1. Introduction
The primary natural sources of inhalant allergens that cause respiratory allergy disorders including asthma and allergic rhinitis (AR) are pollens and fungal spores [
1,
2]. It is thought that there is a higher chance of developing rhinitis when pollen and fungus spores are exposed together outside [
3,
4]. The most prevalent pollen allergy in the world, grass-induced pollinosis affects about 95% of people with sensitivities in Europe [
5]. Approximately 3–10% of people globally are thought to have fungal allergies [
1]. Seasonal overlap may be the reason of the exacerbated symptoms, especially in light of the continuing climate changes, since the majority of patients with inhalant allergies are co-sensitized to several pollen and spore allergens [
1,
3]. Environmental risk factors, such as the length and level of exposure to the allergen, air pollution, and those resulting from the effects of climate change, can affect how severe the allergic reaction is [
2].
Notably, the seasonal co-occurrence of pollen and fungal spores, exacerbated by air pollution and climate change, not only increases the overall exposure burden but also amplifies clinical symptoms in already susceptible individuals [
4,
6,
7]. People who have this overlapping exposure often develop IgE reactions to several seemingly unrelated allergens, a condition known as co-sensitization. The existence of panallergens, which are highly conserved protein families shared by several biological sources and induce IgE cross-reactivity, is a major factor in this phenomenon [
1,
8]. They also add to the complexity of allergic disease [
5,
9]. Pollens are dominated by profilins and polcalcins, two of the most clinically significant panallergens. All eukaryotic cells, including those of trees, grasses, and weeds, include profilins, which are actin-binding proteins that can cause cross-reactive allergic reactions with pollen species as well as with foods derived from plants [
10,
11]. Broad cross-reactivity within pollen families is also linked to polcalcins, calcium-binding proteins that are frequently present in grass pollens [
9]. Mannitol dehydrogenases and enolases, which are important enzymes in glycolysis, are known to be significant cross-reactive allergens in fungus, and they play a part in both food-related and respiratory allergy reactions. [
12,
13]. Because they can cause polysensitization, which makes it more difficult to diagnose and treat allergy illnesses, these panallergens are extremely important from a medical point of view.
Despite increasing recognition that patients are frequently co-exposed to pollen and fungal spores, recent evidence addressing their combined clinical impact remains fragmented. Most existing reviews evaluate these aeroallergens separately, overlook region-specific or meteorologically driven co-occurrence and do not reflect the rapid shifts in exposure patterns driven by contemporary climate variability. No recent systematic review has synthesized their combined clinical effects in the context of accelerated climatic change, nor clarified whether pollen–fungal co-exposure represents a simple temporal coincidence or a clinically meaningful phenomenon with potential synergistic effects. Consequently, clinicians and public health authorities lack consolidated, up-to-date information on the magnitude of risk associated with true co-exposure. This review addresses this gap by integrating contemporary aerobiological, epidemiological, and climatic data.
In addition to clinical studies, we also considered environmental and aerobiological analyses to contextualize exposure patterns and seasonal overlap dynamics, although these were not used to derive clinical outcomes.
This systematic review synthesizes recent evidence (2020–2025) on the impact of co-exposure to pollen and fungal spores on allergic respiratory diseases, with particular emphasis on asthma and allergic rhinitis. By integrating epidemiological, environmental, and aerobiological data, the review examines how simultaneous exposure to these major bioaerosols contributes to the worsening of allergic symptoms, increased hospitalization risk, and seasonal variability in disease burden. The analysis further explores the cumulative and synergistic interactions between pollen and fungal allergens, highlighting their modulation by climatic fluctuations and environmental change.
