•Evidence for urban association across allergic, inflammatory and mental disorders.•Air pollution was environmental driver most frequently associated with disease.•Altered microbial exposure also ...emerged as important environmental driver of disease.•Other urban environmental-risk factors identified as well as key caveats and gaps.
Cities are home to over half the global population; that proportion is expected to rise to 70% by mid-century. The urban environment differs greatly from that in which humans evolved, with potentially important consequences for health. Rates for allergic, inflammatory and auto-immune diseases appear to rise with urbanization and be higher in the more urbanized nations of the world which has led some to suggest that cities promote the occurrence of these diseases. However, there are no syntheses outlining what urban-associated diseases are and what characteristics of cities promote their occurrence.
To synthesize the current understanding of “urban-associated diseases”, and discover the common, potentially modifiable features of cities that may be driving these associations.
We focus on any diseases that have been associated with cities or are particularly prominent in today’s urban societies. We draw on expertise across diverse health fields to examine the evidence for urban connections and drivers.
We found evidence for urban associations across allergic, auto-immune, inflammatory, lifestyle and infectious disease categories. Some conditions (e.g. obesity and diabetes) have complex relationships with cities that have been insufficiently explored. Other conditions (e.g. allergies and asthma) have more evidence demonstrating their relationship with cities and the mechanisms driving that association. Unsurprisingly, air pollution was the characteristic of cities most frequently associated with disease. Other identified urban risk factors are not as widely known: altered microbial exposure and a disconnect from environmental microbiomes, vitamin D deficiency, noise and light pollution, and a transient, over-crowded, impoverished population. However, many complexities and caveats to these relationships beg clarification; we highlight the current knowledge gaps and outline ways to fill those gaps. Identifying urban-associated diseases and their drivers will allow us to prepare for the urban-disease burden of the future and create healthy cities that mitigate that disease burden.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Background and objective
Coal mine dust has a complex and heterogeneous chemical composition. It has been suggested that coal particle chemistry plays a critical role in determining the pathogenesis ...of coal workers' pneumoconiosis (CWP). In this study, we aimed to establish the association between the detrimental cellular response and the chemical composition of coal particles.
Methods
We sourced 19 real‐world coal samples. Samples were crushed prior to use to minimize the impact of particle size on the response and to ensure the particles were respirable. Key chemical components and inorganic compounds were quantified in the coal samples. The cytotoxic, inflammatory and pro‐fibrotic responses in epithelial cells, macrophages and fibroblasts were assessed following 24 h of exposure to coal particles. Principal component analysis (PCA) and stepwise regression were used to determine which chemical components of the coal particles were associated with the cell response.
Results
The cytotoxic, inflammatory and pro‐fibrotic response varied considerably between coal samples. There was a high level of collinearity in the cell responses and between the chemical compounds within the coal samples. PCA identified three factors that explained 75% of the variance in the cell response. Stepwise multiple regression analysis identified K2O (p <0.001) and Fe2O3 (p = 0.011) as significant predictors of cytotoxicity and cytokine production, respectively.
Conclusion
Our data clearly demonstrate that the detrimental cellular effects of exposure to coal mine dusts are highly dependent on particle chemistry. This has implications for understanding the pathogenesis of CWP.
To determine whether chemistry is a key determinant of the lung cell response to coal particles, we examined the correlation between the chemical constituents of 19 coal samples and cellular response. We identified K2O and Fe2O3 as the constituents of the coal associated with the greatest detrimental cell response.
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FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
There has been an increase in the identification of cases of coal workers' pneumoconiosis (CWP) in recent years around the world. While there are a range of possible explanations for this, studies ...have implicated the pyrite content of coal as a key determinant of CWP risk. However, experimental studies to support this link are limited. The aim of this study was to assess the association between the pyrite content, and subsequent release of bioavailable iron, in coal particles and the response of lung cells involved in the pathogenesis of CWP (epithelial cells, macrophages and fibroblasts). Using real-world Australian coal samples, we found no evidence of an association between the pyrite content of the coal and the magnitude of the detrimental cell response. We did find evidence of an increase in IL-8 production by epithelial cells with increasing bioavailable iron (p = 0.01), however, this was not linked to the pyrite content of the coal (p = 0.75) and we did not see any evidence of a positive association in the other cell types. Given the lack of association between the pyrite content of real-world coal particles and lung cell cytotoxicity (epithelial cells and macrophages), inflammatory cytokine production (epithelial cells, macrophages and fibroblasts), and cell proliferation (fibroblasts) our data do not support the use of coal pyrite content as a predictor of CWP risk.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
While the relationship between outdoor particulate matter (PM) and lower respiratory tract infections in children and adolescents is accepted, we know little about the impacts of outdoor PM on the ...risk of developing or aggravating upper respiratory tract infections (URTIs).
