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There has been a long-standing debate about the mechanisms of dry air sensation in indoor environments. We performed a dormitory-based study at Tianjin University, China from November, 2020 to January, 2021, involving 1558 students living in 516 dorm rooms across 4 buildings. Based on questionnaire-reported symptoms, we selected 67 case and 57 control dorm rooms for environmental monitoring, namely, measuring air temperature, humidity, carbon dioxide concentration, and concentrations of volatile organic compounds (VOCs). Our analysis revealed significant VOC-dryness associations (p < 0.05). We found the following to be risk factors: indoor ozone oxidation product (6-methyl-5-hexen-2-one [6-MHO, adjusted odds ratio, AOR: 2.15, 95% confidence interval, 95% CI: 1.18–3.94]) and personal care product emissions (octamethylcyclotetrasiloxane [D4, AOR: 1.51, 95% CI: 1.00–2.28] and dodecamethylcyclohexasiloxane [D6, AOR: 1.84, 95% CI: 1.29–2.63]). While absolute humidity showed no direct association with dry air sensation, it significantly modified VOC effects. Our findings indicate that indoor chemical exposure influences occupants’ dry air sensations.

Indoor dampness and mould exposure are associated with respiratory health, but there is limited evidence on long-term effects in adults. Indoor dampness and mould, and the onset of respiratory symptoms, asthma, and rhinitis, were studied in the Respiratory Health in Northern Europe (RHINE) cohort, in which 8407 adults participated in both the 20-year and 30-year follow-up (RHINE III and IV, respectively). Participants completed a questionnaire on indoor dampness and mould at home and at the workplace, and on respiratory health. In RHINE IV, the prevalence of dampness or mould exposure in the past 10 years was 28.6%, while 15.1% of participants reported a 20-year cumulative exposure. Home exposure of dampness or mould was linked to increased onset of nocturnal chest tightness (OR = 1.80), nocturnal breathlessness (OR = 1.76), productive cough (OR = 1.41), and allergic rhinitis (OR = 1.27) and work exposure of dampness or mould with increased onset of wheeze (OR = 1.58), nocturnal chest tightness (OR = 1.53), doctor-diagnosed asthma (OR = 1.68), and rhinitis (OR = 1.35). Combined home and work exposure showed stronger associations for nocturnal chest tightness (OR = 1.99), doctor-diagnosed asthma (OR = 1.90), and rhinitis (OR = 2.24). Cumulative 20-year exposure accentuated the association with respiratory symptoms. Long-term exposure to dampness or mould at home or at work increased the risk of developing respiratory symptoms, asthma, and rhinitis. Combined exposure at home and work, and a prolonged exposure period, may play a significant role in the development of adverse respiratory outcomes in adults.

Childhood allergic rhinitis (AR) is associated with ozone (O3) exposure, yet the sensitive exposure window (SEW) remains unclear. This multicenter survey of 38,176 children aged 3–6 years across 7 Chinese cities (2019–2020) estimated satellite-based individual maximum daily 8 h average O3 exposure. The SEW and its exposure–response (E–R) relationship were assessed. Doctor-diagnosed AR prevalence was 11.9%. Average O3 exposure from prenatal to AR onset ranged from 67.5 to 76.7 μg/m3. The critical SEW was identified as infancy, specifically 30–38 weeks postnatal (7.5–9.5 months). Per interquartile range (IQR) (10.1 μg/m3) increase in O3, the adjusted odds ratio was 1.29 (95% CI: 1.22–1.36), independent of PM2.5. The E–R relationship was nonlinear, J-shaped, and threshold-free. The SEW effect was stronger in southern cities and mitigated by ≥6 months of exclusive breastfeeding. In conclusion, O3 significantly increases AR risk, with 7.5–9.5 months postnatal being a critical SEW, especially in exclusive breastfeeding <6 months and southern regions

