Mednotes

L7 Public Health Epidemiology of Asthma

Properties2
tagspublichealth, lecture
aliasesL7 Public Health Epidemiology of Asthma

21 min read

Overview

This lecture covers why the respiratory system is especially exposed to the environment, the global and New Zealand burden of respiratory disease, and the epidemiology of the two major obstructive airway diseases, Asthma and COPD (chronic obstructive pulmonary disease) — how they differ in pathology, life-course pattern and risk factors, and where they overlap. It closes by looking at what public health approaches (health promotion frameworks, national policy, smoking control) can do to reduce the burden.

The respiratory system and air pollution

  • The lungs are constantly exposed to the environment: about 5 L of air per minute, defended by cough, mucus and immunological mechanisms.
  • They also receive the entire cardiac output (~5 L/min), separated from pulmonary capillaries by a very thin alveolar wall.
  • Respiration is under autonomic, voluntary and emotional control.
  • WHO reports air pollution as the greatest environmental threat to health: a leading cause of non-communicable disease (including cardiac disease and stroke), causing 7 million premature deaths a year, from both indoor and outdoor sources. It remains a problem in New Zealand.
  • The Great Smog of London (December 1952) is used as a historical illustration of severe outdoor air pollution.

Anatomical pattern of respiratory disease

  • Acute disease by site: airways — acute bronchitis/bronchiolitis (very common); alveoli — pneumonia, including COVID-19 (common); pleura/vasculature — pleural infection, pneumothorax, pulmonary embolism (all less common).
  • Chronic disease by site: airways — lung cancer and the obstructive airway diseases (asthma, COPD/emphysema, bronchiectasis) are all very common; pleura/interstitium — pleural cancer (mesothelioma) and interstitial lung disease (pulmonary fibrosis) are less common.

Global and NZ burden of respiratory disease

  • Global Burden of Disease data (IHME GBD Compare) shows lung cancer and other cancers among the leading non-communicable-disease causes of DALYs; COVID-19, lower respiratory infections and TB are major communicable-disease causes; COPD and asthma sit within the non-communicable cluster, reflecting a large respiratory contribution to global disease burden.
  • Ranking of global causes of death/disability shifted from 1990 to 2010 (Lozano et al., Lancet 2012): COPD rose to become the 3rd leading cause and lung cancer entered the top 5 by 2010, underscoring a rising burden of respiratory disease.
  • The “Big 5” respiratory diseases, each with important public health interventions for prevention and/or management: asthma, COPD, acute respiratory infections, lung cancer, and TB.
  • TB mortality (Massachusetts/USA) fell from ~350–400 per 100,000 in the 1860s to near 0 by the mid-20th century; case-finding, streptomycin (1947) and BCG vaccination (1954) roughly tracked this decline but most of the fall predates these interventions, since the bacillus itself was only identified in 1882.
  • NZ respiratory disease cost an estimated 87.9m; prescriptions 406.1m; years lived with disability 6.28bn — by far the largest component). This excludes ED/outpatient costs, lost work days, and long-term effects of school absence.
  • Total respiratory hospitalisation rate (age-adjusted, per 100,000/year) was roughly stable to slowly rising from 2000 (~1470) through the 2010s (peaking ~1800 around 2017), then fell sharply in 2020 (to ~1150) during the COVID-19 pandemic before rising again toward ~1500 by 2022.
  • During 2020, non-pharmaceutical interventions (e.g. lockdowns) sharply reduced acute non-COVID respiratory infection admissions compared with the typical winter peak seen in 2015–2019.

Airway disease across the life course and spirometry patterns

  • Asthma typically predominates in childhood, COPD in old age, with an uncertain overlap/transition zone between them in adulthood; risk factors shift from genes, in-utero exposures and allergies (early life) to pollution, smoking and occupation (later life).
  • Spirometry basics: FVC = total volume exhaled from full to empty lungs; FEV1 = volume exhaled in the first second.
  • Normal spirometry: volume rises steeply to FEV1 at 1 second, then more gradually to a plateau (FVC) by ~5–6 seconds.
  • Obstructive pattern (very common, e.g. asthma, COPD): FVC may be slightly lower, FEV1 is low, and the FEV1/FVC ratio is low.
  • Restrictive pattern (uncommon): FVC is low, FEV1 is normal or low, but the FEV1/FVC ratio is normal or high.

