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Background Exposure to mold and solid cooking fuels represents a significant environmental health concern, contributing substantially to indoor air pollution among elderly populations. However, the association between mold exposure, household fuel use, and mental health remains poorly understood. Here we examine individual and joint associations of these exposures on depression, anxiety, and their co-occurrence in older adults. Methods We evaluated 9,243 elderly participants from the eighth survey wave of the Chinese Longitudinal Healthy Longevity Survey (CLHLS) to explore the associations between mold exposure, solid fuel use, and depression, anxiety, and their co-occurrence. Multivariable logistic regression models were employed to quantify these relationships, with adjusted odds ratios (aOR) and 95% confidence intervals (CI) reported. Results The study identified a depression prevalence of 13.61% and an anxiety prevalence of 11.79%. Participants exposed to mold demonstrated significantly higher odds of depression (OR = 2.26, 95% CI = 1.93–2.63), anxiety (OR = 2.11, 95% CI = 1.80–2.48), and their co-occurrence (OR = 2.58, 95% CI = 2.10–3.16), compared to participants without mold exposure. Moreover, the use of solid fuels for cooking, as opposed to clean fuels, was correlated with higher occurrence of depression (OR = 1.27, 95% CI = 1.10–1.47), anxiety (OR = 1.31, 95% CI = 1.12–1.52), and their co-occurrence (OR = 1.36, 95% CI = 1.10–1.67). Notably, solid fuel use appeared to attenuate the association between mold exposure and anxiety (Relative excess risk due to interaction [RERI] = -0.22, 95% CI = -0.44, -0.01). Conclusions The study found that exposure to mold and use of solid fuels may be associated with higher prevalence of depression, anxiety, and their co-occurrence. Further prospective studies are warranted to validate our findings.

Chronic inflammatory response syndrome (CIRS) and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) are debilitating multisystem illnesses that share overlapping symptoms and molecular patterns, including immune dysregulation, mitochondrial impairment, and vascular dysfunction. This review provides a chronological synthesis of biomarker development in CIRS, tracing its evolution from early functional tests such as visual contrast sensitivity (VCS) to advanced transcriptomic profiling. Drawing on peer-reviewed studies spanning two decades, we examine the layered integration of neuroendocrine, immunologic, metabolic, and genomic markers that collectively support a multisystem model of innate immune activation specific to environmentally acquired illness. Particular focus is given to the Gene Expression: Inflammation Explained (GENIE) platform’s use of transcriptomics to classify disease stages and distinguish CIRS from other fatiguing conditions. While ME/CFS research continues to explore overlapping pathophysiologic features, it has yet to establish a unified diagnostic model with validated biomarkers or exposure-linked mechanisms. As a result, many patients labeled with ME/CFS may, in fact, represent unrecognized CIRS cases. This review underscores the importance of structured biomarker timelines in improving differential diagnosis and guiding treatment in complex chronic illness and highlights the reproducibility of the CIRS framework in contrast to the diagnostic ambiguity surrounding ME/CFS.

Occupational mold exposure can lead to Aspergillus-associated allergic diseases including asthma and hypersensitivity pneumonitis. Elevated IL-17 levels or disbalanced T-helper (Th) cell expansion were previously linked to Aspergillus-associated allergic diseases, whereas alterations to the Th cell repertoire in healthy occupationally exposed subjects are scarcely studied. Therefore, we employed functional immunoassays to compare Th cell responses to A. fumigatus antigens in organic farmers, a cohort frequently exposed to environmental molds, and non-occupationally exposed controls. Organic farmers harbored significantly higher A. fumigatus-specific Th-cell frequencies than controls, with comparable expansion of Th1- and Th2-cell frequencies but only slightly elevated Th17-cell frequencies. Accordingly, Aspergillus antigen-induced Th1 and Th2 cytokine levels were strongly elevated, whereas induction of IL-17A was minimal. Additionally, increased levels of some innate immune cell-derived cytokines were found in samples from organic farmers. Antigen-induced cytokine release combined with Aspergillus-specific Th-cell frequencies resulted in high classification accuracy between organic farmers and controls. Aspf22, CatB, and CipC elicited the strongest differences in Th1 and Th2 responses between the two cohorts, suggesting these antigens as potential candidates for future bio-effect monitoring approaches. Overall, we found that occupationally exposed agricultural workers display a largely balanced co-expansion of Th1 and Th2 immunity with only minor changes in Th17 responses.