Parabens, a prevalent class of endocrine-disrupting chemicals (EDCs), are ubiquitous in consumer products; however, their role in linking pediatric allergic phenotypes remains poorly understood. This case-control study analyzed paraben levels in urine and indoor dust as proxies for internal and external exposures and investigated their associations with allergic rhinitis only (AR Only), asthma only (AS Only), and comorbidities (AR&AS) among children in Shanghai. The concentrations for each of four paraben compounds were quantitatively measured, and multi-pollutant frameworks—including Bayesian Kernel Machine Regression (BKMR) and Weighted Quantile Sum (WQS) regression—were employed to characterize the mixture exposure and risk. Propylparaben (PrP) was detectable in 100% of urine samples and over 90% of dust samples, and the concentrations ranked the highest out of the four compounds in both samples. Benzylparaben (BzP) was detected in >70% of urine samples and over 50% of dust samples at relatively lower levels. Urinary PrP exhibited significantly positive associations with all phenotypes (OR in 2.18–2.92) and BzP with the AR&AS Comorbidity (OR = 3.55, 95% CI: 1.32–9.55). Dust-borne PrP was associated with AR Only (OR = 2.26, 95% CI: 1.16–4.43), indicating a potential “Portal of Entry” effect via direct nasal deposition. According to BKMR and WQS analyses, urinary PrP and BzP emerged as two primary risk drivers. Using interaction analysis, an additive synergistic effect was observed between urinary PrP and BzP with parental history of allergy, suggesting heightened vulnerability to paraben exposure in genetically predisposed subgroups. In conclusion, children with respiratory allergies were associated with higher exposure to PrP and BzP and exhibited higher susceptibility in those with a parental history of allergy.

Background and objective: Indoor microbial exposures influence respiratory health, yet how men and women respond differently to airborne bacterial communities remains unclear. This study aimed to assess sex-specific associations between indoor airborne bacteria, and lung function, and airway inflammation in adults.

Methods: Airborne dust was collected from the bedrooms of 1038 adults (463 men, 575 women) across five Nordic cities as part of the European Community Respiratory Health Survey (ECRHS) III. Bacterial communities were profiled using 16S rRNA amplicon sequencing. Bacterial and endotoxin loads were quantified via quantitative PCR (qPCR) and the Limulus amebocyte lysate (LAL) assay, respectively. Multivariable linear regression models stratified by sex were used to examine associations with lung function and airway inflammation.

Results: Greater indoor bacterial diversity was associated with higher lung function in men (FEV1 (β= 0.17, 95% CI: 0.05 to 0.29, P = 0.003) and higher FeNO levels in women ((β= 2.44, 95% CI: 0.73 to 4.15, P = 0.005). Endotoxin load was positively associated with FeNO in women ((β= 0.37, 95% CI: 0.05 to 0.70, P = 0.02), but not in men. Genera from Actinobacteriota and Bacilli were associated with higher lung function, while Clostridia was linked to lower lung function and reduced FeNO. In contrast, several genera from Actinobacteriota and Gammaproteobacteria were positively associated with FeNO.

Conclusions: Indoor bacterial exposures were associated with respiratory health in a sex-specific pattern. These findings highlight the importance of microbial composition in shaping adult lung health and underscore the need for sex-specific approaches in future epidemiological research.

Background: While short-term occupational exposures to many agents are associated with increased risk of asthma, the long-term consequences of exposure have not been well understood. We investigated the effects of occupational exposures over two decades on the incidence of asthma.

Methods: This population-based, multicentre cohort was assessed at baseline (European Community Respiratory Health Survey (ECRHS)1) and followed up twice over 20 years (ECRHS2 and ECRHS3). This analysis included data for 5591 participants with complete work histories and free of asthma at baseline. Incident adult-onset asthma was defined as either an asthma attack, woken by an attack of shortness of breath and/or current asthma medication in the last 12 months before each timepoint, without asthma at a previous survey. An updated asthma-specific job exposure matrix was used to estimate exposures to asthmagens. Adjusted Poisson models were fitted with generalised estimating equations to estimate asthma incidence.