2. Materials and Methods
2.1. Eligibility Criteria
This review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We conducted a systematic search in PubMed and Google Scholar from 1 January 2020 to 31 August 2025. PubMed was selected because it indexes the core medical and clinical literature on asthma and allergic rhinitis, while Google Scholar was included to ensure broad retrieval of aerobiology and environmental exposure studies that are often not indexed in Medline or EMBASE. The time interval 2020–2025 was chosen deliberately because the last five years reflect accelerated climatic changes that have substantially altered pollen and fungal spore dynamics, including earlier onset, longer seasons, and greater overlap. Older studies do not accurately capture these contemporary exposure patterns and were therefore excluded. Boolean operators were used to combine relevant terms, including pollen, fungi, asthma, and allergic rhinitis. The search syntax was as follows: “pollen” AND “fungi” AND “allergic” (“asthma” OR “rhinitis”). In PubMed, the following Boolean string was applied: (“pollen”[MeSH] OR “pollen”[tiab]) AND (“fungi”[MeSH] OR “fungal spores”[tiab] OR “mold”[tiab]) AND (“asthma” OR “allergic rhinitis” OR “respiratory allergy”). In Google Scholar, an adapted version (“pollen” AND “fungi” AND “asthma” OR “rhinitis” AND “co-exposure”) was used, with screening of the first 200 results sorted by relevance. Searches were restricted to articles in English. Protocol registration was not undertaken (e.g., PROSPERO), which constitutes a methodological limitation acknowledged in the Discussion.
Recent aerobiological evidence shows that pollen–fungi overlap patterns have shifted significantly since 2020 due to rising temperatures and altered precipitation cycles, supporting the need for a contemporary time window [
14,
15]. Given the narrow focus of our inclusion criteria—requiring explicit assessment of simultaneous exposure to pollen and fungal spores linked to clinical outcomes—additional databases were unlikely to yield further eligible studies. This was confirmed by the high initial retrieval (n = 320) and very small number of studies ultimately meeting co-exposure criteria.
Title and abstract screening were performed independently by two reviewers (A.I. and T.N.V.). Full-text evaluation and data extraction were also conducted independently. Any discrepancies in study selection or data extraction were resolved through discussion and consensus. This dual-review approach minimized selection bias and strengthened methodological rigor.
Eligible studies were human research articles published between 2020 and 2025 that investigated asthma and/or allergic rhinitis in relation to simultaneous airborne exposure to pollen and fungal spores. Only studies that quantified co-exposure within the same day or over a short lag period (up to 48 h), using aerobiological or environmental monitoring methods, were included. We focused on observational clinical designs—such as cohort, time-series, and case-crossover studies—and on aerobiological analyses that incorporated clinical outcomes. Studies examining only pollen or only fungal spores, laboratory or in vitro mechanistic work, animal studies, and articles that lacked extractable exposure or outcome data were excluded. Publications in languages other than English were also excluded. Narrative and climatological reviews were used solely to contextualize exposure patterns and climatic trends but did not contribute primary clinical outcome data to the synthesis.
The database search yielded 320 records, of which 280 remained after removing duplicates. Following title and abstract screening, 220 articles were excluded because they did not report pollen–fungi co-exposure. Sixty full texts were assessed for eligibility, and 48 were excluded due to absence of co-exposure quantification or missing clinical endpoints. Twelve studies met all criteria and were included in the qualitative synthesis. The study selection process is illustrated in
Figure 1 (PRISMA flow diagram).
Narrative and climatological reviews were included only to contextualize exposure dynamics and climatic trends; they did not contribute primary clinical outcome data nor influence effect interpretation. Mechanistic studies were excluded because they do not quantify real-world co-exposure or clinical endpoints.
Narrative reviews, systematic reviews, and climatological or aerobiological analyses were intentionally included only to contextualize exposure dynamics and seasonal overlap, and were not treated as original research studies, nor used to derive clinical associations or effect estimates.
2.2. Quality Assessments
Quality assessment of the included observational studies was performed using the Newcastle–Ottawa Scale (NOS) (
Table 1), which evaluates three domains: selection, comparability, and outcome. Each study could receive a maximum of nine points, with scores ≥ 7 indicating high methodological quality. Narrative reviews, climatological analyses, and mechanistic papers were not subjected to NOS scoring, as they did not contribute primary clinical data to the synthesis.
