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Table of Contents

Whole Allergen

m1 Penicillium chrysogenum

m1 Penicillium chrysogenum Scientific Information

Type:

Whole Allergen

Display Name:

Penicillium chrysogenum

Route of Exposure:

Inhalation

Family:

Trichocomaceae

Species:

Penicillium chrysogenum

Latin Name:

Penicillium chrysogenum

Other Names:

Penicillium notatum

Summary

Penicillium species are outdoor and indoor environmental fungi. P. chrysogenum is one of the most important and well-known Penicillium species due to its use for the production of penicillin. Species belonging to Penicillium genus are ubiquitous soil and airborne fungi; however, the abundance of fungal spores fluctuates depending on rainfall and location. They thrive near organic material or damp building environment but can survive with very little water. P. chrysogenum spores are smooth and spheroidal.  Prevalence of IgE sensitization to Penicillium spp. was found to be 1.5% and 7.3-22% in general population and atopic individuals, respectively. The primary route of exposure to allergens of P. chrysogenum is inhalation, while exposure may occur rarely through ingestion and skin contact. P. chrysogenum can induce respiratory allergic symptoms, such as allergic rhinitis, asthma, and allergic broncho-pulmonary mycosis in sensitized individuals. Penicillium sensitization in children is less frequent than in adults, usually below 10% among asthmatic or atopic subjects. Pen ch 13 and Pen ch 18 (serine and/or vacuolar proteases) are major allergens of P. chrysogenum, but they are not species-specific due to their cross-reactivity with other molds. Of note, there is no cross-reactivity between Penicillium sensitization and drug allergic reactions to β-lactam penicillin, which is a fungal secondary metabolite, synthesized only under specific circumstances.

Allergen

Nature

The genus Penicillium consists of more than 250 ubiquitous filamentous fungi. Some of them are causal agents for allergies and opportunistic infections (1). They are easily recognizable as blue-green molds (2). Penicillium species are both outdoor and indoor environmental fungi; however, they are more predominantly indoor fungi (2, 3). They are employed in the food industry to produce blue mold cheese (2), commercially as enzymes and in the drug industry for the production of compounds against bacteria, fungi or viruses as well as anti-cancer compounds (1). Penicillium chrysogenum (P. chrysogenum) is the most important and well-known species (spp.) due to its use in the production of penicillin (4). Its name reminds of the yellow pigment chrysogine produced during prolonged growth (from chrysos, the Greek word for gold) (5).

Airborne Penicillium spores comprise asexually produced conidia, a major allergenic component of the airborne fungal burden, and ascospores, resulting from sexual reproduction (1, 3).

Habitat

Penicillium genus spp. are soil and airborne fungi, which prefer moderate to cool climate; however, the abundance of fungal spores fluctuates depending on rainfall and location (4, 6, 7). The fungal spore count of airborne Penicillium spp. is usually found to increase with higher temperature and humidity (6, 7). Indoor factors associated with an increase in airborne Penicillium are poor ventilation, higher temperatures, less sunlight, water seepage, and presence of pets (2). The seasonal variability of indoor Penicillium spp. levels is less marked than for other genera because house dust and indoor mold act as reservoirs of spores and allergenic materials (7, 8).

Sources of Penicillium are rotting vegetables and foods, dead plants, and moldy wood (1, 9). Penicillium spp. are usually found near organic material or in humid environments, but some of them can survive with scarce water too (9). Penicillium spp. is a component of human microbiota, and its relative enrichment among fungal communities was reported in bronchial samples from asthmatic patients compared to healthy controls (10). Penicillium spp. has also been detected in healthy human gut, coming from diet or environment as they are unable to grow at 37°C and colonize the gut (11).