Die Zusammenhänge zwischen Schimmelpilzexposition, IgE-vermittelter Sensibilisierung, Entzündungsmarkern und Atemwegssymptomen wurden bei 46 exponierten und 23 nicht exponierten Studienteilnehmenden untersucht. Sowohl die Exposition als auch die klinischen Symptome wurden anhand eines Fragebogens bewertet. Spezifisches (s)IgE gegen eine Schimmelpilzmischung (mx1) war signifikant höher und wurde häufiger bei Exponierten (41%) als bei Nicht-Exponierten (17%) gefunden, was für sIgG gegen eine Schimmelpilzmischung (Gmx6) nicht beobachtet wurde. Schimmelpilz-exponierte Asthmatiker waren in dem Studienkollektiv häufiger gegen Schimmelpilze sensibilisiert (55%) als exponierte Nicht-Asthmatiker (18%). Darüber hinaus waren die Serumkonzentrationen des Club Cell Protein 16 (CC16) bei exponierten Asthmatikern deutlich niedriger im Vergleich zu Nicht-Asthmatikern und Nicht-Exponierten. Positive Assoziationen wurden zwischen Schimmelpilzsensibilisierung, Asthma und Schimmelpilzexposition beobachtet, jedoch nicht bei Personen mit Sensibilisierungen gegen Umweltallergene ohne Schimmelpilzsensibilisierung. Spezifisches IgE gegen mx1, aber nicht sIgG gegen Gmx6 ist ein nützlicher diagnostischer Marker, um Schimmelpilze als Ursache für Atemwegssymptome zu verifizieren. Erstpublikation in Allergologie select, mit freundlicher Genehmigung der Autoren: PubMedCentral Allergologie select Zitierung: Kespohl S, Liebers V, Maryska S, Meurer U, Litzenberger C, Merget R, Raulf M. What should be tested in patients with suspected mold exposure? Usefulness of serological markers for the diagnosis. Allergol Select. 2022; 6: 118-132. DOI 10.5414/ALX02298E

Schimmelpilzbefall in Innenräumen kann zu einer Vielzahl von gesundheitlichen Beeinträchtigungen führen, darunter allergische und nichtallergische Atemwegsbeschwerden. Insbesondere wenn die Beschwerden nicht allergisch bedingt sind, fehlen Diagnoseinstrumente, welche die schimmelpilzbedingten Gesundheitsprobleme erklären könnten. Als Proof-of-Concept wurde in der vorliegenden Studie ein Vollblut-Test (VBT) verwendet, um die zelluläre Reaktion durch Messung der Zytokinfreisetzung (IL-1β und IL-8) nach In-vitro-Stimulation zu bestimmen. Von insgesamt 48 Personen standen Blutproben zur Verfügung. Mittels Fragebogen wurden Beschwerden und eine mögliche Schimmelpilzexposition dokumentiert. Die spezifische In-vitro-Zellreaktivität wurde mit E. coli-Endotoxin und Extrakten verschiedener Schimmelpilze (Aspergillus fumigatus, Penicillium chrysogenum, Aspergillus versicolor und Cladosporium herbarum) getestet. Um die schimmelpilzinduzierte Immunantwort mittels VBT zu charakterisieren, verglichen wir die folgenden Gruppen: Asthmatiker versus Nichtasthmatiker, Schimmelpilz-Sensibilisierte versus nicht Schimmelpilz-Sensibilisierte, Schimmelpilz-Exponierte versus nicht Schimmelpilz-Exponierte. Als Reaktion auf die Stimulation mit Endotoxin wurde bei Schimmelpilz-Sensibilisierten eine signifikant höhere IL-1β-Freisetzung festgestellt als bei nicht Sensibilisierten. Darüber hinaus zeigte das Blut von Asthmatikern im Vergleich zu dem von Nichtasthmatikern eine signifikant höhere IL-8- und IL-1β-Freisetzung nach Stimulation mit P. chrysogenum und Endotoxin. Es wurde jedoch kein signifikanter Unterschied in der Höhe der Zytokinfreisetzung zwischen der schimmelpilzexponierten und der nicht exponierten Gruppe beobachtet, weder nach Endotoxin – noch nach Schimmelpilzstimulation. Zusammenfassend lässt sich sagen, dass der in dieser Studie verwendete VBT kein geeignetes Instrument für die klinische Routinediagnostik ist. Unsere Daten deuten darauf hin, dass der VBT krankheitsbedingte zelluläre Unterschiede widerspiegelt, aber nicht die Schimmelpilzexposition anzeigt. In Kombination mit weiteren Daten kann der VBT jedoch ein hilfreiches und interessantes Werkzeug in der Forschung sein, zum Beispiel bei der Beschreibung der komplexen Immunantwort auf Schimmelpilze. Erstpublikation in Allergologie select, mit freundlicher Genehmigung der Autoren: PubMedCentral Allergologie select Zitierung: Liebers V, Kespohl S, Borowitzki G, Stubel H, Raulf M. Is in vitro cytokine release a suitable marker to improve the diagnosis of suspected mold-related respiratory symptoms? A proof-of-concept study. Allergol Select. 2022; 6: 133-141. DOI 10.5414/ALX02299E