For each included study we extracted: literature data (author, year, region), study design, study population, type of exposure (pollen, fungi, associated pollution, climatic factors), clinical outcomes (severity of symptoms, emergency department visits, hospitalizations, mortality), and reported statistical values (RR, OR, 95% CI, p).
Using the AMSTAR-2 tool, systematic reviews were assessed with emphasis on critical domains including data synthesis, risk-of-bias evaluation, and protocol registration.
3. Results
3.1. Co-Exposure to Pollen and Fungal Spores
The included studies, conducted across a wide range of geographic regions—including Europe (Denmark, Poland, multicenter EU cohorts), Asia (China, South Korea), Africa (South Africa), and North America (Canada)—demonstrate the relevance of pollen–fungi co-exposure in diverse climatic and clinical settings. Across these studies, the most frequently investigated pollen taxa were grasses (Poaceae), birch (Betula), alder (Alnus), and weed species such as Ambrosia, while Alternaria and Cladosporium were the predominant fungal genera assessed. Exposure was quantified mainly through Hirst-type volumetric spore traps, complemented by environmental monitoring stations aligned with meteorological data and, in some cases, health–environment linkage databases. Clinical outcomes encompassed daily or seasonal symptom scores, emergency department visits, asthma exacerbations, hospital admissions, and evaluations of lagged effects following peak exposures. Several studies examining the temporal overlap between taxa found that the highest respiratory morbidity occurred when peak pollen and fungal concentrations coincided within the same 24–72 h window, with three time-series analyses identifying significant 1–2-day lagged increases in asthma exacerbations—particularly associated with elevated Alternaria during periods of high concurrent pollen levels. Together, these findings support the presence of synergistic rather than independent allergenic effects.
Simultaneous exposure to multiple allergens, especially pollen and fungi, significantly intensifies allergic rhinitis symptoms and asthmatic exacerbations. While pollen and fungi have been studied independently, recent studies show that their exposure together has a cumulative and sometimes mutually enhancing effect, increasing respiratory inflammation and the risk of hospitalization.
According to data from multicenter European cohorts (Kazadzis et al., 2025; Olsen et al., 2023) [
4,
6], a 42% increase was observed in asthma ER visits during June–July when grass pollen and Cladosporium spores were co-exposed (RR = 1.42; 95% CI: 1.18–1.71;
p < 0.001). Similarly, in temperate and hemiboreal zones, Alternaria spores exhibited temporal overlap with pollen from birch (Betula) and alder (Alnus), which corresponded with increased hospitalization rates among sensitized individuals [
4,
8]. In China, polysensitized patients had a 1.8-fold increased risk of developing moderate-severe allergic rhinitis (
p < 0.05) during periods of co-exposure, according to a national consensus based on multicenter epidemiologic data. This supports the idea of a cumulative effect of multiple exposure. This effect was more evident in patients living in urban areas where there is more air pollution [
16]. Approximately 2500 school children in Korea were simultaneously exposed to pollen and fungal spores; there was a 27% increase in emergency department visits for asthma (
p = 0.02) As a result, the risk was much higher in the late summer and early fall months, when Ambrosia and Cladosporium levels overlapped [
7].
Across studies, inconsistencies emerged regarding thresholds for defining “high” exposure, co-exposure windows, and lag structures. Some European studies demonstrated strong synergistic effects, while others reported only additive or weak associations. Differences in meteorology, aerobiological methods, and pollution levels likely account for these discrepancies. This variability underscores the need for standardized co-exposure metrics and highlights that the strength of interaction is context-dependent rather than universal.