Taxonomy

The Penicillium genus belongs to the Ascomycota phylum of fungi, which is characterized by meiotic ascospores and mostly airborne conidia. Penicillium conidiophores appear like a paintbrush, hence the name Penicillium was derived from the Latin for paintbrush, “penicillus”, that also gave the name “pencil”. Penicillium spp. are among the most common airborne fungi causing allergy (9). The genus Penicillium comprises of a large variety of species, with 354 accepted as of 2014 (12). P. chrysogenum is closely related to P. rubens, and both were earlier known collectively as P. notatum (9).

Taxonomic tree of Penicillium chrysogenum  (9)
Domain Eukaryota
Kingdom Fungi
Phylum Ascomycota
Class Eurotiomycetes
Order Eurotiales
Family Trichocomaceae
Genus Penicillium
Species P. chrysogenum


Tissue

P. chrysogenum spores are smooth and spheroidal in shape with a size of 3 μm and cylindrical projections (phialides) of 7 μm diameter. Conidiophore branching pattern is bi, ter, and quarterverticillate, with a cylindrical outermost branch (metulae) of 10 μm size (1).

Epidemiology

Worldwide distribution

Like other airborne molds, Penicillium spp. induce IgG and IgE production in humans (13).  Serum specific IgE and SPT can be used to demonstrate Penicillium sensitization, but the agreement between the two methods is low, varying from 29% to 44% as a function of the fungal extract and the study population (14, 15). In mold-sensitized subjects, sensitization to Penicillium spp. is associated with sensitization to other molds, mainly Alternaria spp. and Aspergillus spp. (16, 17).

A review of data from 1980-2000 reported that the prevalence of IgE sensitization to Penicillium spp. in general population was 1.5%, and 7.3% to 22% in atopic individuals (18). Current sensitization rates to Penicillium range from 5 to 8% in general population and atopic patients (19) and are much higher, usually up to 29%, in asthmatic patients (14, 19). Accordingly, a 2016 study on 160 Japanese asthmatic adults found a 21.9% (35/160) prevalence of P. chrysogenum sensitization (20), while 27% (7/26) of Canadian adult patients with allergic rhinitis (AR) or asthma had positive SPT to at least one species of Penicillium, mainly P. chrysogenum (21). A higher prevalence was recently reported in a Chinese study of asthmatic patients sensitized to Aspergillus fumigatus (A. fumigatus), 80% of whom exhibited P. chrysogenum co-sensitization (22). The prevalence of P. chrysogenum sensitization was also higher in a targeted population of patients with suspected mold allergy: 41% in asthmatic patients, and 23% in non-asthmatic ones (14, 19).

A gender bias has been reported in some studies, with fungus, including P. chrysogenum, sensitization apparently more prevalent in male than in female subjects (20, 23). This difference was related to asthma severity, which might be a confounding factor. Conversely, other studies did not find gender-related differences in fungal sensitization (24).

Studies addressing age-related variations of P. chrysogenum sensitization showed that a maximum was reached at 6-8 years, followed by a decrease during adulthood and a subsequent increase in elderly (23-25).

The use of molecular allergens instead of crude extracts for serum specific IgE testing is increasing (19). IgE immunoblot reactivity to Pen ch 13, a major allergen from P. chrysogenum, was found in 17% (35/212) of asthmatic patients (age 3 to 94 years) from Taipei (Taiwan). The prevalence of IgE reactivity to Pen ch 13 increased with age, from 7% in patients ≤10 years to 42% in >70 years, confirming sensitization to airborne Penicillium species is a common finding in older asthmatic patients (25).

Penicillium sensitization is associated with increased prevalence of upper and lower respiratory symptoms including poorer asthma control, and with severe asthma with fungal sensitization (SAFS) (1, 19, 20) . 

Pediatric issues

Penicillium spp. is considered a causative agent of asthma and AR in children according to the American Institute of Medicine (26).