Asthma: definition, pathology and mechanism

  • Asthma is an inflammatory (often allergic) process causing variable airway narrowing. Lung function may be normal between episodes, though inflammation usually persists.
  • It starts mostly in childhood (boys > girls); adult-onset asthma is more common in women than men.
  • Symptoms — wheeze, cough, difficulty breathing, chest tightness — are often intermittent.
  • Pathology progresses from a normal airway (relaxed smooth muscle, open lumen) → asthmatic airway (inflamed, thickened wall) → asthmatic airway during an attack (tightened smooth muscle, mucus plugging, air trapped in the alveoli distal to the obstruction).
  • Histology of asthmatic airways shows structural remodelling versus normal: a markedly thickened basement membrane, hypertrophied smooth muscle, and a narrowed, irregular lumen.
  • Allergic sensitisation can be demonstrated by skin prick testing against a panel of allergens (e.g. pollens, animal dander, mould), read against histamine and negative controls.

Asthma epidemiology: age, sex, ethnicity and geography

  • Cohort data show asthma prevalence shifts from male-predominant in childhood (~10% at age 7) to female-predominant in adulthood, with females overtaking males by the mid-20s and reaching the highest rates (~20–21%) by ages 26 and 45.
  • NZ age-standardised medicated asthma rates (2022/23) cluster around 10–15% across most age groups, with higher rates in young males (5–14 years) and in females aged 15–34 compared with same-age males.
  • The ISAAC study of wheeze prevalence in 13–14 year-olds shows substantial global geographic variation: highest prevalence in parts of the UK/Ireland, Australia/New Zealand and parts of Latin America; lower prevalence across much of Asia and parts of Europe.
  • Comparing a “clean” (Munich) versus “polluted” (Leipzig/Halle, former East Germany) environment in 9–11 year-olds found less asthma (9% vs 7% — clean higher) and atopy (37% vs 18%) in the clean environment, but much more bronchitis in the polluted one (16% vs 34%), i.e. asthma and atopy were more common in the clean, western (Munich) environment while bronchitis was more common in the polluted one.
  • NZ medicated asthma prevalence (2022/23) varies by ethnicity: Māori 18.7% (children and adults); Pacific 16% children / 10.9% adults; Asian 6.7% children / 6.5% adults (lowest); European/Other 12.3% children / 13.2% adults.
  • Asthma hospitalisation rate ratios (relative to non-Māori/non-Pacific, 2000–2022) show persistently elevated rates for Pacific (peaking ~3.7 around 2007, settling ~2.5 by 2022) and Māori (plateauing ~2.5–2.9), while Asian rates stayed close to or below 1.0.
  • There is a clear socioeconomic gradient in asthma hospitalisation: the most deprived quintile (NZDep 9-10) had rates up to ~3.4x the least deprived (NZDep 1-2), with risk increasing progressively across deprivation quintiles.
  • During 2020, asthma admissions fell during the COVID-19 lockdown (April–June) but spiked sharply in July 2020, a pattern that closely tracked a resurgence of positive rhinovirus tests at Waikato hospital once restrictions eased — linking the admission spike to rhinovirus infection.

The hygiene hypothesis

  • Proposed by Strachan (1989): children from bigger families have fewer allergies, and allergy prevalence has increased as family sizes have reduced, raising the question of whether sibling exposure reduces atopy via lower hygiene and more childhood infections. Farming children have also been reported to have fewer allergies/asthma.
  • Immunologically, allergen exposure via dendritic cells can drive naive T-helper cells toward a Th2 response (via STAT6/GATA-3, producing IL-4/5/9/13) leading to allergy, or a Th1 response (via STAT4/T-bet/IL-12, producing IFN-γ/TNF-β) leading to protection against infection — the Th1/Th2 balance underlying the hygiene hypothesis.
  • Cohort data: as the number of children in the house at age 3 increases (1 to 5+), asthma prevalence at both age 9 and age 32 falls (from ~13–23% with one child to ~3–9% with 5+ children).
  • Other reported associations with fewer allergies/asthma: owning cats and dogs, bottle feeding (controversial); and with fewer allergies specifically: parental/personal smoking (controversial), thumb-sucking and nail-biting.
  • Combining “unhygienic” exposures (not breastfed, cats/dogs, crowded house, smoking parent, daycare attendance, thumb-sucking/nail-biting; Shin et al. 2017) showed atopy prevalence at both age 13 and age 32 fell steadily as the number of exposures increased from 1 to 6 (from ~70% down to ~20–45%, both p<0.001).
  • The association was weaker for asthma: at age 13 prevalence was highest with 2 exposures (~21%) and generally declined with more exposures (p=0.010), but at age 32 the pattern was flat (~16–23%) and not statistically significant (p=0.14) — the hygiene hypothesis association is less consistent for asthma than for atopy.
  • This creates a difficult public health message, since the implied “unhygienic” advice (avoid breastfeeding, keep pets, smoke around children, don’t wash hands) runs directly counter to good health practice.