3.2. Cumulative Effect
Mahmoud (2024) demonstrated in a pediatric cohort in Africa that concurrent exposure to pollen and fungi doubled the risk of asthmatic exacerbations in atopic children from agricultural areas (OR = 2.31; 95% CI 1.12–4.73;
p = 0.01) and prolonged hospitalization by 1.4 days compared to children exposed to a single allergen [
7]. A study of 1200 adult patients with allergic rhinitis in Canada found that those who were exposed to pollen, fungi, and pollution at the same time had mean symptom scores that were 1.5 points higher on a 10-point scale (
p < 0.05) than those who were exposed to only one of the factors. This finding points to a complicated relationship between pollutants and allergens that directly affects how symptoms are experienced by patients [
13]. In a study in Europe, Kim et al. found that pollen-fungi overlap was associated with a 56% increased risk of hospitalization for asthma exacerbations (RR = 1.56; 95% CI 1.10–2.21;
p = 0.004). These data highlight the idea that it is not only the amount of allergen that matters, but also the overlap and accumulation of different exposures [
15]. Furthermore, Alternaria exposure increases epithelial barrier permeability and triggers IL-33-driven Th2 inflammation, according to Hughes et al. (2022) [
1], which suggests that cross-reactive or synergistic pathways may be responsible for the observed clinical severity. Thus, the increased morbidity in polysensitized patients may be explained by the cumulative immunological stimulation from several aeroallergens, which may intensify airway inflammation [
1].
Age-specific analyses revealed that children and adolescents experienced the strongest clinical impact of co-exposure. The studies from South Korea, Europe and South Africa consistently reported higher effect sizes among younger age groups, likely reflecting smaller airway caliber, higher outdoor exposure time, and heightened immunologic reactivity. Similarly, outcomes varied across studies: co-exposure was consistently associated with worsening symptom scores in patients with allergic rhinitis, whereas asthma-related outcomes (exacerbations, emergency visits, hospitalizations) demonstrated the most pronounced increases. Several studies also indicated stronger effects in urban settings, where elevated particulate matter (PM2.5) and ozone levels appear to amplify allergenic responses to combined pollen–fungal exposure.
3.3. The Role of Climatic and Environmental Factors
Many recent studies have confirmed the role of climatic and environmental factors in aggravation of allergic symptoms by co-exposure to pollens and fungi. Longitudinal climate analyses show that allergen bioaerosol dynamics are significantly modified by global warming and seasonal thermal variability. This makes exposure seasons overlapping and longer.
Myszkowska et al. (2023) [
3] found a strong association between the yearly temperature amplitude and the number of days with high levels of grass or birch pollen and Alternaria and Cladosporium spores (R
2 = 0.30;
p = 0.0318). The most frequent overlaps were between grass and Cladosporium (June–July) and between birch and Alternaria (May–June), indicating that weather has a direct impact on the duration and intensity of allergy co-occurrence. These data support that climate change prolongs cumulative exposure and increases the risk of severe allergy exacerbations [
3]. On hot and windy days, pollen concentrations increase by up to 35% and fungal spores double. In addition, rainfall stimulates fungal growth and reduces pollen levels, changing exposure patterns according to Burbank, 2025 [
15]. Ziska (2020) analyzed climate data and found that the co-exposure season increased by 20–30 days per year, while symptom severity increased by 15–30 percent [
17]. These findings are supported by Paudel et al. (2021), which showed that simultaneous exposure to pollen and fungi has increased by 20–30 percent in recent decades, further elevating the risk of asthmatic exacerbations [
18]. In a systematic review, Domingo et al. (2024) found that simultaneous exposure to pollutants, pollens and fungi increased the risk of asthmatic exacerbations in children by 20 to 40 percent (
p < 0.01) [
19]. Higher levels of fine particulate matter had a greater effect (PM
2.5) [
19]. Hughes et al. described extreme asthma events in thunderstorms. They examined the phenomenon of asthma in thunderstorms and presented the case of Melbourne in 2016, where a thunderstorm caused an acute asthma outbreak that resulted in over 3000 emergency department patients and 10 deaths [
1].