A cross-sectional study by Nolles et al. (2001) addressing sensitization to fungi among 137 atopic (asthma, AR, or eczema) children from the Netherlands, aged 5 months to 14 years, found a 7.3% prevalence for specific IgE to Penicillium (24). A similar figure of 12.8% was obtained with SPT with P. notatum among 7565 mold-sensitized Mexican children aged 2-18, addressed for asthma, AR, or atopic dermatitis (AD) (27). Other pediatric studies reported higher figures for the prevalence of sensitization to P. chrysogenum, e.g. 7% among 100 Brazilian asthmatic children aged 4 to 14 years assessed with serum specific IgE in 2007 (28). 

Environmental Characteristics

Living environment

In allergology, Aspergillus spp. and Penicillium spp. are the main indoor allergenic fungi (2, 17). Penicillium spp. are more frequent in indoors as compared to outdoor air, although they are found in large number in the soil (2, 3, 7). The prevalence of detectable airborne Penicillium spp. in homes is found to be at least 1 colony forming unit (CFU)/m3 , which is up to 41% (8).

Worldwide distribution

Penicillium species shows geographical variation. P. citrinum was the most common Penicillium species found in Taipei (Taiwan), while five other species P. chrysogenum, P. spinulosum, P. oxalicum, and P. brevicompactum were commonly found in Topeka, Kansas (USA) (29).

A Nigerian study detected Penicillium and Aspergillus to be the most frequently occurring airborne fungal species in five different locations in Lagos State, Nigeria. They were found to be most abundant during the wet season in all locations (6). Another study in urban, suburban and forest areas of Nanchang, China reported a relatively higher abundance of allergenic fungal communities of Penicillium along with Alternaria, and showed the effect of air quality of the three areas (30).  

The amount of airborne Penicillium spp. is subjected to variations resulting from global climate changes and new domestic environmental practices. Flooding causes damp indoor spaces, leading to increased levels of airborne Penicillium, even after apparent damage remediation (31). Similarly, a study conducted in Colorado, United States (US), showed that Penicillium was among the most abundant fungi in flooded homes (32).  On the contrary, airborne dust in Kuwait conveyed minimal, stable levels of Penicillium (1.15%) (33). The possible effect of green walls and roofs has been reported as beneficial for both outdoor and indoor airborne fungal communities (31, 34). 

Route of Exposure

Main

The primary route of exposure to P. chrysogenum allergens is inhalation (35). 

Secondary

P. chrysogenum can induce allergic reaction through ingestion (35) or direct contact (cheilitis) (36).

Clinical Relevance

Penicillium genus is one of the most important fungal allergenic sources, associated mainly with upper and lower respiratory allergy including asthma, AR, allergic fungal sinusitis, and allergic broncho-pulmonary mycosis. It is also responsible for opportunistic infections, onychomycosis, keratomycosis, and non-allergic, non-invasive, fungal sinusitis (1, 33). Beside sensitization, allergy and opportunistic infections, Penicillium spp. release volatile organic compounds (VOCs) and mycotoxins, which can pose health threats through inhalation or ingestion, e.g., ingested mycotoxins from fermented cheese (37). VOCs are responsible of the moldy odor, which can be perceived in presence of growing Penicillium (38). Data on exposure to Penicillium spp., especially in indoor environments, are best interpreted in the context of multiple microbial communities. Indeed, fungal and microbial load and diversity may mitigate immune responses, especially during early life (39).

Allergic rhinitis

Penicillium spp. are reported to induce AR (18).

A study by Kołodziejczyk et al. (2016) addressed the clinical presentation and natural course of AR in outpatients from Poland. Patients (n= 229) sensitized only to molds were compared to patient’s mono- or polysensitized to other airborne allergens. Among the 239 mold-allergic patients, only 14 (5.9%) were sensitized (SPT or specific IgE) to P. chrysogenum, a far lower prevalence than A. fumigatus or Cladosporium herbarum. The study concluded that in mold allergic patients AR is milder, but with significant predisposition for bronchial asthma (40). 

