noticed that the worms appeared in the blood at night, when the mosquitoes that plagued his patients were most active. In the late 1870s he fed mosquitoes on the blood of an infected man and found the worms developing inside the insect's body. This was the first demonstration that a mosquito could play a part in the life cycle of a human parasite, and it encouraged Manson to argue, from the early 1890s, that malaria might be transmitted in a similar way.

Ronald Ross, the man who settled the question, was born in India in 1857, the son of a British general, and was sent to England as a child. He trained in medicine at St Bartholomew's Hospital in London, though his real interests were writing and mathematics, and he joined the Indian Medical Service in 1881 largely because it offered a secure income. In 1894, on leave in London, he met Manson, who persuaded him that the mosquito was the missing link in the story of malaria and that the necessary experiment could be carried out in India.

Back in India, Ross began dissecting mosquitoes that had fed on patients suffering from malaria, examining their stomachs under a microscope. Progress was painfully slow. He was often posted to places where there were few patients, his equipment was primitive and he had little spare time, so that after more than two years he had nothing to show for his efforts. Then, in August 1897 at Secunderabad, he fed mosquitoes of a kind he described as dappled-winged on a patient named Husein Khan, and on 20 August he found in the wall of one insect's stomach a cluster of pigmented cells like those Laveran had seen in human blood.

One discovery, however, was not proof. Ross could show that the mosquito took up the parasite, but not that it could pass it on. Denied permission to continue the work with human volunteers, he turned to birds. In Calcutta in 1898, with the help of Indian assistants, he fed mosquitoes on sparrows infected with a malaria parasite of birds and then allowed the same insects to bite healthy sparrows. The healthy birds developed the disease, and the chain was complete: a mosquito that had bitten an infected bird could transmit the parasite to another.

In Italy, meanwhile, the zoologist Giovanni Battista Grassi had been following a different line of inquiry. Working in the Roman Campagna, where malaria was then common, he identified the species of mosquito that carried the human parasite and described the stages of its development in the insect's body. His results, published in 1898 and 1899, were arguably the fuller account of human malaria, and he and Ross quarrelled bitterly for the rest of their lives over who deserved the credit.

Ross left India in 1899 and joined the Liverpool School of Tropical Medicine, which had been founded a year earlier. He led an expedition to Sierra Leone, where he tried to apply the theory in practice, and he spent the rest of his career arguing that malaria could be controlled by protecting people from bites and by destroying the places where mosquitoes bred. He was awarded the Nobel Prize in 1902 and knighted in 1911.

The practical consequences were enormous. Screening windows, sleeping under nets, clearing drains and treating patients with quinine became standard measures wherever malaria was endemic, and they saved many thousands of lives long before any vaccine existed. The disease has not been defeated, however. It still infects more than two hundred million people each year and kills several hundred thousand, most of them young children in sub-Saharan Africa, and the mosquitoes have developed resistance to many of the insecticides used against them.

Ross himself remained a combative figure, quick to detect slights and tireless in defending his reputation. He wrote poetry and novels, and he spent years developing a mathematical method for analysing epidemics that was largely ignored at the time. When he died in 1932, the mosquito's role in malaria was beyond doubt; how best to defeat the disease was not.

Take a deep breath and you draw roughly half a litre of air into your lungs. Spread out flat, the surface across which that air meets your blood would cover some seventy square metres. The entire barrier separating air from blood is generally less than a thousandth of a millimetre thick. These two facts, an enormous area and an extremely thin membrane, are the whole secret of gas exchange: oxygen must cross from the air into the blood, and carbon dioxide must cross in the opposite direction.

Air enters through the nose or the mouth and passes down the trachea, a tube held open by rings of cartilage, which divides into two bronchi, one for each lung. These branch repeatedly into narrower tubes called bronchioles, and at the ends of the finest of them hang clusters of tiny air sacs, the alveoli. There are thought to be several hundred million of them in a pair of adult lungs. The airways themselves play no part in gas exchange; their walls are too thick, and the air inside them is not in close contact with blood.

