GAtherton

Asthma and Aspergillosis

How fungal spores interact with asthma and other lung diseases

Every day we inhale thousands of microscopic fungal spores from the environment. One of the most common fungi in the air is Aspergillus fumigatus. In healthy lungs these spores are removed quickly by the lungs’ natural defence systems and cause no illness.

However, in people with asthma—particularly severe asthma—the interaction between the lungs and Aspergillus can be very different. The fungus may trigger allergic inflammation, grow in mucus within the airways, or occasionally contribute to chronic lung disease.

Understanding this relationship helps explain several important conditions including:

  • Aspergillus sensitisation

  • Severe Asthma with Fungal Sensitisation (SAFS)

  • Allergic Bronchopulmonary Aspergillosis (ABPA)

  • Aspergillus bronchitis

  • Chronic Pulmonary Aspergillosis (CPA)

Although asthma is the most common condition linked to Aspergillus allergy, other lung diseases such as bronchiectasis, Chronic Obstructive Pulmonary Disease (COPD), and tuberculosis-related lung damage can also create environments where the fungus becomes important.

Why Asthma Creates a Favourable Environment for Aspergillus

Asthma is a disease of airway inflammation and hyper-reactivity. The bronchi narrow during attacks because the airway wall becomes swollen and the surrounding smooth muscle contracts.

Several features of asthma make it easier for Aspergillus spores to remain in the lungs.

Mucus production

Asthma often causes increased production of thick airway mucus.

Normally mucus traps inhaled particles and moves them upward toward the throat via the mucociliary escalator.

In asthma:

  • mucus becomes thicker

  • clearance becomes less efficient

  • spores remain trapped

This trapped environment allows fungal spores to persist in the airway mucus.

Allergic immune responses

Many asthma patients have Type-2 (T2) inflammation (50-70%), involving immune pathways driven by:

  • Immunoglobulin E (IgE)

  • Interleukin-4

  • Interleukin-5

  • Interleukin-13

  • eosinophils

These pathways respond strongly to fungal allergens. When the immune system recognises Aspergillus proteins it may trigger allergic inflammation in the airways.

Fungal sensitisation is increasingly recognised as an important contributor to severe asthma (PMID: 24735832).

Aspergillus Sensitisation

Many people with asthma develop allergic sensitisation to Aspergillus.

Sensitisation means the immune system produces antibodies against fungal proteins.

Features include:

  • positive Aspergillus skin test or IgE blood test

  • worsening asthma symptoms

  • increased exacerbations

Studies suggest 10–25% of patients attending severe asthma clinics show Aspergillus sensitisation (PMID: 24735832).

However, sensitisation alone does not necessarily cause lung damage.

Severe Asthma with Fungal Sensitisation (SAFS)

Some patients with severe asthma have fungal sensitisation but do not meet the criteria for ABPA.

This condition is known as Severe Asthma with Fungal Sensitisation (SAFS).

Typical features include:

  • severe or poorly controlled asthma

  • fungal allergy

  • moderate IgE elevation

A randomised controlled trial demonstrated that antifungal therapy may improve symptoms in some SAFS patients (PMID: 18948425).

Allergic Bronchopulmonary Aspergillosis (ABPA)

Allergic Bronchopulmonary Aspergillosis is the most important Aspergillus-related disease associated with asthma.

ABPA occurs when Aspergillus grows within airway mucus and triggers a strong allergic immune response.

Typical findings include:

  • very high total IgE levels

  • Aspergillus-specific IgE and IgG antibodies

  • eosinophilia

  • mucus plugs containing fungal hyphae

  • central bronchiectasis

ABPA occurs in approximately:

  • 1–2% of all asthma patients

  • up to 10–15% of severe asthma patients

These figures come from global prevalence estimates of ABPA in asthma populations (PMID: 23210682/.

Modern diagnostic criteria for ABPA were updated by the International Society for Human and Animal Mycology (ISHAM) in 2024 (PMID: 38423624).

Asthma and Aspergillus Disease Pathway


Possible interactions between asthma and Aspergillus. Some patients develop allergic disease (ABPA) which may lead to airway damage such as bronchiectasis (NB Progression to CPA is very rare).

When ABPA Causes Bronchiectasis

Repeated inflammation from ABPA may damage airway walls and lead to bronchiectasis.

Bronchiectasis occurs when airways become:

  • permanently widened

  • distorted

  • unable to clear mucus effectively

Instead of being cleared from the lungs, mucus pools in the airways.

This retained mucus creates an environment where microorganisms—including fungi—can grow.

Aspergillus Bronchitis

In some patients with bronchiectasis or chronic lung disease, Aspergillus may persist in airway mucus and cause chronic airway infection rather than allergy.

Symptoms may include:

  • chronic cough

  • sputum production

  • repeated positive Aspergillus cultures

IgE levels are usually lower than in ABPA.

Chronic Pulmonary Aspergillosis (CPA)

Chronic Pulmonary Aspergillosis is a slowly progressive fungal infection of damaged lung tissue.

CPA usually develops in lungs containing:

  • cavities

  • severe structural damage

Common underlying diseases include:

  • tuberculosis

  • sarcoidosis

  • severe COPD

Globally, the most common cause of CPA is previous tuberculosis infection (PMID: 22271943).

Asthma alone rarely causes CPA, but severe bronchiectasis or ABPA-related lung damage may occasionally lead to it.

Aspergillosis and Immune Competence

Different forms of aspergillosis occur depending on lung damage and immune function.

Other Lung Diseases Linked to Aspergillus

Although asthma is the most common condition associated with Aspergillus allergy, several other lung diseases can predispose to fungal disease.

Bronchiectasis

Dilated airways trap mucus, allowing fungi and bacteria to persist.

COPD

Chronic airway inflammation may lead to Aspergillus bronchitis or chronic pulmonary aspergillosis.

Tuberculosis

Post-tuberculosis lung cavities are the most common global cause of chronic pulmonary aspergillosis (PMID: 22271943).

Key Messages

  • Asthma is one of the most important diseases associated with Aspergillus-related lung conditions.

  • Many asthma patients develop fungal sensitisation.

  • A smaller proportion develop Allergic Bronchopulmonary Aspergillosis (ABPA).

  • Repeated inflammation from ABPA can lead to bronchiectasis.

  • Chronic pulmonary aspergillosis is rare in asthma alone but may occur if significant lung damage develops.

Understanding these interactions helps guide diagnosis and treatment for people living with asthma and Aspergillus-related disease.

Further reading

Agarwal R, Chakrabarti A, Shah A, Gupta D, Meis JF, Guleria R, Moss R, Denning DW; ABPA complicating asthma ISHAM working group. Allergic bronchopulmonary aspergillosis: review of literature and proposal of new diagnostic and classification criteria. Clin Exp Allergy. 2013 Aug;43(8):850-73. doi: 10.1111/cea.12141. PMID: 23889240.

Denning DW, Pleuvry A, Cole DC. Global burden of chronic pulmonary aspergillosis as a sequel to pulmonary tuberculosis. Bull World Health Organ. 2011 Dec 1;89(12):864-72. doi: 10.2471/BLT.11.089441. Epub 2011 Sep 27. PMID: 22271943; PMCID: PMC3260898.

by GAtherton

Weekly Aspergillosis Research Update – Week 10, 2026

Focus: chronic aspergillosis, allergic Aspergillus disease, and long-term lung damage

This week’s papers are especially relevant to people living with Allergic Bronchopulmonary Aspergillosis (ABPA), allergic bronchopulmonary mycosis, and Chronic Pulmonary Aspergillosis (CPA). The strongest themes are the potential value of Immunoglobulin E (IgE) as a marker of future lung decline, the growing role of biologic therapies in steroid-sparing care, and improved tools for diagnosing CPA in people with previous tuberculosis.

Acute invasive aspergillosis papers are included lower down for context, but this update prioritises chronic and longer-term disease.

Chronic and allergic Aspergillus disease

High total serum IgE level at diagnosis was associated with a progressive decline in lung function in asthmatic patients with allergic bronchopulmonary mycosis

Kodama Y, Takaoka S, Nakashima T, Matsunaga K, Terada K, Yamashita Y, Masumitsu H, Miyasaka A, Muraoka T, Masumoto N, Kaneko T, Watanabe M, Tsurikisawa N.
Allergy Asthma Clin Immunol. 2026 Mar 8. doi: 10.1186/s13223-026-01024-2.