Asthma

Exposure to Penicillium spp. is a risk factor for asthma at all stages of its natural history inluding development, persistence, and severity, both in adults and in children (3, 41)

A prospective birth cohort study was conducted with 880 infants at high risk for developing asthma (defined as at least one older sibling with physician-diagnosed asthma) from Connecticut and western Massachusetts, USA. In this study, higher indoor concentrations of Penicillium spp. were linked with an increased rate of wheeze [RR =2.46; 95% Confidence Interval (CI) 1.63-3.70] and persistent cough (RR= 1.84; 95% CI 1.22-2.80) during the first year of life, after adjustment for potential confounding factors such as  seasonal and housing characteristics, maternal asthma, and socio-economic status (2, 8). The same research group confirmed these findings in a cohort of 1233 asthmatic children (age 5-10 years): exposure and sensitization to any indoor airborne Penicillium species conveyed a higher risk of wheeze [Odds ratio (OR) 2.12, 95% CI 1.12-4.04], persistent cough (OR 2.01, 96% CI 1.05-3.85), and elevated asthma severity score (OR 1.99, 95% CI 1.06-3.72) in comparison to those who were not sensitized or exposed to Penicillium species (42).

The association between indoor mold growth and wheezing episodes in children was also found in a Finnish pediatric cohort study (3). In adult asthmatic patients, multiple reports found that Penicillium sensitization was associated with poor asthma control or higher severity score for asthma (20, 43). According to a cross sectional study by Woolnough et al. (2017) a significant correlation was observed between IgE sensitization to filamentous fungi and lung damage in asthma patients (44).  

Similarly, a meta-analysis of 33 epidemiologic studies observed that adverse respiratory outcomes were increased by 30-50% in houses with damp indoor environment and mold growth (45). Current researches from the US, Europe, and World Health Organization (WHO) indicated damp indoor environment to be an important factor in inducing asthma (3).

At the pathophysiological level, Penicillium allergens exert both IgE-dependent and IgE-independent actions with synergistic effects. The alkaline serine proteases of Penicillium group 13 allergens (e.g., Pen ch 13) disrupt interepithelial tight junctions through direct action on occludin and induce bronchial epithelial cells to release proinflammatory cytokines (46, 47). IgE-mediated effects include histamine degranulation, which can be demonstrated in vitro through basophil activation triggered by Pen ch 13 (47).

Atopic Dermatitis

P. chrysogenum was commonly found in homes from Canada, which may be responsible for upper or lower respiratory tract infection and also skin reactions in allergic individuals (21). Among patients from Taiwan (n= 133, 1-67 years) with fungal sensitization, Penicillium sensitization was found in 74.6 % (44/59) patients with isolated AD and in 71% (22/31) of those diagnosed with both AD and respiratory disease (asthma or AR), at higher levels than in patients with isolated asthma or AR (41%, 18/43) (48). 

Other diseases

A study evaluating fungi in sick building syndrome among 48 schools in the US found Penicillium spp. in 5.2% of samples, with P. chrysogenum as the predominant species (49).

Penicillium spp. has been linked to the development of hypersensitivity pneumonitis, often in the context of occupational allergies in highly diverse fields: wind instrument players, food industry workers, foresters, mushroom producers  (50, 51).

Other topics

Penicillium spp. are also reported to produce several mycotoxins such as ochratoxin, citrinin, cyclopiazonic acid, mycophenolic acid, rubratoxin B, and patulin. These mycotoxins, especially ochratoxin and citrinin, can cause acute lesions and further can develop into cancer (52). P. chrysogenum is reported to cause black esophagus, endophthalmitis, and keratitis (35). 