Asthma mortality and management

  • NZ experienced two distinct asthma mortality epidemics (1960s–2000s data): one peaking around 1966–68 and a much larger one peaking around 1979–81, both clearly exceeding rates in England and Wales, Australia, USA, Canada and West Germany, which stayed comparatively low and flat. All countries’ rates converged to low levels by the 1990s–2000s. [flag: axis title/units not legible on the slide itself] The historically debated role of a specific reliever inhaler/medication in driving the NZ epidemics is flagged on the graph but not further specified in the transcript.
  • Historically, ineffective/harmful “treatments” existed, e.g. Dr Batty’s Asthma Cigarettes (marketed since 1802).
  • The UK National Review of Asthma Deaths (NRAD, Royal College of Physicians, May 2014) identified contributing factors in asthma deaths: excessive prescribing of reliever medication, under-prescribing of preventers (inhaled steroids), use of long-acting beta agonists alone, 45% of patients dying without seeking medical assistance, and guidelines not being followed in 46% of cases.
  • Poor asthma control is defined as: symptoms more than twice a week, needing a reliever inhaler on 2 or more days a week, any symptoms at night or on waking, or some limitation of activities — many patients tolerate symptoms worse than this without recognising it as poor control.
  • Anti-Inflammatory Reliever (AIR) therapy: using a plain bronchodilator alone (e.g. Ventolin) as a reliever is discouraged; the preferred approach uses a combination inhaler containing both an inhaled corticosteroid and a bronchodilator (e.g. budesonide/formoterol, Symbicort) as the reliever.
  • NZ dispensing data (age 12+, PHARMAC, 2010–2023) show SABA dispensing remaining consistently highest throughout (with a slight late decline), ICS-alone dispensing declining steadily, and ICS/formoterol (budesonide/formoterol) rising sharply from around 2019 — coinciding with GINA 2019 guidance and its approval as a sole reliever — to overtake other ICS/LABA combinations by 2023.
  • Over the same period, the trend in asthma hospital discharge rates (age 12+) was flat around 9–9.5 per 100,000 from 2013–2018, then declined to roughly 7–7.5 per 100,000 by 2023, temporally associated with the shift toward AIR/combination reliever therapy.
  • A real-world case example (NZ Herald, 2010): a 4-year-old boy died from an unexpectedly severe, rapidly progressive asthma attack, illustrating how quickly asthma can become fatal.

COPD: definition, phenotypes and pathology

  • COPD (chronic obstructive pulmonary disease, also called CORD, COAD or COLD) is an inflammatory (non-allergic) process, usually caused by smoking or other inhaled pollutants (occasionally seen in non-smokers, mostly from chronic asthma). Damage predisposes to chronic/acute infection.
  • Unlike asthma, lung function is NOT normal between exacerbations. It starts in adulthood, after years of smoking. Symptoms: wheeze, cough, sputum, difficulty breathing.
  • Two classic clinical phenotypes: “Blue Bloater” (chronic bronchitis) — shortness of breath, cough with sputum, cyanosis, crackles and wheeze, peripheral oedema, low O2, high CO2; “Pink Puffer” (emphysema) — shortness of breath, little/no cough, chest overexpansion, no cyanosis, quiet breath sounds, no peripheral oedema, slightly low O2, normal CO2.
  • Mechanistically: loss of alveolar wall attachments around the airway causes emphysema (loss of elastic recoil, airway collapse); smooth muscle constriction with fibrosis/inflammation of the airway wall causes chronic bronchitis. Histology confirms destroyed alveolar architecture (emphysema) alongside a thickened, distorted airway wall (bronchitis) compared with normal lung.
  • COPD is best understood via a Venn diagram: chronic bronchitis and emphysema overlap to define COPD, which can further overlap with asthma, all falling within the broader category of airflow obstruction — COPD is not a single distinct disease entity but a composite of overlapping conditions.