Results: Ever high exposure to high molecular weight sensitisers (rate ratio (RR)=1.31; 95% CI 1.15 to 1.63), irritants (RR=1.29; 1.09-1.54), biocides (RR=1.42; 1.12-1.79), only low exposure to low molecular weight sensitisers (RR=1.26; 1.08-1.47), mites (RR=1.48; 1.12-1.94) and reactive chemicals (RR=1.24; 1.06-1.45) were associated with increased incidence of asthma. Asthma incidence also increased with ever high or cumulative exposure to these exposures and for specific exposure to wood dust, cleaning agents and bleach. The population-attributable fraction for adult-onset asthma due to occupational exposures was 18% (16.9-19.4%).

Conclusion: This strengthens the evidence that occupational exposures to sensitisers and chemical irritants contribute substantial risk and a substantive attributable fraction of adult-onset asthma. Control of implicated hazardous exposures and periodic screening of exposed workers should be considered.

Ambient ozone (O₃) links to childhood allergic rhinitis (AR), but the nasal microbiome’s role remains unclear. We did a case-control study in Shanghai (176 AR children, 114 controls). AR children had higher 12-month O₃ (OR=1.21, 95 %CI:1.11–1.29 per 10 μg/m³) and reduced nasal microbial α-diversity (P < 0.05). Co-occurrence network analysis showed the nasal microbial community in AR children had reduced connectivity and lost keystone taxa compared to controls. O₃ was negatively correlated with α-diversity (P < 0.05) which indices mediated annual (9.15 %, 95 %CI:3.17–18.45 %) and warm-season (14.21 %, 95 %CI:5.27–27.84 %) O₃-AR links; predicted microbial functional pathways in particular steroid hormone biosynthesis (8.77 % for annual O₃, 18.49 % for warm-season O₃) and limonene/pinene degradation (7.46 % for warm-season O₃) (P < 0.05) mediated the O₃-AR link too. Our findings highlighted the nasal microbiome’s potential role in mediating the link between O₃ exposure and childhood AR. This fills gaps in the mechanism on ambient O₃ and childhood AR in perspective of the mediation by nasal microbiome and its functional pathways and offers actionable insights for O₃ - targeted environmental management and precise pediatric health protection.

Background: The indoor microbiome significantly impacts human health. Different sampling methods are used to characterize this environment, but it is unclear how these methods affect the resulting microbial profiles and health-related interpretations. This study aimed to compare the bacterial communities captured by two common methods, i.e., passive collection of settled air dust and active vacuuming of surface dust, and to evaluate how sampling choice influences epidemiological associations with respiratory health.

Methods: We collected paired settled air dust (n = 86) and vacuumed surface dust (n = 83) samples from 87 university dormitory rooms. The bacterial composition was characterized by sequencing the V3-V4 region of the 16S rRNA gene. We analyzed differences in bacterial diversity, taxonomic composition, predicted functional profiles, and associations with self-reported student health data (rhinitis, asthma, and respiratory infections).

Results: The two sampling methods captured drastically different bacterial communities (PERMANOVA R² = 0.65, p < 0.001). Vacuumed dust samples were dominated by the genus Pseudomonas (75.1% mean relative abundance), whereas air dust samples were more diverse and primarily composed of Ralstonia (15.6%), Pelomonas (11.3%), and Anoxybacillus (9.3%). Air dust samples exhibited significantly higher alpha diversity (observed taxa: 906.2 ± 179.6) compared to vacuumed dust (345.1 ± 82.3, p < 0.001). These compositional differences led to distinct predicted functional pathways and divergent associations with health outcomes. For asthma, airborne Collinsella was associated with strongly increased odds (OR 2.17, p = 0.003), while Paracoccus was associated with decreased odds (OR 0.062, p = 0.006). By contrast, associations in vacuumed dust were limited to taxa with small effect sizes, such as Peptoclostridium (OR 1.07, p = 0.004). Furthermore, while airborne genera like Slackia were associated with respiratory infections (OR 5.94, p = 0.005), no significant bacterial associations for respiratory infections were found in vacuumed dust.