Molecular Aspects

Allergenic molecules

Fungi contain numerous and varied antigens (3). As of 25th January, 2021, six allergenic molecules have been identified, characterized and published officially by World Health Organization/International Union of Immunological Studies (WHO/IUIS) Allergen Nomenclature Sub-Committee for P. chrysogenum. The table below provides detailed information on each of the allergenic protein (2, 4, 53):

Allergens Molecular Weight (kDa) Biochemical name Allergenicity
Pen ch 13 34 Alkaline serine protease
  • Major allergen (2)
  • Among sera of 70 asthmatic patients, 17 (25%) showed IgE binding on immunoblots for P. chrysogenum (P. notatum) (29).
  • Thirty-five (17%) of 212 sera of asthmatic patients showed IgE binding on immunoblots (25)
  • Pen ch 13 showed 47% sequence identity with Pen ch 18 (41)
Pen ch 18 32 Vacuolar serine protease
  • Major allergen (2)
  • Of 17 sera of asthmatic patients sensitized to P. chrysogenum (P. notatum). 14 (82%) showed IgE binding on immunoblots (29)
  • Among 13 sera of asthmatic patients, 10 (77%) showed IgE binding on immunoblots (41)
Pen ch 20 68 N-acetylglucosaminidase
  • Minor allergen
Pen ch 31   Calreticulin
  • Minor allergen
Pen ch 33 16  
  • Minor allergen
Pen ch 35 36.5 Transaldolase
  • Minor allergen

Cross-reactivity

P. chrysogenum protein (33 kDa) was found to be cross reactive with P. brevicompactum’s 33 kDa protein (47). Serine proteases are thought to be the major pan-fungal allergen group found in most of the airborne fungal species (41, 47). Cross reactivity among serine protease allergens from the species such as P. oxalicum, P. chrysogenum, P. citrinum, P. brevicompactum, A. fumigatus, A. flavus, A. oryzae, R. mucilaginosa, and C. cladosporioides is reported. Serine protease Pen ch 13 and Pen ch 18 identified in P. chrysogenum are reported to be the most cross-reactive proteins (47).

Further, studies have demonstrated cross-reactivity between Pen ch 13 (P. chrysogenum) and Pen c 13 (a major allergen of P. citrinum) with Asp f 13 (A. fumigatus) and Asp fl 13 (A. flavus) in a dose-related manner (46, 47). This IgE cross reactivity among the serine proteases of different fungal species indicated that atopic patients primarily sensitized by either of these prevalent fungal species may develop allergic symptoms by exposure to other environmental fungi (47). Pen ch 13 and Pen ch 18 are homologous to Asp f 13 and Asp f 18 with considerable sequence similarity (2). Pen ch 18 has shown about 63-83% homology with other allergens of the same class (vacuolar serine protease) of A. fumigatus, Saccharomyces cerevisiae, and P. oxalicum (41). 

Compiled By

Author: Turacoz Healthcare Solutions

Reviewer: Dr. Christian Fischer

 

