雅思阅读 173: The Air We Breathe（我们呼吸的空气）

改编自 European Respiratory Journal / Frontiers in Pediatrics（2025-2026年）。雅思阅读 Section 3 难度，约 1050 词。 素材来源：https://pmc.ncbi.nlm.nih.gov/articles/PMC12278304/

Reading Passage

A. Asthma is no longer regarded as a single, uniform illness. Once described simply as a narrowing of the airways that came and went, it is now understood as a family of conditions whose origins stretch back into early childhood and whose triggers lie as much in the surrounding environment as in the patient's own body. The most striking shift in recent research has been the recognition that the lungs of children are not miniature versions of adult lungs. They are organs still under construction, growing in spurts from birth through adolescence, and that growth can be derailed by exposures that an adult would tolerate without obvious harm. A child who inhales polluted air year after year does not merely suffer occasional attacks; the very architecture of the bronchial tree may be altered, leaving a smaller airway calibre that never fully recovers. This reframing has moved asthma from the consulting room of the allergist into the wider domain of public health, because the exposures that damage developing lungs are distributed across whole cities rather than confined to individual households. Where an earlier generation of doctors saw an unlucky disposition, modern epidemiology sees an environmental wound inflicted in slow motion, one school run and one congested street at a time.

B. Particulate matter smaller than 2.5 micrometres — known as PM2.5 — has become the focus of this concern. These particles are so tiny that deep inhalation carries them past the upper respiratory tract and into the alveoli, the delicate sacs where oxygen crosses into the bloodstream. From there, their chemical burden can enter the circulation itself. A long-running cohort study of school children in Taiwan, published in 2025, tracked youngsters exposed to differing neighbourhood concentrations of PM2.5 over several years and found that sustained exposure was associated with measurably impaired lung growth. Children who began wheezing during the study showed, on average, a reduction of about 13 millilitres in the forced expiratory volume they could push out in one second — a small figure in isolation, but one that compounds across a decade of development. The same children also showed elevated levels of fractional exhaled nitric oxide, a biomarker of airway inflammation that does not depend on symptoms alone. Crucially, the damage appeared even in youngsters who had not yet received a formal asthma diagnosis, suggesting that pollution can slow lung development before the clinical label is ever attached.

C. The indoor environment, long treated as a refuge from outdoor pollution, has turned out to be no safe harbour. US birth-cohort analyses published in 2025 found that several early-life exposures cluster together rather than act alone: fine particles from outside that seep through windows, dampness and mould associated with water damage, and the absence of household dogs — a finding that echoes the so-called hygiene hypothesis, in which early microbial exposure seems protective. The statistical methods used were deliberately conservative, adjusting for income, ethnicity and maternal smoking, yet the associations survived. What these studies cannot yet tell us is which exposure matters most. A child breathing a mixture of traffic fumes, cooking emissions and dust from a damp carpet is exposed to all of them simultaneously, and untangling their separate contributions requires the kind of multi-pollutant modelling that epidemiologists are only now beginning to standardise. The practical message, however, is already clear: reducing indoor dampness, banning smoking in the home and keeping particles out at the window all help, even when their precise weighting is unknown.

D. Not all triggers are chemical. Pollen season, dust storms and the atmospheric plumes they generate have long been associated with acute asthma attacks, but recent work has sharpened the picture. Research conducted in the Eastern Mediterranean, where arid climate and strong seasonal winds sweep sand across populated coastlines, found that children already sensitised to allergens experienced a further worsening during dust events. Their exhaled nitric oxide climbed, their peak flow dipped, and the effect was most pronounced in those whose immune systems had already recognised common environmental allergens. Black carbon — the soot produced by incomplete combustion in diesel engines and older heating systems — shows a similar pattern, with a three-day lag between exposure and hospital attendance. In winter, when domestic burning and temperature inversions trap soot close to the ground, the same concentration of black carbon appears more likely to tip a vulnerable child into an acute exacerbation than it does in summer.

E. These findings carry an uncomfortable implication: the childhood asthma epidemic of the past half-century cannot be explained by genes alone, because the human genome has not changed in that time. Something in the modern environment has shifted, and the most plausible candidates are the combustion products that accompany dense urban living. Air quality standards, once set chiefly with adult cardiovascular disease in mind, are increasingly being rewritten around the developing lung. The most effective interventions turn out to be population-level ones — shifting fleets away from diesel, restricting emissions near schools, and improving housing stock — rather than the prescription of yet another inhaler. None of this means that individual treatment has failed; bronchodilators and controller inhalers remain essential. But the research suggests that the largest gains in childhood respiratory health will come not from treating attacks after they occur, but from ensuring that the air a child grows up breathing allows the lungs to reach their full genetic potential. The child who wheezes at seven may be telling us something about the city, not just about themselves. The challenge for the next decade of respiratory medicine is therefore as political as it is clinical: to read the wheeze as a data point about the air, and to regulate the sources of that air as rigorously as clinicians regulate the dose of an inhaler.

Questions 1-4

Choose the correct heading for paragraphs B, C, D and E from the list of headings below.

List of Headings i. Why genes alone cannot explain the asthma epidemic ii. The biology of PM2.5 and a long-term children's study iii. Why indoor air offers no reliable protection iv. The history of asthma diagnosis v. Non-chemical triggers and seasonal variation vi. The cost of asthma medication worldwide vii. How inhalers are manufactured

1. Paragraph B: ____
2. Paragraph C: ____
3. Paragraph D: ____
4. Paragraph E: ____

Questions 5-8

Choose the correct letter, A, B, C or D.

5. Why are children's lungs considered especially vulnerable? A. They are simply smaller versions of adult lungs. B. They are still growing and their development can be derailed. C. They contain more alveoli than adult lungs. D. They cannot absorb oxygen efficiently.

6. What did the Taiwanese school study find about children who began wheezing? A. Their lung function improved over time. B. They showed an average reduction of about 13 millilitres in FEV1. C. They were already formally diagnosed with asthma. D. Their exhaled nitric oxide fell sharply.

7. What is notable about black carbon exposure? A. It affects children immediately on the same day. B. It is linked to exacerbations with roughly a three-day delay. C. It is more harmful in summer than in winter. D. It has no measurable effect on asthma.

8. Where does the author argue the biggest gains in childhood respiratory health will come from? A. Developing stronger bronchodilators. B. Population-level improvements in air quality and housing. C. Identifying susceptible genes. D. Prescribing more inhalers.

Questions 9-13

Do the following statements agree with the claims of the writer?

Write:

• TRUE if the statement agrees with the information
• FALSE if the statement contradicts the information
• NOT GIVEN if there is no information on this

9. PM2.5 particles are large enough to be filtered out by the upper respiratory tract.
10. In the Taiwanese study, lung-growth impairment appeared even in children without a formal asthma diagnosis.
11. The absence of dogs in the home was found to be protective against childhood asthma.
12. Air quality standards have historically been set primarily with the developing child lung in mind.
13. Asthma is now more prevalent in rural areas than in cities.

Questions 14-15

Complete the summary below using NO MORE THAN TWO WORDS from the passage.

Sustained exposure to fine particulate matter was associated with impaired lung growth and elevated levels of fractional exhaled (14) __________, a biomarker of airway inflammation that does not rely on (15) __________ alone.

答案与解析

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