Breathing itself is a mechanical process. The diaphragm, a dome-shaped sheet of muscle beneath the lungs, contracts and flattens, enlarging the chest cavity, while muscles between the ribs assist. Because the pressure inside the lungs then falls below that of the atmosphere, air flows in without any effort being made to suck it. When the muscles relax, the elastic recoil of the lungs pushes the air out again.

What makes the alveoli special is their lining. Each sac is formed from a single layer of flattened cells, and the capillaries that wrap around it are made of cells flattened in the same way, so that between the air and the blood there is very little tissue: a film of moisture, two cell layers and a shared basement membrane. Diffusion slows sharply as distance increases, and this arrangement allows gases to cross in a fraction of a second. Scavenging cells called macrophages also patrol the alveolar surface, engulfing dust and microbes.

The driving force behind the movement is a difference in concentration, or more precisely in partial pressure. Fresh air in an alveolus contains oxygen at a partial pressure of about 13 kilopascals, whereas the blood arriving from the body's tissues has used much of its oxygen and is at about five. Oxygen therefore diffuses into the blood, while carbon dioxide, which is more concentrated in the blood than in the alveolar air, diffuses out. The two gases move independently, each down its own gradient, until the partial pressures on either side are nearly equal.

Most of the oxygen that enters the blood does not dissolve in the plasma but attaches to haemoglobin, the iron-containing protein packed into red blood cells. Each red cell carries some 270 million haemoglobin molecules, and each of these can bind four molecules of oxygen. The bond is strong enough to capture oxygen in the lungs, where the gas is plentiful, yet weak enough to release it in the tissues, where it is scarce and where warmth and acidity weaken it still further.

Carbon dioxide is handled differently. Only a small fraction travels dissolved in the plasma; most is converted inside red blood cells into bicarbonate by an enzyme called carbonic anhydrase, and carried in that form. Because carbon dioxide is far more soluble in water than oxygen, it crosses the alveolar lining roughly twenty times more readily, so a failure to breathe out properly raises its level in the blood long before oxygen levels fall. It is carbon dioxide, rather than oxygen, that the body mainly monitors: receptors in a part of the brainstem called the medulla respond to the acidity of the blood and adjust the depth and rate of breathing.

Keeping the sacs open takes a little chemical engineering. The inner surface of every alveolus is wet, and water surfaces tend to contract; without help, small sacs would empty into larger ones and the lungs would gradually collapse. The solution is surfactant, a mixture of lipids and proteins secreted by specialised cells in the alveolar wall known as type II cells. It lowers surface tension, and does so more strongly in small sacs than in large ones, which stabilises the whole structure. Babies born very prematurely may produce too little surfactant and need it supplied as a drug.

Blood flow and airflow must also be matched. In an upright person, gravity makes both ventilation and blood flow greater at the base of the lungs, and the two distributions, although not identical, correspond closely enough for most purposes. Where a region of lung is poorly ventilated, the small arteries supplying it constrict, so that blood is diverted towards regions where it can pick up oxygen. This response, hypoxic pulmonary vasoconstriction, is the opposite of what happens elsewhere in the body, where low oxygen causes vessels to widen.

The delicate structure is easily damaged. In emphysema, the walls between neighbouring sacs break down, merging many small alveoli into a few large ones, so that the total surface area falls drastically. Fibrosis, in which scar tissue thickens the barrier between air and blood, and pulmonary oedema, in which fluid leaks into the air spaces, reduce diffusion in different ways. How far damaged lungs can repair themselves is disputed: removing one lung from a young animal can trigger a limited burst of new alveolar growth in the remaining one, but whether adult human lungs retain a comparable capacity is unclear.