Last reviewed: February 2021

References
  1. Abastabar M, Mirhendi H, Hedayati MT, Shokohi T, Rezaei-Matehkolaei A, Mohammadi R, et al. Genetic and Morphological Diversity of the Genus Penicillium From Mazandaran and Tehran Provinces, Iran. Jundishapur J Microbiol. 2016;9(1):e28280.
  2. Fukutomi Y, Taniguchi M. Sensitization to fungal allergens: Resolved and unresolved issues. Allergol Int. 2015;64(4):321-31.
  3. Knutsen AP, Bush RK, Demain JG, Denning DW, Dixit A, Fairs A, et al. Fungi and allergic lower respiratory tract diseases. J Allergy Clin Immunol. 2012;129(2):280-91; quiz 92-3.
  4. Chang C, Leung PSC, Todi S, Zadoorian L. Definition of Allergens: Inhalants, Food, and Insects Allergens.  Allergy and Asthma2019. p. 1-58.
  5. Lagashetti AC, Dufosse L, Singh SK, Singh PN. Fungal Pigments and Their Prospects in Different Industries. Microorganisms. 2019;7(12).
  6. Odebode A, Adekunle A, Stajich J, Adeonipekun P. Airborne fungi spores distribution in various locations in Lagos, Nigeria. Environ Monit Assess. 2020;192(2):87.
  7. Bush RK, Portnoy JM. The role and abatement of fungal allergens in allergic diseases. J Allergy Clin Immunol. 2001;107(3 Suppl):S430-40.
  8. Gent JF, Ren P, Belanger K, Triche E, Bracken MB, Holford TR, et al. Levels of household mold associated with respiratory symptoms in the first year of life in a cohort at risk for asthma. Environ Health Perspect. 2002;110(12):A781-6.
  9. Levetin E, Horner WE, Scott JA, Environmental Allergens W. Taxonomy of Allergenic Fungi. J Allergy Clin Immunol Pract. 2016;4(3):375-85 e1.
  10. Sharma A, Laxman B, Naureckas ET, Hogarth DK, Sperling AI, Solway J, et al. Associations between fungal and bacterial microbiota of airways and asthma endotypes. J Allergy Clin Immunol. 2019;144(5):1214-27.e7.
  11. Hallen-Adams HE, Suhr MJ. Fungi in the healthy human gastrointestinal tract. Virulence. 2017;8(3):352-8.
  12. Visagie CM, Houbraken J, Frisvad JC, Hong SB, Klaassen CH, Perrone G, et al. Identification and nomenclature of the genus Penicillium. Stud Mycol. 2014;78:343-71.
  13. Raulf M, Joest M, Sander I, Hoffmeyer F, Nowak D, Ochmann U, et al. Update of reference values for IgG antibodies against typical antigens of hypersensitivity pneumonitis. Allergo Journal International. 2019;28(6):192-203.
  14. O'Driscoll BR, Powell G, Chew F, Niven RM, Miles JF, Vyas A, et al. Comparison of skin prick tests with specific serum immunoglobulin E in the diagnosis of fungal sensitization in patients with severe asthma. Clin Exp Allergy. 2009;39(11):1677-83.
  15. Kespohl S, Maryska S, Bunger J, Hagemeyer O, Jakob T, Joest M, et al. How to diagnose mould allergy? Comparison of skin prick tests with specific IgE results. Clin Exp Allergy. 2016;46(7):981-91.
  16. Mari A, Schneider P, Wally V, Breitenbach M, Simon-Nobbe B. Sensitization to fungi: epidemiology, comparative skin tests, and IgE reactivity of fungal extracts. Clin Exp Allergy. 2003;33(10):1429-38.
  17. Larenas-Linnemann D, Baxi S, Phipatanakul W, Portnoy JM, Environmental Allergens W. Clinical Evaluation and Management of Patients with Suspected Fungus Sensitivity. J Allergy Clin Immunol Pract. 2016;4(3):405-14.
  18. Simon-Nobbe B, Denk U, Poll V, Rid R, Breitenbach M. The spectrum of fungal allergy. Int Arch Allergy Immunol. 2008;145(1):58-86.
  19. Kespohl S, Raulf M. Mold Sensitization in Asthmatic and Non-asthmatic Subjects Diagnosed with Extract-Based Versus Component-Based Allergens. Adv Exp Med Biol. 2019;1153:79-89.