We aimed to review the literature examining the relationship between outdoor PM exposure and URTIs in children and adolescents. A systematic search of EMBASE, MEDLINE, PubMed, Scopus, CINAHL and Web of Science databases was undertaken on April 3, 2020 and October 27, 2021. Comparable short-term studies of time-series or case-crossover designs were pooled in meta-analyses using random-effects models, while the remainder of studies were combined in a narrative analysis. Quality, risk of bias and level of evidence for health effects were appraised using a combination of emerging frameworks in environmental health.
Out of 1366 articles identified, 34 were included in the systematic review and 16 of these were included in meta-analyses. Both PM2.5 and PM10 levels were associated with hospital presentations for URTIs (PM2.5: RR = 1.010, 95%CI = 1.007–1.014; PM10: RR = 1.016, 95%CI = 1.011–1.021) in the meta-analyses. Narrative analysis found unequivocally that total suspended particulates were associated with URTIs, but mixed results were found for PM2.5 and PM10 in both younger and older children.
This study found some evidence of associations between PM and URTIs in children and adolescents, the relationship strength increased with PM10. However, the number of studies was limited and heterogeneity was considerable, thus there is a need for further studies, especially studies assessing long-term exposure and comparing sources.
•Outdoor particulate matter could be linked to upper respiratory tract infections.•Larger particles could trigger more upper respiratory infections than smaller ones.•The source of particulate matter could influence the association with infections.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Vitamin D has a range of non-skeletal health effects and has been implicated in the response to respiratory infections. The aim of this study was to assess the effect of vitamin D on the response of ...epithelial cells, neutrophils and macrophages to lipopolysaccharide (LPS) stimulation. BEAS-2B cells (airway epithelial cell line) and primary neutrophils and macrophages isolated from blood samples were cultured and exposed to LPS with and without vitamin D (1,25(OH)
D). The production of IL-6, IL-8, IL-1β and TNF-α of all cells and the phagocytic capacity of neutrophils and macrophages to E. coli were assessed. Vitamin D had no effect on BEAS-2B cells but enhanced the production of IL-8 in neutrophils (p = 0.007) and IL-1β in macrophages (p = 0.007) in response to LPS. Both vitamin D (p = 0.019) and LPS (p < 0.001) reduced the phagocytic capacity of macrophages. These data suggest that the impact of vitamin D on responses to infection are complex and that the net effect will depend on the cells that respond, the key response that is necessary for resolution of infection (cytokine production or phagocytosis) and whether there is pre-existing inflammation.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Engineered stone (ES) is a popular building product, due to its architectural versatility and generally lower cost. However, the fabrication of organic resin-based ES kitchen benchtops from slabs has ...been associated with alarming rates of silicosis among workers. In 2024, fifteen years after the first reported ES-related cases in the world, Australia became the first country to ban the use and importation of ES. A range of interacting factors are relevant for ES-associated silicosis, including ES material composition, characteristics of dust exposure and lung cell-particle response. In turn, these are influenced by consumer demand, work practices, particle size and chemistry, dust control measures, industry regulation and worker-related characteristics. This literature review provides an evidence synthesis using a narrative approach, with the themes of product, exposure and host. Exposure pathways and pathogenesis are explored. Apart from crystalline silica content, consideration is given to non-siliceous ES components such as resins and metals that may modify chemical interactions and disease risk. Preventive effort can be aligned with each theme and associated evidence.
Exposure to geogenic (earth-derived) particulate matter (PM) is linked to an increased prevalence of bronchiectasis and other respiratory infections in Australian Indigenous communities. Experimental ...studies have shown that the concentration of iron in geogenic PM is associated with the magnitude of respiratory health effects, however, the mechanism is unclear. We investigated the effect of geogenic PM and iron oxide on the invasiveness of non-typeable Haemophilus influenzae (NTHi). Peripheral blood mononuclear cell-derived macrophages or epithelial cell lines (A549 & BEAS-2B) were exposed to whole geogenic PM, their primary constituents (haematite, magnetite or silica) or diesel exhaust particles (DEP). The uptake of bacteria was quantified by flow cytometry and whole genome sequencing (WGS) was performed on NTHi strains. Geogenic PM increased the invasiveness of NTHi in bronchial epithelial cells. Of the primary constituents, haematite also increased NTHi invasion with magnetite and silica having significantly less impact. Furthermore, we observed varying levels of invasiveness amongst NTHi isolates. WGS analysis suggested isolates with more genes associated with heme acquisition were more virulent in BEAS-2B cells. The present study suggests that geogenic particles can increase the susceptibility of bronchial epithelial cells to select bacterial pathogens in vitro, a response primarily driven by haematite content in the dust. This demonstrates a potential mechanism linking exposure to iron-laden geogenic PM and high rates of chronic respiratory infections in remote communities in arid environments.
•Geogenic particles are linked to severe respiratory infections in Indigenous Australian communities, but the mechanism is unknown.•Particles containing haematite increased susceptibility of the airway epithelium to invasion by non-typeable Haemophilus influenzae.•Whole genome sequencing identified genes related to heme acquisition that were associated with this response.•This has implications for communities exposed to high levels of iron-laden particles.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
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