In little more than two decades, bans on smoking in enclosed public places have gone from being controversial to being unremarkable. The frontier has since moved outdoors. Cities have restricted smoking in parks, on beaches, at bus stops, outside hospital entrances and at pavement tables, and each new restriction provokes the same argument between those who see a necessary protection of health and those who see an intrusion into private life. The question deserves to be taken seriously, and my answer is that it cannot be settled in general terms, because the spaces we call outdoor differ enormously from one another.

The health argument is where supporters begin, and it is not contemptible. Tobacco smoke contains dozens of substances known to cause cancer, and no threshold has been found below which exposure is risk-free. The difficulty is one of scale. Outdoors, smoke is dispersed by wind and mixed with a vast volume of air, so that concentrations fall steeply within a metre or two of the burning cigarette. Measurements taken on pavement terraces where smoking is allowed have found particle levels well above background, sometimes approaching those recorded indoors, particularly where a wall or roof traps the air. But sitting for an hour beside a smoker on a still evening is not the same as walking through a plume on a windy street, and the evidence that brief outdoor exposure damages the health of bystanders is thin, though thin is not the same as absent.

The strongest case for legal restriction therefore concerns places that are outdoors only in a technical sense: bus shelters, stadium concourses, covered terraces, the narrow strip of pavement where a café's tables are set out. In such places non-smokers cannot easily move away, the air may be almost as still as indoors, and exposure can last an hour or more. Staff deserve particular consideration. A waiter cannot choose to serve at a different table, and if employers are obliged to provide a safe workplace, a terrace that functions as an extension of an indoor room falls under the same principle as an indoor bar. Restrictions of this kind command wide support and cost little to enforce, because the premises are identifiable and their owners can be held responsible.

Blanket bans on smoking in large parks, on beaches or along quiet footpaths are a different proposition. Here the risk to others is negligible, the distance between people is usually considerable, and the interference with personal liberty is plain. Enforcement in such places is bound to be sporadic and selective. Where police or officials do act, they tend to act on the people who are most visible, and there is evidence from some cities that such enforcement falls disproportionately on the poor and on minorities. A rule that cannot be applied consistently, and that everyone can see is not being applied consistently, does more harm than the practice it forbids, because it teaches people that laws are optional.

There is, however, a stronger justification for some outdoor restrictions than secondhand smoke: cigarette ends. Most filters are made of cellulose acetate, a form of plastic that persists in the environment for years rather than breaking down, and discarded butts carry nicotine and other residues that are toxic to fish and other aquatic organisms. They are among the items most frequently collected during beach clean-ups around the world, and cigarettes dropped from car windows or left smouldering on dry ground are a well-documented cause of wildfires. A ban on smoking on a beach or in a forest can therefore be defended, but the argument is environmental rather than medical, and it should be made in those terms rather than dressed up as a measure to protect bystanders.

Supporters also point to children. A child who sees adults smoking at the school gate or in a playground may come to regard the habit as ordinary, and there is some research linking the sight of smoking with the likelihood that a young person will try it. The evidence is suggestive rather than conclusive, because it is difficult to separate what children see from everything else that shapes their behaviour, including advertising, family habits and friends. Even so, restrictions in playgrounds and near school entrances are cheap, popular and unlikely to be widely resented, and if they reduce the chances of a child taking up smoking even slightly, they are worth having. Parents, in particular, tend to welcome them.

The conclusion I would draw is that the useful question is not whether smoking should be banned outdoors but where. I would restrict it at the entrances to buildings and hospitals, at bus stops and taxi ranks, in queues, in the seated areas of sports grounds, in playgrounds, and at the pavement tables of cafés and pubs, where employees must work and customers cannot easily move. I would not send enforcement officers after a single smoker on a deserted beach or halfway up a mountain, where the case rests on litter and fire risk and is better met by ashtrays, deposit schemes and clean-up campaigns. The danger of a total ban is that it invites the public to treat all restrictions as absurd, and so undermines the ones that genuinely protect people. A carefully limited law will be more effective, and more respected, than a universally ambitious one.