PMID: https://pubmed.ncbi.nlm.nih.gov/41796390/

Why this matters

This is one of the most important chronic-disease papers in this batch. It suggests that very high total IgE at diagnosis may not just reflect current disease activity, but may also predict future lung damage.

Key points

  • Patients with allergic bronchopulmonary mycosis (ABPM), including many with Allergic Bronchopulmonary Aspergillosis (ABPA), who had higher IgE levels at diagnosis showed a more progressive decline in lung function over time.

  • This raises the possibility that baseline IgE could help identify patients at higher risk of long-term airway damage.

  • It supports the idea that some patients may need closer monitoring and earlier treatment escalation rather than waiting for repeated flare-ups.

Relevance

For patients and clinicians, this paper reinforces that IgE is not just a number to follow during treatment. A very high starting IgE may signal the need for more careful long-term planning, especially in people with asthma, mucus plugging, recurrent exacerbations or bronchiectasis.

Biologics Use in Eosinophilic Lung Disease: Controversies and Consensus

Pérez de Llano L, Rivas DD, Pavord I, Aslam MMS, Lugogo N.
J Allergy Clin Immunol Pract. 2026 Mar;14(3):583-596.e12. doi: 10.1016/j.jaip.2026.01.022.

PMID: https://pubmed.ncbi.nlm.nih.gov/41786384/

Why this matters

This review is highly relevant to current ABPA care because biologics are increasingly being used to reduce reliance on oral corticosteroids, especially in people with severe asthma and recurrent eosinophilic inflammation.

Key points

  • The review discusses biologics including omalizumab, mepolizumab, benralizumab, dupilumab and tezepelumab.

  • It highlights growing evidence that biologics may help some patients with ABPA by reducing steroid burden, improving asthma control and lowering exacerbation frequency.

  • The authors also stress that evidence in ABPA is still developing and remains less robust than in severe eosinophilic asthma.

Relevance

This is a useful overview of where the field is heading. For many patients with ABPA, the major clinical problem is not only fungal sensitisation but the long-term harm caused by repeated steroid courses. Biologics are becoming an increasingly important part of steroid-sparing strategy, though patient selection remains crucial.

Differential Diagnosis of Eosinophilic Lung Diseases

Emmi G, Bass J, Baratella E, Akuthota P, Loscocco GG.
J Allergy Clin Immunol Pract. 2026 Mar;14(3):542-557. doi: 10.1016/j.jaip.2026.01.027.

PMID: https://pubmed.ncbi.nlm.nih.gov/41786383/

Why this matters

ABPA is still often missed, mislabelled or diagnosed late. This review is useful because it places ABPA in the wider context of eosinophilic lung disease, where several conditions can look similar.

Key points

  • The paper compares ABPA with other eosinophilic lung diseases such as chronic eosinophilic pneumonia, eosinophilic granulomatosis with polyangiitis, and drug-related eosinophilic lung disease.

  • It emphasises the importance of combining history, imaging, blood eosinophils, total IgE, fungal sensitisation and radiology.

  • The review underlines how easily overlap can occur, especially in people with severe asthma.

Relevance

For patients, this matters because getting the diagnosis right affects treatment. Not every eosinophilic lung disease is ABPA, and not every worsening in an asthma patient with high eosinophils is due to fungus. For clinicians, it is a helpful reminder to keep a broad differential diagnosis.

Chronic Pulmonary Aspergillosis

Performance of the LDBio Aspergillus ICT lateral flow assay and western blot for diagnosing chronic pulmonary aspergillosis in post-tuberculosis patients: a prospective study from South India

Samaddar A, Pramanik P, Voleti H, Akshata JS, Nagarathna S, Thennarasu K, Nagraja C.
Microbiol Spectr. 2026 Mar 6:e0384725. doi: 10.1128/spectrum.03847-25.

PMID: https://pubmed.ncbi.nlm.nih.gov/41789940/

Why this matters

This is the key CPA paper in this week’s list. It focuses on a major real-world problem: how to diagnose CPA more effectively in people left with lung damage after tuberculosis.

Key points

  • The study found that the LDBio Aspergillus immunochromatographic test (ICT) performed well in diagnosing CPA in post-tuberculosis patients.

  • Western blot also performed strongly, and combining the tests improved diagnostic confidence.

  • The results support the use of simpler, more accessible serology in settings where advanced imaging or specialist fungal laboratories may be limited.

Relevance

CPA after tuberculosis remains underdiagnosed worldwide. This paper is especially important because it supports the use of practical, lower-complexity diagnostics that may help identify patients earlier. That has implications far beyond India, particularly in regions where post-tuberculosis lung disease is common.

Host susceptibility and chronic disease risk

Oncostatin M receptor deficiency as a novel candidate genetic cause of autosomal recessive hyper-IgE syndrome

Andersen S, Assing K, Jensen J, Rasmussen LD, Laursen CB, Dellgren CD, Hinke DM, Degn SE, Mogensen TH.
J Hum Immun. 2026 Mar 3;2(3):e20250119. doi: 10.70962/jhi.20250119.

PMID: https://pubmed.ncbi.nlm.nih.gov/41783139/

Why this matters

Some patients develop chronic or severe Aspergillus disease because of an underlying immune problem that may not be obvious at first. This paper adds a possible new genetic explanation.

Key points

  • The authors describe a patient with very high IgE, eczema, bone fractures and Chronic Pulmonary Aspergillosis (CPA).

  • They identified a rare variant in the oncostatin M receptor (OSMR) gene.

  • The paper proposes OSMR deficiency as a possible new cause of autosomal recessive hyper-IgE syndrome.

Relevance

Although rare, studies like this help explain why a small number of people develop unusual susceptibility to chronic fungal disease. Over time, this kind of work may improve genetic diagnosis, immune work-up and personalised management in patients with recurrent or unexplained Aspergillus disease.

Important diagnostic lesson

Peripheral T-cell lymphoma-NOS presenting with cavitary lung lesions mimicking invasive aspergillosis

Lopez Ventosa J, Rodriguez A, Garcia N, Tirado M, Nieves Rivera J.
BMJ Case Rep. 2026 Mar 4;19(3):e268805. doi: 10.1136/bcr-2025-268805.

PMID: https://pubmed.ncbi.nlm.nih.gov/41781006/

Why this matters

Although this is not a chronic aspergillosis paper, it is worth noting because it highlights a key problem in lung medicine: cavities and positive biomarkers do not always equal Aspergillus infection.

Key points

  • A patient with cavitary lung lesions and a positive serum galactomannan was initially treated for presumed aspergillosis.

  • Tissue biopsy did not support fungal infection.

  • The final diagnosis was peripheral T-cell lymphoma.

Relevance

This is a valuable reminder that malignancy, tuberculosis and other diseases can mimic CPA or invasive aspergillosis, and that tissue diagnosis remains important when the picture does not fit cleanly.

Acute invasive aspergillosis: important context papers

How to safely discontinue antifungal treatment in invasive pulmonary aspergillosis? - Clinical considerations in haematology

Stemler J, Sprute R, Koehler P, Cornely OA.
Clin Microbiol Infect. 2026 Mar 6:S1198-743X(26)00106-0. doi: 10.1016/j.cmi.2026.03.001.

PMID: https://pubmed.ncbi.nlm.nih.gov/41796963/

25 years of improvement in mortality in invasive aspergillosis in haematology patients: will it be sustained or is it under threat?

Maertens JA, Vanbiervliet Y, Mercier T, Aerts R, Lagrou K, Slavin MA.
J Antimicrob Chemother. 2026 Mar 4;81(4):dkag077. doi: 10.1093/jac/dkag077.