COPD: lung function decline and trajectories

  • The Fletcher-Peto diagram (FEV1 decline with age in men, by smoking history): never-smokers (or those not susceptible) decline gradually from 100% (age 25) to ~70–75% by 75, staying above the disability threshold (~30% of value at 25). Susceptible regular smokers decline steeply, crossing the disability threshold around age 60 and the death threshold (~10%) by ~70. Stopping smoking at 45 or 65 flattens the subsequent decline to run roughly parallel to the never-smoker slope, but stopping later (65) still leaves substantially worse lung function than stopping earlier (45) — smoking cessation helps at any age, but earlier cessation preserves more lung function.
  • Lange et al. (2015) describe four lung-function trajectories from childhood to adulthood, based on peak attained FEV1 and subsequent rate of decline: TR1 — normal peak, slow decline, no COPD (71.5% of people); TR2 — small lungs (low peak) but slow decline, no COPD (16.9%); TR3 — normal peak but rapid decline, leading to COPD (5.5%); TR4 — small lungs (low peak) with steady decline, leading to COPD (6.1%). This shows COPD can arise either from accelerated decline from a normal peak, or from never reaching a healthy peak lung function in the first place, not only from the classic accelerated-decline (Fletcher-Peto) model.

COPD epidemiology: international and NZ patterns

  • OECD data (2015 or nearest year) on combined asthma/COPD avoidable hospital admissions (age-sex standardised per 100,000) show New Zealand notably high at 371, well above the OECD34 average of 237, among the higher-admission countries alongside Australia, Ireland, Turkey and (highest) Hungary; Japan, Italy and Portugal had the lowest rates.
  • COPD hospitalisation in adults 45+ (NZ, 2022) shows both ethnicity and deprivation strongly associated with risk: Māori have by far the highest rates and steepest deprivation gradient (682.0 at NZDep 1-2 rising to 1820.6 at NZDep 9-10), followed by Pacific (582.9 to 1197.4); Asian rates are much lower across all deprivation levels (84.1 to 197.0); non-Māori/non-Pacific rates are intermediate with a clear gradient (223.6 to 782.9).
  • Similar to other respiratory admissions, COPD hospital admissions in 2020 were markedly lower than the 2015–2019 typical winter peak, with a smaller, delayed winter peak that year — a COVID-19 pandemic effect.
  • Adult COPD mortality (age-adjusted, per 100,000/year) rose from ~117 (2000) to a peak of ~135 (2001), then declined fairly steadily over two decades to ~78 by 2019, dipped further to ~58 in 2020 (provisional data, likely a pandemic effect), before rising again to ~68–88 in 2021 — an overall long-term downward trend in NZ COPD mortality.