  20. Tanaka A, Fujiwara A, Uchida Y, Yamaguchi M, Ohta S, Homma T, et al. Evaluation of the association between sensitization to common inhalant fungi and poor asthma control. Ann Allergy Asthma Immunol. 2016;117(2):163-8.e1.
  21. Tarlo SM, Fradkin A, Tobin RS. Skin testing with extracts of fungal species derived from the homes of allergy clinic patients in Toronto, Canada. Clin Allergy. 1988;18(1):45-52.
  22. Luo W, Hu H, Wu Z, Wei N, Huang H, Zheng P, et al. Molecular allergen sensitization of Aspergillus fumigatus between allergic bronchopulmonary aspergillosis and A fumigatus‐sensitized asthma in Guangzhou, Southern China. Journal of Clinical Laboratory Analysis. 2020;34(10):e23448.
  23. Ezeamuzie CI, Al-Ali S, Khan M, Hijazi Z, Dowaisan A, Thomson MS, et al. IgE-mediated sensitization to mould allergens among patients with allergic respiratory diseases in a desert environment. Int Arch Allergy Immunol. 2000;121(4):300-7.
  24. Nolles G, Hoekstra MO, Schouten JP, Gerritsen J, Kauffman HF. Prevalence of immunoglobulin E for fungi in atopic children. Clin Exp Allergy. 2001;31(10):1564-70.
  25. Chou H, Chang CY, Tsai JJ, Tang RB, Lee SS, Wang SR, et al. The prevalence of IgE antibody reactivity against the alkaline serine protease major allergen of Penicillium chrysogenum increases with the age of asthmatic patients. Ann Allergy Asthma Immunol. 2003;90(2):248-53.
  26. Reboux G, Rocchi S, Vacheyrou M, Millon L. Identifying indoor air Penicillium species: a challenge for allergic patients. J Med Microbiol. 2019;68(5):812-21.
  27. Fernandez-Soto R, Navarrete-Rodriguez EM, Del-Rio-Navarro BE, Sienra-Monge JJL, Meneses-Sanchez NA, Saucedo-Ramirez OJ. Fungal Allergy: Pattern of sensitization over the past 11 years. Allergol Immunopathol (Madr). 2018;46(6):557-64.
  28. de Barros Bezerra GF, Haidar DM, da Silva MA, Filho WE, Dos Santos RM, Rosa IG, et al. IgE serum concentration against airborne fungi in children with respiratory allergies. Allergy Asthma Clin Immunol. 2016;12:18.
  29. Shen HD, Lin WL, Tam MF, Wang SR, Tzean SS, Huang MH, et al. Characterization of allergens from Penicillium oxalicum and P. notatum by immunoblotting and N-terminal amino acid sequence analysis. Clin Exp Allergy. 1999;29(5):642-51.
  30. Pan Y, Luo L, Xiao H, Zhu R, Xiao H. Spatial variability of inhalable fungal communities in airborne PM2.5 across Nanchang, China. Sci Total Environ. 2020;746:141171.
  31. Vardoulakis S, Dimitroulopoulou C, Thornes J, Lai KM, Taylor J, Myers I, et al. Impact of climate change on the domestic indoor environment and associated health risks in the UK. Environ Int. 2015;85:299-313.
  32. Emerson JB, Keady PB, Brewer TE, Clements N, Morgan EE, Awerbuch J, et al. Impacts of flood damage on airborne bacteria and fungi in homes after the 2013 Colorado Front Range flood. Environ Sci Technol. 2015;49(5):2675-84.
  33. Al Salameen F, Habibi N, Uddin S, Al Mataqi K, Kumar V, Al Doaij B, et al. Spatio-temporal variations in bacterial and fungal community associated with dust aerosol in Kuwait. PLoS One. 2020;15(11):e0241283.
  34. Pyrri I, Zoma A, Barmparesos N, Assimakopoulos MN, Assimakopoulos VD, Kapsanaki-Gotsi E. Impact of a green roof system on indoor fungal aerosol in a primary school in Greece. Sci Total Environ. 2020;719:137447.
  35. Egbuta MA, Mwanza M, Babalola OO. Health Risks Associated with Exposure to Filamentous Fungi. Int J Environ Res Public Health. 2017;14(7).