PMID: https://pubmed.ncbi.nlm.nih.gov/41790511/

Invasive aspergillosis in liver transplant recipients in France (2007-21): a nationwide, retrospective, matched case-control study

Le Hyaric C, Melenotte C, Lefebvre F, Saliba F, Botterel F, El-Domiaty N, Dumortier J, Persat F, Do R, Pasquier G, Camus C, Gangneux JP, Kamar N, Iriart X, Monsel A, Fekkar A, Conti F, Vuotto F, Loridant S, Durand F, Bonnal C, Barbaz M, Chesnay A, Vignals C, Lefranc M, Guerin R, Moniot M, Weil D, Bellanger AP, Decaens T, Maubon D, Lebossé F, Artzner T, Morel G, Letscher-Bru V, Herbrecht R, Ader F, Lortholary O, Lefort A, Guichon C, Danion F.
Lancet Microbe. 2026 Mar 2:101272. doi: 10.1016/j.lanmic.2025.101272.

PMID: https://pubmed.ncbi.nlm.nih.gov/41785881/

Treatment Monitoring and Outcome Prediction in Invasive Aspergillosis using Immunologic Markers

Pereira A, Scott J, Sarlea A, Sprute R, Aerts R, Lass-Flörl C, Mikulska M, Sedik S, Garcia-Vidal C, Gangneux JP, Giacobbe DR, Prattes J, Grothe J, Biswas S, Monzo-Gallo P, Bassetti M, Maertens J, Kumar V, Koehler P, Cunha C, Netea MG, Carvalho A, Hoenigl M.
J Infect Dis. 2026 Mar 4:jiag140. doi: 10.1093/infdis/jiag140.

PMID: https://pubmed.ncbi.nlm.nih.gov/41778487/

by GAtherton

Bronchiectasis in Aspergillosis Patients

Many people with aspergillosis also develop bronchiectasis, a condition in which some of the airways in the lungs become permanently widened and damaged. Understanding bronchiectasis can help explain many symptoms experienced by patients with Allergic Bronchopulmonary Aspergillosis (ABPA – Allergic Bronchopulmonary Aspergillosis) and Chronic Pulmonary Aspergillosis (CPA – Chronic Pulmonary Aspergillosis).

Although bronchiectasis cannot usually be reversed, it can often be managed effectively, and understanding how it works helps patients recognise symptoms and flare-ups early.

The airways of the lungs

Your lungs contain a branching network of tubes called bronchi and bronchioles that carry air in and out of the lungs.

Air travels through the trachea (windpipe) into the bronchi, which then divide repeatedly into smaller and smaller tubes called bronchioles. At the ends of the bronchioles are millions of tiny air sacs called alveoli, where oxygen moves into the bloodstream.

The lining of the airways produces a thin layer of mucus that traps dust, bacteria and fungal spores that we breathe in every day.

Tiny hair-like structures called cilia move this mucus upward toward the throat, where it can be swallowed or coughed out. This system acts like a self-cleaning escalator, helping keep the lungs clear.

What is bronchiectasis?

In bronchiectasis, some of the airways become permanently widened and damaged.

When this happens:

  • the airway walls become inflamed and weakened

  • the tubes widen and lose their normal shape

  • mucus becomes harder to clear

  • bacteria and fungi can grow in trapped mucus

Over time, this leads to repeated infections and inflammation.

Doctors often describe bronchiectasis as a vicious cycle:

  1. Infection or inflammation damages the airway

  2. The airway widens and mucus clearance becomes poor

  3. Mucus builds up in the airway

  4. Bacteria and fungi grow in the mucus

  5. Infection and inflammation occur again

Without treatment, this cycle can gradually worsen airway damage.

Why bronchiectasis is common in aspergillosis

Bronchiectasis is particularly common in patients with aspergillosis, especially in ABPA.

In ABPA, the immune system reacts strongly to Aspergillus spores in the airways. This causes:

  • allergic inflammation in the bronchi

  • thick mucus plugs

  • repeated airway irritation

Over time, this inflammation can damage the airway walls and lead to bronchiectasis, often affecting the central airways of the lungs.

Once bronchiectasis develops, mucus becomes harder to clear, which can allow bacteria and fungi such as Aspergillus to persist in the lungs.

Symptoms of bronchiectasis

Many symptoms of bronchiectasis overlap with those of aspergillosis.

Common symptoms include:

  • persistent cough

  • regular sputum (phlegm) production

  • breathlessness

  • fatigue

  • frequent chest infections

Sputum may be:

  • clear

  • yellow or green

  • occasionally blood-streaked

In people with ABPA, patients sometimes cough up thick mucus plugs, which may appear brown or rubbery.

How bronchiectasis is diagnosed

Bronchiectasis is usually diagnosed using a High Resolution CT (HRCT) scan of the lungs.

On a CT scan, doctors may see:

  • widened airways

  • thickened airway walls

  • mucus plugs

  • airways extending closer to the edge of the lung than normal

Radiologists sometimes describe a typical appearance called the “signet ring sign”, where the widened airway appears larger than the nearby blood vessel.

Bronchiectasis and aspergillosis flare-ups

Because bronchiectasis and aspergillosis affect the same airways, it can sometimes be difficult for patients to recognise whether worsening symptoms are caused by:

  • a bronchiectasis infection, or

  • an aspergillosis flare-up.

Understanding the differences can help patients recognise when to seek medical advice.

Bronchiectasis exacerbations

Bronchiectasis flare-ups are usually caused by bacterial infection in trapped mucus.

Patients may notice:

  • increased sputum production

  • sputum becoming yellow or green

  • increased coughing

  • fever or feeling unwell

  • breathlessness

Many patients describe bronchiectasis exacerbations as feeling like a chest infection.

Treatment usually involves:

  • antibiotics

  • airway clearance physiotherapy

  • increased mucus clearance

Aspergillosis flare-ups

Aspergillosis flare-ups are usually caused by fungal activity or immune reactions to Aspergillus.

Patients may notice:

  • worsening wheezing

  • chest tightness

  • increased breathlessness

  • thick mucus plugs

Some patients cough up:

  • brown mucus

  • rubbery mucus plugs

  • mucus shaped like small airway casts

In Chronic Pulmonary Aspergillosis, patients may also experience:

  • persistent cough

  • fatigue

  • weight loss

  • occasionally coughing blood

Treatment may involve:

  • steroid treatment

  • antifungal medication

  • biologic therapies in ABPA

Key differences patients often notice

Feature Bronchiectasis flare-up Aspergillosis flare-up
Main cause Bacterial infection in trapped mucus Fungal activity or immune reaction to Aspergillus
Sputum colour Yellow or green Brown mucus plugs or thick sticky mucus
Fever More common Less common
Wheezing Sometimes present Often worse
Feeling like a chest infection Common Less typical
Response to antibiotics Usually improves Usually little improvement
Mucus plugs Less common More common in ABPA
Blood tests Usually unchanged IgE may rise in ABPA

Both conditions can occur together

In reality, bronchiectasis and aspergillosis often interact with each other.

For example:

  • ABPA can cause bronchiectasis

  • bronchiectasis allows fungi and bacteria to remain in mucus

  • infection and fungal inflammation can occur at the same time

Doctors may investigate flare-ups using:

  • sputum cultures

  • blood tests (for example IgE levels in ABPA)

  • CT scans

  • inflammatory markers

Why airway clearance is important

Because bronchiectasis makes mucus harder to clear, airway clearance physiotherapy becomes a key part of treatment.

Common techniques include:

  • Active Cycle of Breathing Technique (ACBT)

  • Autogenic drainage

  • oscillating devices such as Flutter or Acapella

Regular airway clearance helps:

  • remove mucus from the lungs

  • reduce infections

  • improve breathing

  • reduce cough

For patients with aspergillosis, clearing mucus may also help remove fungal material from the airways.

When patients should seek medical advice

Patients should contact their healthcare team if they notice:

  • rapidly increasing sputum

  • fever or feeling unwell

  • coughing blood

  • severe breathlessness

  • large mucus plugs

Early treatment can often prevent a mild flare-up from becoming a more serious infection.

The key message

Bronchiectasis means that some airways in the lungs have become permanently widened, making mucus harder to clear.

However, many people with aspergillosis and bronchiectasis live active lives with stable lung function.

With good treatment, airway clearance, and early management of infections, bronchiectasis can often be well controlled for many years.

by GAtherton

Damp & Mould Health Evidence Monitor: 4 March 2026

Date of check

4 March 2026

🆕 New papers since last check

Early-life indoor mould exposure and lung function

Journal: Environmental Research: Health
Published: Feb 2026

Summary
Children exposed to serious indoor mould in early life showed:

  • reduced lung function in adolescence

  • increased risk of asthma during childhood

This study used long-term cohort data and objective lung function testing, strengthening the evidence that early mould exposure can have lasting respiratory consequences.