Public health approaches to respiratory disease

  • The Ottawa Charter for Health Promotion framework (enable, mediate, advocate at its core, surrounded by five action areas: build healthy public policy, create supportive environments, strengthen community action, develop personal skills, reorient health services) is used as a prompt for thinking about respiratory health interventions at population, community and whānau/individual levels.
  • The Asthma and Respiratory Foundation NZ’s 2023 political manifesto set out eight policy themes for the NZ government: prioritising respiratory wellness as a national health priority (reducing acute respiratory hospitalisations, reducing Māori/Pacific disparities); a national respiratory strategy (spirometry capacity, accurate diagnosis, workforce investment, bronchiectasis prevention/funding, lung cancer screening); improved services via multi-disciplinary teams; tackling youth vaping (banning disposable vapes, limiting nicotine content, retailer/advertising restrictions); investing in vaccination (RSV, influenza); health literacy (culturally appropriate education, particularly for Māori children’s asthma); healthy housing (enforcing healthy homes standards in rentals); and indoor/outdoor clean air (banning unflued gas heaters, reducing solid-fuel burning, EV fleets, air quality monitoring and a national strategy).
  • NZ smoking prevalence fell substantially from 1983–2020: adult (15+) current smoking declined from ~32% (1984) to ~14% (2020); Year 10 student regular smoking declined more steeply, from ~28% (~1999) to ~5% (2020) — a projection pointed toward a 5% target by ~2024–2025. This decline coincided with numerous tobacco control policies and campaigns (tobacco control programmes, warning labels, price rises, indoor smokefree laws, standardised packaging, the Smokefree 2025 goal, and vaping regulation).
  • The Smokefree Environments and Regulated Products (Smoked Tobacco) Amendment Act 2022 (SERPA) would have introduced denicotinisation (reducing nicotine from 8–13 to 0.8 mg/g), a 90% reduction in tobacco retailers, and a smoke-free generation (no sales to anyone born after 2006), predicted to reduce smoking to under 5% (non-Māori by 2025, Māori by 2027), with over 8000 fewer deaths and over $2 billion in health savings — but the policy was subsequently cancelled/repealed.

Summary points

  • The respiratory system is highly exposed to the environment.
  • The “Big 5” (asthma, COPD, acute respiratory infections, lung cancer, TB) are all influenced by public health measures.
  • Respiratory disease carries a huge burden, seen daily in clinical practice.
  • Asthma and COPD show important overlaps and differences in epidemiology.
  • Both primary prevention (preventing disease occurrence) and secondary prevention (preventing exacerbations) are needed.

Self-test

  1. Explain why the respiratory system is particularly vulnerable to environmental exposures.
  2. According to WHO, what is the scale and nature of the global health impact of air pollution?
  3. List the “Big 5” respiratory diseases discussed as public health priorities.
  4. Describe the difference between an obstructive and a restrictive spirometry pattern, in terms of FVC, FEV1 and the FEV1/FVC ratio.
  5. Define asthma and describe its typical age/sex pattern of onset.
  6. Describe the progression of airway pathology from a normal airway to an asthmatic airway during an attack.
  7. Distinguish the immunological pathway (Th1 vs Th2) underlying protection from infection versus allergy.
  8. Describe how asthma prevalence changes with age and sex across the life course, from childhood to middle age.
  9. Distinguish the pattern of asthma versus atopy prevalence in relation to childhood “unhygienic” exposures, according to the hygiene hypothesis studies presented.
  10. List examples of “unhygienic” childhood exposures reported to be associated with fewer allergies or asthma.
  11. Describe the ethnic disparities in NZ medicated asthma prevalence and in asthma hospitalisation rates.
  12. Describe the relationship between socioeconomic deprivation and asthma hospitalisation rates in NZ.
  13. What contributing factors did the National Review of Asthma Deaths (NRAD) identify in asthma deaths?
  14. Define poor asthma control according to the criteria given.
  15. Explain the rationale for Anti-Inflammatory Reliever (AIR) therapy and why a bronchodilator-only reliever is discouraged.
  16. Distinguish the chronic bronchitis (“Blue Bloater”) and emphysema (“Pink Puffer”) phenotypes of COPD.
  17. Describe the two structural mechanisms of airflow obstruction in COPD and how each arises.
  18. Explain, using the Fletcher-Peto diagram, why the age at which a smoker quits matters for lung function.
  19. Describe the four lung-function trajectories (Lange et al.) leading to COPD or not, and their approximate population proportions.
  20. Explain how the Venn diagram relates chronic bronchitis, emphysema, asthma and COPD to one another.
  21. Describe how COPD hospitalisation rates in NZ vary by ethnicity and deprivation.
  22. A patient presents with recurrent wheeze that started in childhood, is intermittent, and is normal on lung function testing between episodes. A second patient has chronic wheeze, cough with sputum, and abnormal lung function even between exacerbations, having smoked for 30 years. Distinguish which condition each patient more likely has and why.
  23. Describe the long-term trend in NZ smoking prevalence from 1983–2020 and the type of policies associated with it.
  24. Explain what the SERPA (2022) policy proposed and what ultimately happened to it.

Answers

Graph View

Backlinks