  36. Jaqueti P, García MI, Campanón-Toro MV, Sobrino M, Gallardo A, Dávila I. Cheilitis Associated With Sensitization to Penicillium notatum in a Clarinetist. J Investig Allergol Clin Immunol. 2020;30(4):292-3.
  37. Anelli P, Haidukowski M, Epifani F, Cimmarusti MT, Moretti A, Logrieco A, et al. Fungal mycobiota and mycotoxin risk for traditional artisan Italian cave cheese. Food Microbiol. 2019;78:62-72.
  38. Inamdar AA, Morath S, Bennett JW. Fungal Volatile Organic Compounds: More Than Just a Funky Smell? Annu Rev Microbiol. 2020;74:101-16.
  39. Karvonen AM, Hyvärinen A, Rintala H, Korppi M, Täubel M, Doekes G, et al. Quantity and diversity of environmental microbial exposure and development of asthma: a birth cohort study. Allergy. 2014;69(8):1092-101.
  40. Kołodziejczyk K, Bozek A. Clinical Distinctness of Allergic Rhinitis in Patients with Allergy to Molds. BioMed research international. 2016;2016:3171594-.
  41. Shen HD, Chou H, Tam MF, Chang CY, Lai HY, Wang SR. Molecular and immunological characterization of Pen ch 18, the vacuolar serine protease major allergen of Penicillium chrysogenum. Allergy. 2003;58(10):993-1002.
  42. Gent JF, Kezik JM, Hill ME, Tsai E, Li DW, Leaderer BP. Household mold and dust allergens: exposure, sensitization and childhood asthma morbidity. Environ Res. 2012;118:86-93.
  43. Masaki K, Fukunaga K, Matsusaka M, Kabata H, Tanosaki T, Mochimaru T, et al. Characteristics of severe asthma with fungal sensitization. Ann Allergy Asthma Immunol. 2017;119(3):253-7.
  44. Woolnough KF, Richardson M, Newby C, Craner M, Bourne M, Monteiro W, et al. The relationship between biomarkers of fungal allergy and lung damage in asthma. Clin Exp Allergy. 2017;47(1):48-56.
  45. Fisk WJ, Lei-Gomez Q, Mendell MJ. Meta-analyses of the associations of respiratory health effects with dampness and mold in homes. Indoor Air. 2007;17(4):284-96.
  46. Caraballo L, Valenta R, Puerta L, Pomés A, Zakzuk J, Fernandez-Caldas E, et al. The allergenic activity and clinical impact of individual IgE-antibody binding molecules from indoor allergen sources. World Allergy Organ J. 2020;13(5):100118.
  47. Shen HD, Tam MF, Tang RB, Chou H. Aspergillus and Penicillium allergens: focus on proteases. Curr Allergy Asthma Rep. 2007;7(5):351-6.
  48. Chang FY, Lee JH, Yang YH, Yu HH, Wang LC, Lin YT, et al. Analysis of the serum levels of fungi-specific immunoglobulin E in patients with allergic diseases. Int Arch Allergy Immunol. 2011;154(1):49-56.
  49. Cooley JD, Wong WC, Jumper CA, Straus DC. Correlation between the prevalence of certain fungi and sick building syndrome. Occupational and environmental medicine. 1998;55(9):579-84.
  50. Soumagne T, Reboux G, Metzger F, Roussel S, Lefebvre A, Penven E, et al. Fungal contamination of wind instruments: Immunological and clinical consequences for musicians. Sci Total Environ. 2019;646:727-34.
  51. Greenberger PA. Mold-induced hypersensitivity pneumonitis. Allergy Asthma Proc. 2004;25(4):219-23.
  52. Koteswara Rao V, Girisham S, Madhusudhan Reddy S. Prevalence of toxigenic Penicillium species associated with poultry house in Telangana, India. Arch Environ Occup Health. 2016;71(6):353-61.
  53. WHO/IUIS. "Allergen-Penicillium chrysogenum"  Retrieved from http://www.allergen.org/search.php?allergenname=&allergensource=Penicillium+chrysogenum&TaxSource=&TaxOrder=&foodallerg=all&bioname=. Last date of access 25th January 2021 2019