PMID: 39162373
PubMed link:
https://pubmed.ncbi.nlm.nih.gov/39162373/

Damp and mouldy homes: impact on lung health in childhood

Authors: Moorcroft C, Whitehouse A, Grigg J
Journal: Archives of Disease in Childhood (2025)

Summary
This clinical review explains how damp housing contributes to:

  • childhood asthma

  • recurrent respiratory infections

  • allergic disease

It emphasises that paediatric clinicians frequently encounter children whose symptoms are linked to poor housing conditions.

PMID: 39814530
PubMed link:
https://pubmed.ncbi.nlm.nih.gov/39814530/

Damp housing and mental health effects

Journal: Environmental Health Perspectives

Summary
A major review examining whether damp and mould exposure affects mental health.
Evidence suggests associations with:

  • anxiety

  • depression

  • psychological stress

Mechanisms may include chronic illness, housing insecurity, and inflammatory responses to mould exposure.

PMID: 39162373
PubMed link:
https://pubmed.ncbi.nlm.nih.gov/39162373/

📊 Summary

New or important items identified

• Evidence continues to strengthen the link between damp housing and respiratory disease
• Long-term cohort data show effects on lung development
• Emerging research also suggests mental health impacts

by GAtherton

Weeks 6–7 Aspergillosis Literature Update

22 February – 3 March 2026

1️⃣ Chronic Pulmonary Aspergillosis (CPA) & Structural Lung Disease

Clinical impact of chronic pulmonary aspergillosis in patients with pulmonary nontuberculous mycobacterial disease

Annals of Medicine
Lee MR et al., 24 Feb 2026
PMID: 41736260
🔗 https://pubmed.ncbi.nlm.nih.gov/41736260/

Key Findings

  • CPA subtypes identified:

    • Chronic cavitary pulmonary aspergillosis (CCPA)

    • Chronic fibrosing pulmonary aspergillosis (CFPA)

    • Subacute invasive pulmonary aspergillosis (SAIA)

  • CPA significantly worsened:

    • Mortality

    • Lung function trajectory

    • Treatment burden

Relevance

  • Reinforces strong NTM–CPA interaction.

  • Supports routine Aspergillus IgG screening in deteriorating NTM patients.

  • Highly relevant for structured longitudinal services such as NAC.

Post-tuberculosis lung disease and pulmonary aspergillosis management

Expert Review of Anti-infective Therapy
Sehgal IS et al., 22 Feb 2026
PMID: 41674445
🔗 https://pubmed.ncbi.nlm.nih.gov/41674445/

Highlights

  • CPA is the most frequent fungal sequela of treated tuberculosis.

  • Diagnostic delay remains common.

  • Imaging + Aspergillus IgG remain central tools.

Strategic Implication

Post-TB surveillance pathways should incorporate fungal screening protocols.

2️⃣ Invasive Aspergillosis (IA) – ICU & CNS

Why do we urgently need a new treatment for cerebral aspergillosis?

Expert Review of Anti-infective Therapy
Soman R et al., 27 Feb 2026
PMID: 41758247
🔗 https://pubmed.ncbi.nlm.nih.gov/41758247/

Core Issues

  • Extremely high mortality.

  • Poor CNS penetration of many antifungals.

  • Delayed diagnosis remains common.

Direction of Travel

  • CNS-penetrant azoles

  • Host-directed adjunctive therapy

  • Earlier molecular diagnostics

Clinical characteristics of probable invasive pulmonary aspergillosis in the ICU

(Research Square – preprint; not yet indexed in PubMed)

Key Themes

  • Rising IPA incidence in ICU.

  • Increasing recognition in non-classical immunocompromised hosts.

  • Diagnostic uncertainty persists.

Invasive Aspergillus Tracheobronchitis Presenting as Subglottic Stenosis

Respirology Case Reports
Sato T et al., 1 Mar 2026
(Indexing pending — searchable in PubMed by title)

Significance

  • Airway-dominant invasive disease.

  • Reminds clinicians that IA is not purely parenchymal.

3️⃣ Diagnostics – AI, Biomarkers & Rapid Testing

Identification of Aspergillus at section and species levels by AI-based microscopic morphology recognition

Journal of Clinical Microbiology
Tan M et al., 27 Feb 2026
PMID: 41757926
🔗 https://pubmed.ncbi.nlm.nih.gov/41757926/

Why It Matters

  • Species-level ID influences resistance prediction.

  • AI microscopy may support antifungal stewardship.

  • Potential synergy with resistance-genotyping services.

Performance evaluation of chemiluminescence immunoassay for quantitative (1,3)-β-D-glucan

Medical Mycology
Yuan K et al., 24 Feb 2026
PMID: 41733444
🔗 https://pubmed.ncbi.nlm.nih.gov/41733444/

Implication

Improved BDG quantification could refine:

  • Diagnostic confidence

  • Antifungal escalation decisions

  • AMS compliance

Rapid and reliable diagnosis of mucormycosis using colorimetric LAMP

Journal of Clinical Microbiology
Gu Y et al., 26 Feb 2026
PMID: 41746213
🔗 https://pubmed.ncbi.nlm.nih.gov/41746213/

Broader Context

Improving differentiation between mould pathogens is increasingly critical in ICU and transplant settings.

Evaluation of the Aspergillus Lateral Flow Assay

(Preprint; not indexed in PubMed)

Movement toward rapid, bedside semi-quantitative testing continues.

4️⃣ Immunology & Host Response

Ferroptosis-related biomarkers and subtypes in invasive aspergillosis

Toxicology Research
Tang L et al., 23 Feb 2026
PMID: 41756099
🔗 https://pubmed.ncbi.nlm.nih.gov/41756099/

Emerging Theme

  • Ferroptosis signatures in IA.

  • Potential for biomarker-guided host-directed therapy.

Immune Exhaustion in Chronic Infection and Cancer

MedComm
Song Y et al., 26 Feb 2026
PMID: 41768369
🔗 https://pubmed.ncbi.nlm.nih.gov/41768369/

Relevance

  • T-cell exhaustion pathways implicated in invasive pulmonary aspergillosis models.

  • Checkpoint biology may influence future antifungal immunotherapy.

Helminth Immune Modulation and Invasive Fungal Infections in Sub-Saharan Africa

Journal of Fungi
Fonte L et al., 23 Feb 2026
PMID: 41745302
🔗 https://pubmed.ncbi.nlm.nih.gov/41745302/

Implication

Immune skewing in endemic regions may influence:

  • IA susceptibility

  • Allergic bronchopulmonary aspergillosis (ABPA) patterns

Proposition for a New Classification of Hypersensitivity Reactions

Clinical Reviews in Allergy & Immunology
Szegedi A et al., 26 Feb 2026
PMID: 41746569
🔗 https://pubmed.ncbi.nlm.nih.gov/41746569/

Relevance to ABPA

Supports more nuanced immunophenotyping in complex hypersensitivity states.

5️⃣ Therapeutics & Antifungal Strategy

Influence of Extended Itraconazole Antifungal Prophylaxis After Lung Transplant

Journal of Transplantation
Fischer S et al., 26 Feb 2026
PMID: 41769149
🔗 https://pubmed.ncbi.nlm.nih.gov/41769149/

Clinical Angle

Balancing prolonged prophylaxis with resistance development and toxicity.

Auranofin and iodoquinol as repurposing drugs against filamentous fungi

Microbiology Spectrum
Xisto MIDdS et al., 27 Feb 2026
PMID: 41757906
🔗 https://pubmed.ncbi.nlm.nih.gov/41757906/

Takeaway

Repurposed agents remain essential in the slow antifungal pipeline landscape.