Over the past 20 years, exposure to mycotoxin producing mold has been recognized as a significant health risk. Scientific literature has demonstrated mycotoxins as possible causes of human disease in water-damaged buildings (WDB). This study was conducted to determine if selected mycotoxins could be identified in human urine from patients suffering from chronic fatigue syndrome (CFS). Patients (n = 112) with a prior diagnosis of CFS were evaluated for mold exposure and the presence of mycotoxins in their urine. Urine was tested for aflatoxins (AT), ochratoxin A (OTA) and macrocyclic trichothecenes (MT) using Enzyme Linked Immunosorbent Assays (ELISA). Urine specimens from 104 of 112 patients (93%) were positive for at least one mycotoxin (one in the equivocal range). Almost 30% of the cases had more than one mycotoxin present. OTA was the most prevalent mycotoxin detected (83%) with MT as the next most common (44%). Exposure histories indicated current and/or past exposure to WDB in over 90% of cases. Environmental testing was performed in the WDB from a subset of these patients. This testing revealed the presence of potentially mycotoxin producing mold species and mycotoxins in the environment of the WDB. Prior testing in a healthy control population with no history of exposure to a WDB or moldy environment (n = 55) by the same laboratory, utilizing the same methods, revealed no positive cases at the limits of detection.

Background Previous studies have suggested an increased risk of asthma related to indoor dampness problems, but their role in the etiology of Asthma-COPD Overlap Syndrome has not been studied. We utilized a population-based incident case–control study to assess potential effect of indoor dampness and molds at home and at work on development of ACOS. Methods We recruited systematically all new cases of asthma diagnosed during a 2.5-year study period (1997–2000) and randomly selected controls from the source population of adults 21–63 years old and representing 500,000 persons-years in the Pirkanmaa Hospital District, South Finland. Exposure indicators included water damage, damp stains or paint peeling, visible mold, and mold odor, asked separately for home and workplace. The clinically diagnosed case series consisted of 521 adults with newly diagnosed asthma. Altogether 25 of them satisfied the criteria for ACOS-cases, i.e. FEV1/FVC < 0.70 in post-bronchodilator spirometry. The control series, including 932 controls, were from a random sample of source population, after excluding 76 (7.5%) controls with asthma. Results In logistic regression analysis adjusting for confounders, the risk of ACOS was significantly related to presence of mold odor in the workplace (OR 3.43; 95% CI 1.04–11.29), but not to other dampness indicators. The fraction of ACOS attributable to workplace mold odor was 70.8% (95% CI 3.8–91.1%) among the exposed. The risk of ACOS was not related to mold exposures at home. Conclusions Present results provide new evidence of the significant relation between workplace exposure to mold odor and adult-onset ACOS.