Among the 12 included publications, original observational studies constituted the clinical evidence base, while review and environmental analyses were retained solely for contextual interpretation and are clearly identified as such in
Table 2.
All observational studies scored between 7 and 9 points on the Newcastle–Ottawa Scale, indicating overall high methodological quality across the included clinical evidence.
Environmental and review articles were included for context but did not contribute primary clinical outcome data.
4. Discussion
According to recent data, the respiratory system is affected by the simultaneous exposure to several aeroallergens in a way that is both additive and synergistic. Individuals who are allergic to both pollen and fungal spores typically exhibit more severe clinical symptoms than those who are just exposed to one allergen. Long-term mucosal irritation, overlapping inflammatory pathways, and increased immune activation resulting from simultaneous exposure to multiple allergens, contribute to the cumulative effect. The burden of allergic inflammation is increased by this combined exposure, which raises the incidence of hospitalizations, ER visits, and asthma exacerbations.
In our view, the evidence strongly suggests that the interaction of multiple allergenic triggers induces effects on the respiratory system that are amplified rather than merely additive. Burte et al. (2017) and Siroux et al. (2018) reported that polysensitization is tightly associated with asthma–rhinitis multimorbidity, implying that this immunologic profile represents a distinct disease endotype rather than a continuum of monosensitization [
20,
21].
Our findings align with these observations: when multiple allergenic sources—such as pollen and fungal spores—interact simultaneously, the impact on respiratory function and symptom burden becomes synergistically amplified. This raises the question, also emphasized by Bousquet et al. (2015; 2023) in the MeDALL and ARIA frameworks, of whether polysensitized patients should be recognized as a separate clinical category within future allergy management guidelines [
22,
23]. Stratifying patients by sensitization patterns, as suggested by Patchett et al. (2023), could enhance prognostic precision and support personalized therapeutic strategies, including allergen immunotherapy selection and multimorbidity risk assessment [
24]. However, as noted by Bousquet et al. (2023), current international guidelines do not uniformly acknowledge polysensitization as an independent category, underlining the need for further clinical validation and standardized integration into allergy practice [
23].
From a pathophysiological perspective, the synergistic effect of pollen–fungi co-exposure likely arises from convergent mechanisms involving epithelial barrier disruption, oxidative stress, and amplified type-2 inflammation. Fungal proteases and pollen-derived NADPH oxidases increase epithelial permeability and promote the release of alarmins such as IL-33 and TSLP, activating downstream eosinophilic and mast-cell pathways, as described by Hughes et al., 2022 [
1] and Xu et al., 2025 [
8]. In parallel, air pollutants such as ozone and NO
2 induce protein nitration, enhancing the allergenicity of both pollen and fungal antigens, while particulate matter generates oxidative stress that further compromises epithelial integrity. Notably, fungal genera differ in their pathogenic potential: Alternaria produces potent serine proteases that.
Age-specific differences have also emerged as an important factor. Studies by Oh (2022) and Kim et al. (2025) [
14,
16] reported a stronger association between co-exposure and asthma exacerbations in children and adolescents, likely due to smaller airway caliber, higher outdoor activity, and the developmental immaturity of immune and epithelial responses. These findings highlight the need for pediatric-focused preventive strategies during overlap periods of high aeroallergen activity.
The influence of climatic variability and environmental change appears to play a crucial modulatory role. Rising global temperatures, altered precipitation patterns, and increased CO
2 levels have extended the flowering and sporulation seasons by up to 20–30 days annually, intensifying the duration and frequency of pollen–fungi co-occurrence (Ziska, 2020; Burbank, 2025; Myszkowska et al., 2023) [
3,
15,
17]. This climatic synchronization contributes to longer cumulative exposure windows and may partly explain the growing incidence of severe allergic exacerbations observed in recent decades.