Arp9 modulates drug resistance and aflatoxin biosynthesis in Aspergillus flavus

PLoS Pathogens
Ma D et al., 2 Mar 2026
PMID: 41770810
🔗 https://pubmed.ncbi.nlm.nih.gov/41770810/

Strategic Significance

Links:

  • Chromatin regulation

  • Temperature adaptation

  • Drug resistance

  • Environmental pathogenic evolution

6️⃣ Radiology & Case-Based Insights

Radiologic Characterization of Invasive Fungal Infections of the Paranasal Sinuses and Skull Base

Cureus
S S et al., 23 Feb 2026
PMID: 41743147
🔗 https://pubmed.ncbi.nlm.nih.gov/41743147/

Clinical Utility

Supports ENT + radiology diagnostic differentiation.

Atypical Manifestations of Aspergillosis

Respirology Case Reports
Zahiri L et al., 1 Mar 2026
(Indexing pending — searchable by title)

Message

Aspergillosis remains a spectrum disease influenced heavily by host immunity.

📊 2-Week Synthesis

Emerging Patterns

  1. Increasing ICU and CNS complexity

  2. Strong CPA overlap with structural lung disease (NTM, TB)

  3. Rapid diagnostic evolution (AI, BDG quantification, LAMP, LFA)

  4. Growing focus on host biology (ferroptosis, immune exhaustion)

  5. Continued therapeutic gap — particularly cerebral disease

by GAtherton

National Aspergillosis Centre, Antifungal Therapeutic Drug Monitoring (TDM), Molecular Resistance Testing & Antimicrobial Stewardship

How the National Aspergillosis Centre Supports UK Clinicians

Long-term antifungal therapy in aspergillosis presents a distinct antimicrobial stewardship (AMS) challenge. Treatment is often prolonged, drug exposure is highly variable, and resistance may emerge during therapy.

The National Aspergillosis Centre (NAC), working closely with the Mycology Reference Centre Manchester (Manchester UK"], provides national expertise through:

  • Therapeutic drug monitoring (TDM)

  • Molecular resistance testing

  • Specialist Advice & Guidance

  • Remote multidisciplinary team (MDT) review

  • Standardised laboratory processes

Together, these services enable UK clinicians to optimise antifungal therapy while aligning with national AMS strategy and antimicrobial resistance (AMR) policy.

The National AMS Framework: Why This Matters

Antifungal stewardship sits within the wider UK antimicrobial resistance strategy.

Key national resources include:

1️⃣ NHS England – Digital Vision for Antimicrobial Stewardship

https://www.england.nhs.uk/long-read/digital-vision-for-antimicrobial-stewardship-in-england/

Emphasises:

  • Data-driven optimisation

  • Decision support

  • Clear documentation

  • Measurable stewardship interventions

2️⃣ Antimicrobial Prescribing & Stewardship Competency Framework

https://www.gov.uk/government/publications/antimicrobial-prescribing-and-stewardship-competencies

Defines clinician responsibilities including:

  • Right drug

  • Right dose

  • Right duration

  • Monitoring for toxicity

  • Review and stop decisions

3️⃣ English Surveillance Programme for Antimicrobial Utilisation and Resistance (ESPAUR)

https://www.gov.uk/government/publications/english-surveillance-programme-for-antimicrobial-utilisation-and-resistance-espaur-report

Supports:

  • National resistance monitoring

  • Stewardship benchmarking

  • Reduction of inappropriate antimicrobial exposure

4️⃣ Chronic Pulmonary Aspergillosis (CPA) Service Specification

https://www.england.nhs.uk/publication/chronic-pulmonary-aspergillosis-service-adults/

This specialised service model explicitly includes:

  • Optimisation of antifungal therapy

  • Toxicity monitoring

  • Therapeutic drug monitoring

Antifungal stewardship is embedded within the commissioned service design.

Why Aspergillosis Requires Enhanced Stewardship

Unlike short-course antibacterial therapy, aspergillosis often involves:

  • Long-term triazole therapy

  • Structural lung disease

  • High interaction burden

  • Emerging environmental resistance

  • Potential for treatment failure despite adequate adherence

Effective stewardship therefore requires both:

  1. Assurance of adequate drug exposure (TDM)

  2. Assurance of organism susceptibility (molecular testing)

1️⃣ Therapeutic Drug Monitoring (TDM)

Triazole antifungals demonstrate:

  • High pharmacokinetic variability

  • Concentration-dependent toxicity

  • Reduced efficacy if under-dosed

TDM enables:

✔ Early detection of subtherapeutic exposure
✔ Prevention of toxicity
✔ Dose optimisation
✔ Reduction of avoidable escalation

This directly fulfils AMS competency expectations.

2️⃣ Molecular Resistance Testing

Azole resistance in Aspergillus fumigatus is increasingly recognised in the UK.

Through MRCM, NAC supports:

CYP51A Mutation Analysis

Common mutations include:

  • TR34/L98H

  • TR46/Y121F/T289A

These may arise:

  • Environmentally (azole fungicide pressure)

  • During long-term therapy

Phenotypic Susceptibility Testing

Where viable isolates are available:

  • Minimum inhibitory concentration (MIC) testing

  • Clinical interpretation to guide therapy

Why Resistance Testing Is Essential for AMS

If a patient deteriorates despite adequate serum levels:

  • Continuing the same azole is not stewardship

  • Escalating empirically without evidence increases antimicrobial pressure

Molecular confirmation ensures:

✔ Rational switching
✔ Avoidance of ineffective therapy
✔ Contribution to national resistance surveillance

This aligns with ESPAUR and national AMR objectives.

3️⃣ Remote Advice & Guidance & MDT Review

The NAC provides structured national clinician support.

This strengthens stewardship by:

✔ Refining diagnosis
✔ Preventing indication drift
✔ Setting defined review points
✔ Supporting stop decisions
✔ Reducing empirical prolonged therapy

Early specialist review is one of the most effective stewardship interventions.

Integrated Stewardship Model

Clinical Situation TDM Molecular Testing
Initiation of azole Yes Not routine
Poor response + low level Adjust dose Not primary
Poor response + adequate level Confirm exposure Essential
Long-term therapy Periodic monitoring Consider if progression
Relapse on therapy Check level Strongly consider

Exposure optimisation + susceptibility confirmation = complete antifungal stewardship.

Practical Workflow for UK Teams

Step 1 – Define Indication

  • Syndrome

  • Treatment objective

  • Planned review date

Step 2 – Baseline Safety Checks

  • Interaction review

  • Liver function tests

  • ECG where appropriate

Step 3 – Perform TDM

Include:

  • Drug

  • Dose

  • Time of last dose

  • Time of sampling

Step 4 – If Clinical Failure Occurs

  • Confirm adequate drug exposure

  • Consider molecular resistance testing

Step 5 – Define Stop/Review Criteria

Avoid open-ended therapy without documented reassessment.

Demonstrating AMS Compliance in Practice

Using NAC-supported services allows Trusts to evidence:

✔ Documented indication
✔ Dose optimisation
✔ Toxicity mitigation
✔ Rational escalation
✔ Defined review intervals
✔ Resistance surveillance contribution
✔ Specialist consultation

This is measurable, defensible antimicrobial stewardship.

Conclusion

Antifungal stewardship in aspergillosis cannot rely on restriction alone.

It requires:

  • Precision dosing

  • Genetic resistance detection

  • Structured specialist review

  • Alignment with national AMS frameworks

Through integrated therapeutic drug monitoring, molecular resistance testing, and national clinical support, the National Aspergillosis Centre provides a UK model for precision antifungal stewardship aligned with national antimicrobial resistance strategy.

by GAtherton

🏥 Good News: New AI “Digital Scribe” Helping Doctors Spend More Time With Patients

We’re pleased to share some exciting developments from Manchester University NHS Foundation Trust that could directly improve your experience at clinic appointments.

A new technology called Ambient Voice Technology (AVT) is gradually being introduced across parts of the Trust. Think of it as a secure “digital scribe” that supports your clinician during your consultation.

What does it do?

With your permission, the system listens to the natural conversation between you and your doctor or nurse. It then:

  • Creates the clinical notes automatically

  • Drafts follow-up actions

  • Updates the electronic patient record (*i.e. another reason to use myMFT)

This means your clinician doesn’t need to spend as much time typing or looking at a screen — and can focus more fully on you.

📊 What Have the Early Results Shown?

Colleagues from Manchester University NHS Foundation Trust recently presented results from the Dragon Copilot trial at the Microsoft AI Tour in London.