Conclusion: The choice between sampling settled air dust versus vacuumed surface dust provides profoundly different views of the indoor bacteriome, which can lead to contradictory conclusions in epidemiological studies of asthma and respiratory illness. Our findings underscore that the selection of an environmental sampling strategy is a critical methodological decision that can dictate the outcome and potential health implications of indoor microbiome research. Researchers must align their sampling method with a clear exposure hypothesis to ensure valid health risk assessments. Future indoor air quality standards and epidemiological studies should consider implementing multi-method sampling to capture a comprehensive profile of microbial exposure.

BACKGROUND: The role of the indoor microbiome in sick building syndrome (SBS) is well-recognized, yet prior studies have been limited to single-center analyses, limiting a broader understanding and applicability of their findings.

METHODS: We conducted a multicenter indoor microbiome and metabolome investigation for SBS, involving 1139 middle school students across three regions in Malaysia (Johor Bahru, Terengganu, and Penang). Using high-throughput amplicon sequencing and untargeted LC-MS, indoor microbiome and metabolites were characterized from classroom dust samples.

RESULTS: The study found that the prevalence of SBS symptoms was high across all three centers (51.0% to 54.6%). Environmental characteristics, including indoor NO₂ and CO₂ concentrations and total weight of indoor dust, were positively associated with SBS (p < 0.01, linear regression). Curtobacterium in Terengganu was negatively associated with SBS, and Clostridium perfringens in Johor Bahru was positively associated with SBS (p < 0.01, FDR < 0.05). Whereas all identified fungal taxa, including an uncharacterized uc_f_Auriculariaceae_sp., Duportella kuehneroides, and Wallemia mellicola, were positively associated with SBS (p < 0.01, FDR < 0.05) in Johor Bahru and Terengganu. Mediation analysis revealed that the adverse health effects of NO₂ on SBS were partially mediated by the increased abundance of uc_f_Auriculariaceae_sp. (p < 0.05, total effect mediated 51.40%). Additionally, potential protective metabolites (S-adenosylmethionine, N-acetylserotonin, sphinganine, 4-hydroxy-2-quinolone, and (2E,4Z,8E)-Colneleic acid) were mainly derived from environmental microorganisms, conferring protective effects against nasal symptoms and tiredness. In contrast, synthetic chemicals were associated with higher SBS symptoms, inducing eye and nasal symptoms.

CONCLUSIONS: This study emphasizes both the significance of fostering a balanced indoor microbiome/metabolite and the necessity to reduce exposure to deleterious substances, providing new insights for future targeted intervention strategies.

Higher air temperature and increased ambient ozone (O₃) concentration have been associated with childhood rhinitis risk. However, the potential mediating role of elevated O₃ in the increased childhood rhinitis risk due to higher air temperature exposure has not been examined. This large-scale cross-sectional study included 40,103 preschool children from 7 Chinese capital cities. Information on ever-rhinitis, current-rhinitis, and doctor-diagnosed allergic rhinitis (AR) was collected using a standardized questionnaire. Average air temperature (TEMavg) and O₃ concentration in the whole year, warm season, and cold season were estimated at 1 km spatial resolution. The findings revealed that exposure to higher air temperature (annual TEMavg, warm season TEMavg, and cold season TEMavg) and ambient O₃ (annual O₃, and warm season O₃) were associated with an elevated risk of ever-rhinitis, current-rhinitis, and doctor-diagnosed AR. Moreover, elevated O₃ concentration played important mediation effects on the relationships between higher air temperature and childhood rhinitis risk, with the mediated proportions ranging from 19.92% to 35.14% for the whole year, 18.62% to 32.82% for the warm season, and 3.85% to 13.32% for the cold season. Our study highlighted that controlling O₃ pollution may be an effective approach to mitigate the increasing childhood rhinitis risk due to global warming.