Importantly, several observed associations may partly reflect co-seasonality, shared meteorological drivers, or unmeasured confounders. Elevated PM2.5 and ozone frequently coincided with peak pollen and fungal days and may potentiate airway inflammation through oxidative and nitrosative stress. Socioeconomic factors, including access to healthcare and urban vs. rural residence, also contributed to variability in clinical outcomes across regions. While synergistic effects are strongly suggested, distinguishing biological interaction from parallel exposure trends remains a key research priority.
Environmental, aerobiological, climatological, and review articles included in
Table 2 were used exclusively to contextualize exposure dynamics, bioaerosol behavior, and climatic overlap patterns. These publications did not generate primary data, did not represent original observational research, and were not incorporated into the synthesis or interpretation of asthma or allergic rhinitis outcomes.
A quantitative meta-analysis was not feasible due to profound heterogeneity across studies, including differences in the pollen and fungal taxa assessed, exposure thresholds, measurement techniques, lag structures, clinical endpoints, and statistical models. Pooling effect estimates under these conditions would introduce substantial bias.
5. Limitations and Future Directions
This review has several limitations. The included studies showed methodological heterogeneity, particularly in the quantification of aeroallergens and definitions of co-exposure, which may affect comparability. Most were observational and region-specific, limiting causal inference and generalizability. Furthermore, standardized thresholds for simultaneous pollen–fungi exposure and integrated meteorological data remain lacking.
Future research should focus on developing unified co-exposure indices, conducting prospective multicenter studies, and integrating aerobiological, climatic, and clinical datasets to establish predictive models for allergic exacerbations under changing environmental conditions.
In addition, most included studies were observational, which limits causal inference. Heterogeneity in exposure definitions, co-exposure thresholds, and outcome measurement further restricts comparability across regions. Future research should harmonize exposure metrics, clinical endpoints, and lag analyses to enable robust pooled estimates and mechanistic interpretation.
6. Conclusions
This review provides an updated synthesis of recent evidence (2020–2025) specifically examining pollen–fungal co-exposure. By integrating aerobiological, climatic, and clinical data, our findings suggest patterns of interaction that may contribute to increased respiratory morbidity and that have been less emphasized in earlier literature. The findings indicate that co-exposure to pollen and fungi may enhance airway inflammation and worsen symptoms in asthma and allergic rhinitis, although the magnitude of this effect varies across studies. While these observations point toward a possible synergistic influence, current evidence remains insufficient to define pollen–fungi co-exposure as a distinct clinical entity, and further standardized research is needed to clarify its pathophysiological and clinical relevance. Nonetheless, awareness of this dual exposure during overlap seasons and high-risk meteorological conditions may help guide preventive approaches. Integrating bioaerosol monitoring and incorporating co-exposure alerts into early-warning systems could support timely public health responses, particularly for children and urban populations.
For clinicians, increased vigilance is warranted during documented pollen–fungi overlap days, particularly among children, adolescents, and highly polysensitized patients. Preventive treatment adjustment—such as early initiation or temporary intensification of inhaled corticosteroids or antihistamines—may help reduce exacerbation risk. For public health authorities, integrating pollen and fungal spore monitoring into early-warning systems and issuing co-exposure alerts could enhance preventive behavior and reduce acute respiratory events.
Author Contributions
Conceptualization, A.-M.I.; Methodology, A.-M.I.; Data Curation, A.-M.I. and T.N.-V.; Writing—Original Draft Preparation, A.-M.I., T.N.-V. and M.G.; Writing—Review and Editing, A.-M.I., O.C.M. and C.U.; Supervision, C.U. All authors have read and agreed to the published version of the manuscript.
Funding
This research received no external funding.
Institutional Review Board Statement
Not applicable.
Informed Consent Statement
Not applicable. This systematic review did not include any individual participant data.
Data Availability Statement
No new data were created or analyzed in this study. Data sharing is not applicable to this article.
Conflicts of Interest
The authors declare no conflicts of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.
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