The findings are encouraging:

✅ 88% of clinicians report saving around 2 minutes per appointment on documentation
✅ 88% say it improves quality and increases face-to-face time with patients
✅ Reduced mental workload for clinicians
✅ Significant reduction in after-clinic administrative work

Two minutes may not sound like much — but across a full clinic list, it adds up. Over time, this could help improve efficiency, reduce waiting times, and improve the overall clinic experience.

💻 How Is It Being Used?

The Dragon Copilot system connects directly into the Trust’s Hive Electronic Patient Record system. It is currently being used in:

  • Outpatient clinics

  • Manchester Royal Infirmary’s Emergency Department

Further expansion is planned in the coming weeks.

❤️ Why This Matters for NAC Patients

For patients with chronic conditions such as aspergillosis, consultations are often detailed and complex. Anything that:

  • Frees up clinician time

  • Improves note accuracy

  • Reduces administrative burden

  • Supports more focused, human interaction

…is a positive step forward.

The aim is not to replace clinicians — but to support them, so your appointment time is spent on what matters most: listening, explaining, planning, and answering your questions.

We’ll continue to keep you updated as this technology develops. It’s encouraging to see innovation being used to strengthen patient-centred care.

If you’d like to learn more, a short video featuring Trust leaders and clinicians was showcased at the Microsoft AI Tour and is available via Trust communications channels.

by GAtherton

Watch the World Aspergillosis Day 2026 talks

World Aspergillosis Day 2026 brought together patients, carers, clinicians and researchers to explore how new science and better understanding can improve care for aspergillosis.

Below you can watch the full set of 12 recorded talks from the day, including expert presentations and lived-experience perspectives. You can play them in order, or open the playlist menu to jump to any session.

If you find these videos helpful, please share them — it helps more people living with aspergillosis (and those supporting them) access reliable information and support.

Watch the World Aspergillosis Day 2026 talks

World Aspergillosis Day 2026 brought together patients, carers, clinicians and researchers to explore how new science and better
understanding can improve care for aspergillosis.

Below you can watch the full set of 12 recorded talks from the day, including expert presentations and
lived-experience perspectives. You can play them in order, or open the playlist menu to jump to any session.

If you find these videos helpful, please share them — it helps more people living with aspergillosis (and those supporting them)
access reliable information and support.

Prefer a direct link to the playlist on YouTube?
Open the WAD2026 playlist.

by GAtherton

Using AI Safely When You Have Aspergillosis

Artificial intelligence (AI) tools (for example, ChatGPT and other “medical chatbots”) can help people living with aspergillosis understand information, prepare for appointments, and feel more confident asking questions.

Used well, AI can be like a helpful explainer.
Used badly, it can be misleading — especially for conditions like aspergillosis where treatment decisions are complex.

This page explains what is safe, what is not safe, and how to use AI in a way that supports (not replaces) your clinical team.

Who is this page for?

This guidance is for people affected by:

  • Chronic Pulmonary Aspergillosis (CPA)

  • Allergic Bronchopulmonary Aspergillosis (ABPA)

  • Severe Asthma with Fungal Sensitisation (SAFS)

  • Aspergillus bronchitis

  • Other long-term Aspergillus-related lung problems

A simple rule that keeps you safe

AI should improve your understanding — it should not change your treatment.

If an AI tool suggests starting, stopping, or changing medication, do not act on it without speaking to your clinician.

What AI is good for

AI tools are usually helpful for:

Explaining medical words in plain language

Examples:

  • “What is Aspergillus Immunoglobulin G (IgG)?”

  • “What does ‘eosinophils’ mean?”

  • “What is a CT scan finding such as ‘cavity’ or ‘bronchiectasis’?”

Understanding medicines (general information)

AI can explain:

  • What a medicine is for

  • How it works in the body

  • Common side effects (in general terms)

  • Why monitoring is needed

This can be helpful for antifungal medicines such as itraconazole, voriconazole, posaconazole, and isavuconazole.

Preparing for appointments

AI can help you create a list of questions, for example:

  • “What monitoring do I need while on antifungals?”

  • “What symptoms should prompt urgent review?”

  • “How do we judge whether treatment is working?”

Summarising research articles

If you paste a paragraph from a paper (or describe it), AI can often translate it into patient-friendly language.
(Always remember: AI can sometimes get details wrong — see below.)

Organising your story

Many people find it useful to ask AI to format:

  • A timeline of symptoms

  • A list of medicines and dates

  • A short “what I want from this appointment” summary

This can make consultations more productive.

What AI is NOT safe for

AI should not be used for:

Diagnosis

Aspergillosis diagnosis usually depends on a careful combination of:

  • Symptoms and clinical history

  • Imaging (often computed tomography, CT)

  • Blood tests

  • Sputum tests / microbiology

  • Sometimes bronchoscopy results

AI cannot reliably “diagnose” from symptoms or a single test result.

Treatment decisions

Do not use AI to decide:

  • Whether you should start or stop antifungals

  • Steroid doses or tapering plans

  • Whether you “should” try biologics (for example, omalizumab)

  • Whether a side effect is safe to ignore

These decisions must be individualised and clinician-led.

Urgent situations

If you have worsening breathlessness, fever, chest pain, or coughing blood (haemoptysis), seek medical advice urgently.
AI is not an emergency service.

Why aspergillosis needs extra caution

Aspergillosis care can be complicated because:

  • Some antifungal medicines have important drug interactions

  • Blood levels may need monitoring (therapeutic drug monitoring)

  • Side effects can overlap with symptoms of lung disease

  • Different Aspergillus-related conditions can look similar but need different management

AI tools can also:

  • Over-generalise from asthma guidance

  • Confuse chronic disease with invasive disease

  • “Hallucinate” (invent) facts, references, or confident-sounding explanations

  • Be out of date

Privacy and confidentiality: what not to share with AI

To protect your privacy, avoid typing in:

  • Your full name

  • Date of birth

  • NHS number

  • Home address

  • Phone number

  • Identifiable clinic letters or reports (unless anonymised)

A safer way to write questions

Instead of pasting an entire letter, use a summary like:

“Adult with chronic lung disease, on itraconazole 200 mg daily, recent CT shows cavities, asking about monitoring and side effects.”

That’s usually enough for education and planning questions.

A safe “4-step” way to use AI

  1. Ask AI to explain (terms, tests, general concepts)

  2. Ask AI to help you prepare questions

  3. Discuss those questions with your clinician

  4. Only change treatment after clinical advice

A quick safety checklist

Before trusting an AI answer, ask:

  • Is this general education, or is it telling me what I should do?

  • Does it recommend changing my medicine or dose?

  • Does it mention checking interactions or monitoring?

  • Does it conflict with my current plan?

  • Is this situation urgent?

If any answer worries you: pause and ask your care team.

Example prompts patients can use safely

You can copy/paste these into an AI tool:

  • “Explain Chronic Pulmonary Aspergillosis (CPA) in plain language.”

  • “What questions should I ask about long-term itraconazole treatment?”

  • “What monitoring is commonly recommended for antifungal medicines?”

  • “Can you help me write a one-page symptom and medication summary for my clinic appointment?”

  • “Here is a paragraph from a research paper — can you summarise it in patient-friendly language and list any uncertainties?”

Tip: If you want a more cautious response, add:
“Please be conservative and tell me what you’re unsure about.”

Signs an AI answer may be unreliable

Be cautious if the AI:

  • Sounds very confident but gives no clear reasoning

  • Gives exact doses or taper schedules

  • Claims “this is definitely ABPA/CPA” from limited information

  • Provides references you cannot find elsewhere

  • Dismisses side effects, interactions, or monitoring

  • Encourages you to delay medical care

Final reminder

AI can be a helpful tool for understanding and preparing — but it is not a substitute for a specialist team.

If you are unsure, or something feels wrong, it is always reasonable to contact your clinician, specialist nurse, or GP.