The American Academy of Pediatrics recently issued guidelines regarding the potential toxic effect of indoor molds. We now report another case of an infant with pulmonary hemorrhage whose residential environmental assessment revealed the presence of the toxigenic mold Stachybotrys atra. We used a questionnaire to identify environmental factors that could predispose the home to fungal contamination. We collected air samples from multiple locations in the home that we felt would reflect areas of relevant exposure. Surface samples were collected with a piece of transparent tape for semiquantitative measurement of spores present. We classified spores into their respective genera based on shape, size, and color. We also measured mycotoxin levels. Air sampling revealed significantly elevated total spore counts in the patient's bedroom and in the attic. Aspergillus/ Penicillium species were predominant. Stachybotrys spores were found in the air sampled in the patient's bedroom, as well as from surfaces sampled in the patient's closet and the attic ceiling. Additionally, a small patch of Stachybotrys-contaminated area in the closet ceiling was sent for mycotoxin analysis. This material proved to be highly toxigenic. As the link between the presence of Stachybotrys in the home and pulmonary hemorrhage in infants increases, further efforts should be made to educate physicians, health care providers, and new parents about the potential toxic effects of this mold.

Adverse health effects of fungal bioaerosols on occupants of water-damaged homes and other buildings have been reported. Recently, it has been suggested that mold exposure causes neurological injury. The authors investigated neurological antibodies and neu-rophysiological abnormalities in patients exposed to molds at home who developed symptoms of peripheral neuropathy (i.e., numbness, tingling, tremors, and muscle weakness in the extremities). Serum samples were collected and analyzed with the enzyme-linked im-munosorbent assay (ELISA) technique for antibodies to myelin basic protein, myelin-associ-ated glycoprotein, ganglioside GM 1 , sulfatide, myelin oligodendrocyte glycoprotein, α-B-crystallin, chondroitin sulfate, tubulin, and neurofilament. Antibodies to molds and mycotoxins were also determined with ELISA, as reported previously. Neurophysiologic evaluations for latency, amplitude, and velocity were performed on 4 motor nerves (median, ulnar, peroneal, and tibial), and for latency and amplitude on 3 sensory nerves (median, ulnar, and sural). Patients with documented, measured exposure to molds had elevated titers of antibodies (immunoglobulin [I g ]A, I g M, and I g G) to neural-specific antigens. Nerve conduction studies revealed 4 patient groupings: (1) mixed sensory-motor polyneuropathy (n = 55, abnormal), (2) motor neuropathy (n = 17, abnormal), (3) sensory neuropathy (n = 27, abnormal), and (4) those with symptoms but no neurophysiological abnormalities (n = 20, normal controls). All groups showed significantly increased autoantibody titers for all iso-types (I g A, I g M, and I g G) of antibodies to neural antigens when compared with 500 healthy controls. Groups 1 through 3 also exhibited abnormal neurophysiologic findings. The authors concluded that exposure to molds in water-damaged buildings increased the risk for development of neural autoantibodies, peripheral neuropathy, and neurophysiologic abnormalities in exposed individuals.

Home mold exposure is a commonly overlooked cause of hypersensitivity pneumonitis. This is in part due to the limited literature supporting the association as well as the lack of exposure characterization available in reported cases. Notably, climate change, extreme weather patterns and frequent flooding continue to create conditions that promote home mold growth. As remediation has the potential to improve outcomes, clinicians need to remain vigilant in searching for and identifying potential mold exposure in suspected HP patients. The purpose of this study is to describe a large retrospective cohort of patients with home mold associated HP. HP patients were identified retrospectively from our single center interstitial lung disease (ILD) database between 2011-2019. Patients with a moderate, high, or definite confidence diagnosis of HP were included. The presence of residential mold exposure was confirmed by medical chart review by a pulmonologist trained in exposure assessment. Home mold exposure was identified as the culprit antigen in 54 of 231 hypersensitivity pneumonitis patients. An invasive procedure (bronchoalveolar lavage, transbronchial biopsy, and/or surgical lung biopsy) was performed to confirm the diagnosis of HP in 85.7% of the cohort. Home mold was principally caused by chronic and/or recurring water intrusion. The most common locations of mold within the home included the bathroom, bedroom, and air conditioning unit. Transplant free survival was 97.7 months, which did not differ from the 50 HP patients in our cohort with HP associated with a mold exposure outside the home or patients in our cohort with HP associated with avian antigen exposure. Of the 41 patients who removed the exposure, 5 (12.2%) had a > 10% improvement in FVC, including 4 with fibrotic HP. Our study is the largest to report an association between HP and home mold exposure and is the first report from the region of north Texas. As climate change continues to disrupt weather patterns causing storms and flooding in certain areas, clinicians should remain alert to the presence of mold and its potential contribution to development of HP.