Medical disclaimer

This page is for general information only and is not medical advice. Always follow the guidance of your healthcare team, especially regarding diagnosis, medicines, and urgent symptoms.

by GAtherton

Travelling with Aspergillosis: A Comprehensive Guide to Safe and Stable Travel

This guide is for people living with:

  • Chronic Pulmonary Aspergillosis (CPA)
  • Allergic Bronchopulmonary Aspergillosis (ABPA)
  • Severe asthma (including fungal sensitisation)
  • Bronchiectasis
  • Fibrotic or structurally abnormal lung disease

Most people with stable disease can travel successfully. The goal is not restriction — it is risk reduction through preparation, environmental awareness, and early action if symptoms change.

Contents

1. Understanding Travel Risk in Aspergillosis

Travel risk arises from four domains:

  1. Structural lung vulnerability (cavities, fibrosis, bronchiectasis)
  2. Inflammatory instability (ABPA activity, asthma control)
  3. Environmental exposure (humidity, dust, pollution)
  4. Healthcare accessibility (if deterioration occurs)

Travel is usually safe when disease is stable and exposures are predictable.

2. Coordinating With Your Medical Team

Respiratory Clinic

  • Review recent imaging (particularly in CPA)
  • Assess haemoptysis history
  • Consider fit-to-fly testing if oxygen saturation borderline
  • Discuss standby rescue medication

GP

  • Ensure medication supply exceeds travel duration
  • Provide updated medication summary
  • Support vaccination review
  • Assist with insurance documentation

3. Assessing Stability Before Travel

Delay travel if within 4–6 weeks of:

  • Significant haemoptysis
  • Escalating breathlessness
  • Recent hospital admission
  • New antifungal initiation

Stable inflammatory markers and symptom plateau are reassuring.

4. Choosing a Destination: Environmental Determinants

Key determinants:

  • Humidity: promotes indoor mould growth
  • Flood history: water damage increases fungal load
  • Air pollution: triggers bronchospasm
  • Dust burden: irritates inflamed airways
  • Healthcare infrastructure: safety net if unwell

5. Regional Risk Patterns Explained

Lower Overall Respiratory Stress

  • Scandinavia
  • New Zealand
  • Canada (outside wildfire season)

Cooler climates limit mould growth; strong building codes reduce damp housing.

Moderate Risk

  • Mediterranean Europe

Generally safe when stable; monitor wildfire smoke and heat stress.

Higher Respiratory Stress

  • Tropical monsoon climates
  • Flood-prone regions
  • Highly polluted megacities
  • Dust storm zones

Humidity increases fungal proliferation; particulate pollution worsens airway inflammation.

6. Air Pollution & AQI Monitoring

Air pollution can exacerbate cough, bronchospasm, breathlessness and fatigue in people with chronic lung disease. In some urban environments, pollution may pose a greater day-to-day risk than fungal exposure.

The most widely used measure of air quality is the Air Quality Index (AQI), which combines several pollutants into a single score.

Key Pollutants That Matter in Lung Disease

  • PM2.5 – fine particulate matter small enough to penetrate deep into the lungs
  • PM10 – larger inhalable particles
  • Ozone (O₃) – irritates airways, especially in heat
  • Nitrogen dioxide (NO₂) – associated with traffic pollution

PM2.5 is particularly important in aspergillosis and severe asthma because it can:

  • Trigger airway inflammation
  • Increase mucus production
  • Worsen bronchospasm
  • Reduce exercise tolerance

Reliable Air Quality Monitoring Resources

These sites provide real-time data and forecasts:

  • World Air Quality Index (WAQI)
    https://waqi.info
    Interactive global map with live AQI data for cities worldwide.
  • IQAir (AirVisual)
    https://www.iqair.com
    Detailed pollutant breakdowns, 7-day forecasts and wildfire smoke tracking.
  • UK Daily Air Quality Index (DEFRA)
    https://uk-air.defra.gov.uk
    Official UK monitoring network with health advice bands.

These platforms also offer mobile apps, which are useful for checking conditions while travelling.

How to Interpret AQI in Practical Terms

AQI Category Practical Advice for Lung Conditions
0–50 Good Ideal conditions for outdoor activity
51–100 Moderate Usually safe; monitor symptoms
101–150 Unhealthy for sensitive groups Reduce strenuous outdoor activity; consider indoor plans
151–200 Unhealthy Limit time outdoors; avoid exertion
200+ Very Unhealthy/Hazardous Stay indoors with filtered air if possible

For many patients with CPA, ABPA or severe asthma, an AQI above 100 warrants caution. Above 150, limiting outdoor exposure is advisable.

Wildfire Smoke

Wildfire smoke contains high concentrations of PM2.5 and organic particulates. Even patients who are stable at home may experience:

  • Increased cough
  • Chest tightness
  • Increased sputum production
  • Fatigue

If travelling during wildfire season:

  • Check AQI daily
  • Plan indoor activities when levels are elevated
  • Use air-conditioned or filtered indoor environments
  • Carry rescue inhalers

Urban Pollution vs Rural Dust

Urban areas are more affected by traffic-related pollutants (NO₂, PM2.5), while rural or desert areas may present dust exposure. Both can aggravate inflamed airways.

The risk is cumulative. Short exposure is usually tolerated; prolonged high-level exposure increases the likelihood of symptom flare.

Key principle: checking AQI before and during travel is one of the simplest and most effective risk-reduction steps for people with chronic lung disease.

7. Heat, Humidity & Hydration Physiology

Hot climates place additional physiological stress on people with chronic lung disease.

Why Heat Matters

In warm environments, the body increases sweating and respiratory water loss to regulate temperature. This leads to:

  • Increased insensible fluid loss (fluid lost through breathing and skin)
  • Reduced plasma volume if intake is inadequate
  • Thickening of airway secretions

In bronchiectasis and chronic pulmonary aspergillosis (CPA), mucus clearance is already impaired. Dehydration increases mucus viscosity, making sputum:

  • Harder to expectorate
  • More likely to stagnate in damaged airways
  • Potentially more prone to secondary infection

Patients may notice thicker sputum, increased cough, or chest tightness in hot weather.

Humidity: Helpful or Harmful?

Humidity has mixed effects:

  • Moderate humidity can help prevent airway drying.
  • High humidity can increase environmental mould growth, particularly indoors if ventilation is poor.

In tropical or monsoon climates, poorly ventilated buildings may have higher fungal spore burdens due to damp conditions.

Heat, Fatigue & Breathlessness

Heat increases cardiovascular demand. The heart works harder to dissipate heat, which can:

  • Increase perceived breathlessness
  • Increase fatigue
  • Reduce exercise tolerance

This does not necessarily indicate worsening lung disease — but it can feel similar.

Hydration Strategy

Practical recommendations:

  • Begin hydrating the day before travel
  • Drink fluids regularly rather than waiting for thirst
  • Aim for pale straw-coloured urine
  • Increase intake during flights and hot excursions

Limit:

  • Excess alcohol (diuretic effect)
  • High caffeine intake

Additional Practical Measures

  • Plan outdoor activity early morning or evening
  • Rest during peak heat (midday)
  • Use air-conditioned environments when available
  • Continue airway clearance routines while travelling

Key principle: in chronic lung disease, hydration supports mucus clearance and reduces avoidable exacerbation risk during hot weather.

8. Travel Insurance & Full Medical Disclosure

Travel insurance is not a formality — it is a critical safety net for people with chronic lung disease.

When purchasing insurance, you must declare all pre-existing medical conditions. This typically includes:

  • Chronic Pulmonary Aspergillosis (CPA)
  • Allergic Bronchopulmonary Aspergillosis (ABPA)
  • Severe asthma
  • Bronchiectasis
  • Pulmonary fibrosis
  • Long-term steroid therapy
  • Adrenal insufficiency (if present)
  • Oxygen use (even if only occasional)

Why Full Disclosure Matters

If you fail to declare a relevant condition, the insurer may:

  • Refuse to cover medical treatment abroad
  • Decline repatriation costs
  • Refuse to reimburse cancelled flights or accommodation
  • Invalidate the entire policy

This applies even if the emergency appears unrelated. Insurers may review your full medical history during a claim.

What Insurers Typically Ask

You may be asked:

  • Have you been hospitalised in the past 12 months?
  • Have you had medication changes recently?
  • Have you had haemoptysis?
  • Are you awaiting tests or investigations?
  • Are you on long-term steroids?

Answer these questions carefully and honestly.

Policies and Stability

Some insurers will decline cover if:

  • You have been hospitalised recently
  • You are awaiting investigations
  • Your condition is considered unstable

This is another reason to travel during a period of clinical stability.

European Travel (UK Patients)

If travelling within Europe, ensure you carry:

  • Your GHIC (Global Health Insurance Card)

However, GHIC does not replace travel insurance. It may not cover:

  • Private healthcare
  • Mountain rescue
  • Repatriation to the UK

Practical Tips

  • Purchase insurance as soon as you book travel
  • Keep written confirmation of declared conditions
  • Carry the insurer’s emergency contact number with you
  • Inform the insurer early if you require hospital care abroad

In summary: full disclosure protects you. Insurance is only effective if the insurer understands your medical background from the outset.

9. Medication Planning & Contingency Prescriptions

  • Carry 1–2 weeks extra supply
  • Bring medications in original packaging
  • Carry clinic letter
  • Consider written rescue plan

10. Specific Considerations for Azole Antifungals

Azoles have significant drug–drug interactions.

  • Inform any clinician abroad you are taking an azole
  • Avoid grapefruit
  • Be aware of sun sensitivity (voriconazole)
  • Take itraconazole with food

11. Air Travel: What Actually Happens in the Cabin?

Commercial aircraft cabins are pressurised to simulate an altitude of approximately 6,000–8,000 feet (1,800–2,400 metres).

This means the partial pressure of oxygen is lower than at sea level. For healthy individuals this causes only a small drop in oxygen saturation (typically 3–4%).

Are Most People with Aspergillosis OK to Fly?

Yes — most stable patients fly without difficulty.

People who are:

  • Clinically stable
  • Not oxygen-dependent
  • Without recent haemoptysis
  • With resting oxygen saturations ≥95%

generally tolerate commercial flights well, including medium and long-haul travel.

Many patients report anxiety before their first flight after diagnosis, but in stable disease, significant problems are uncommon.

Who Should Consider Fit-to-Fly Testing?

Assessment may be appropriate if you have:

  • Resting oxygen saturation consistently below 95%
  • Advanced pulmonary fibrosis
  • Extensive cavitation
  • Significant breathlessness at minimal exertion
  • Recent clinical deterioration

The test commonly used is a Hypoxic Challenge Test (HCT), which simulates cabin oxygen conditions to determine whether supplemental oxygen is required during flight.

Where would I have a Hypoxic Challenge Test (HCT)?

In the UK, a Hypoxic Challenge Test is usually arranged through a hospital respiratory physiology department.

You cannot book this test directly. It must be requested by:

  • Your respiratory consultant or clinic, or
  • Occasionally your GP (who would refer you to a hospital service)

The test is typically performed in:

  • A hospital lung function laboratory
  • A respiratory physiology unit
  • A specialist respiratory centre

During the test, you breathe a gas mixture containing a lower oxygen concentration (usually around 15%) to simulate aircraft cabin conditions. Your oxygen saturation is monitored continuously. If levels fall below safe thresholds, in-flight oxygen may be recommended.

Do Most People Need This Test?

No. Many stable patients with normal resting oxygen saturation (typically ≥95%) do not require hypoxic challenge testing.

The test is generally considered if you:

  • Have resting oxygen saturation below 95%
  • Have advanced pulmonary fibrosis
  • Are already using oxygen
  • Have significant exertional desaturation

If you are unsure, ask your respiratory team whether assessment is appropriate for you.

Symptoms During Flight: What Is Normal?

Mild symptoms that can occur in stable patients include:

  • Slight increase in breathlessness on walking the aisle
  • Fatigue
  • Dry cough (often due to low humidity)

These are usually temporary and not dangerous.

Severe symptoms (marked breathlessness at rest, chest pain, dizziness, confusion) are uncommon and require crew notification.

Anxiety vs Physiological Breathlessness

It is very common for people with chronic lung disease to experience heightened awareness of their breathing during flights. The enclosed environment, reduced cabin pressure and awareness of altitude can all increase anxiety.

Anxiety-related breathlessness typically presents as:

  • A sensation of not getting a “satisfying” breath
  • Chest tightness without wheeze
  • Rapid breathing (hyperventilation)
  • Tingling in fingers or lips
  • Light-headedness

Hyperventilation lowers carbon dioxide levels in the blood. This can cause dizziness, tingling and a feeling of air hunger — even when oxygen levels are normal.

Physiological hypoxia (true low oxygen levels) is less common in stable patients who have been assessed as fit to fly. When it occurs, it is more likely in those with advanced fibrosis, low baseline oxygen saturations, or recent instability.

Features more suggestive of physiological compromise include:

  • Persistent breathlessness at rest
  • Worsening cyanosis (bluish lips or fingers)
  • Marked fatigue or confusion
  • Objective low oxygen saturation if measured

For patients who have undergone fit-to-fly assessment and been cleared to travel, significant in-flight hypoxia is uncommon.

Practical Strategies

  • Use slow, paced breathing (e.g. inhale for 4 seconds, exhale for 6 seconds)
  • Focus on extended exhalation to reduce hyperventilation
  • Keep shoulders relaxed and posture upright
  • Avoid repeatedly “checking” your breathing
  • Remind yourself that mild symptoms are common and expected

Understanding the difference between anxiety-related breathlessness and true hypoxia can significantly reduce distress during flight.

Deep Vein Thrombosis (DVT) Risk

Chronic lung disease does not automatically increase DVT risk, but long-haul immobility does.

General advice:

  • Move legs regularly
  • Stay hydrated
  • Avoid excess alcohol

12. Cabin Dryness & Post-Flight Airway Irritation

Cabin humidity is typically 10–20% (normal indoor comfort is 40–60%).

Low humidity can:

  • Dry airway lining
  • Reduce mucociliary clearance
  • Thicken secretions
  • Trigger cough or mild bronchospasm

This is often why people feel they have “caught a cold” the day after flying. In most cases, it is airway irritation rather than infection.

How to Reduce Dryness Effects

  • Hydrate well before and during flight
  • Limit alcohol and caffeine
  • Use isotonic saline nasal spray
  • Continue preventer inhalers
  • Keep rescue inhaler accessible
  • Avoid direct overhead air vents blowing onto your face
  • Consider mask use — masks increase humidity of inhaled air

Symptoms typically settle within 24–48 hours.

When to Seek Advice After Flying

Seek medical advice if you develop:

  • Progressively worsening breathlessness
  • Persistent fever
  • Significant haemoptysis
  • Chest pain

In stable patients, serious in-flight deterioration is uncommon.

12. Cabin Dryness & Post-Flight Irritation

Cabin humidity is 10–20%.

Dry air:

  • Reduces mucociliary clearance
  • Thickens secretions
  • Triggers cough
  • Irritates airways

Hydration and saline sprays reduce symptoms. Post-flight irritation commonly lasts 24–48 hours and does not necessarily indicate infection.

13. Travelling with Oxygen

Confirm airline device approval and battery duration. Plan well in advance.

14. Accommodation Risk Reduction

Request:

  • Hard flooring
  • No damp odour
  • No renovation dust
  • Pet-free rooms

Chains Often Reported as Allergy-Conscious

  • Hyatt
  • Hilton
  • Marriott
  • Scandic
  • Premier Inn

Newer business hotels often have better HVAC filtration.

15. High-Spore & Dust Exposure Environments

  • Compost handling
  • Construction sites
  • Flood-damaged buildings
  • Agricultural dust

Avoid heavy inhalation exposure.

16. Infection Prevention

  • Hand hygiene
  • Avoid close contact with visibly unwell individuals
  • Maintain vaccination schedule

17. Haemoptysis Planning

If you have a history of haemoptysis:

  • Know your previous pattern
  • Carry clinic contact details
  • Seek urgent care if volume increases significantly

18. Red Flag Symptoms

  • Increasing breathlessness
  • New or worsening haemoptysis
  • Persistent fever
  • Severe chest pain

19. Advanced Planning Checklist

  • Travel when stable
  • Plan with GP and respiratory clinic
  • Carry documentation
  • Monitor AQI
  • Hydrate on flights
  • Avoid damp & heavy dust
  • Know red flags

With preparation, most people with stable aspergillosis travel safely and successfully.

by GAtherton