Atmospheric particulate matter (PM) is one of the most dangerous air pollutants of anthropogenic origin; it consists of a heterogeneous mixture of inorganic and organic components, including transition metals and polycyclic aromatic hydrocarbons. Although previous studies have focused on the effects of exposure to highly concentrated PM on the respiratory and cardiovascular systems, emerging evidence supports a significant impact of air pollution on the gastrointestinal (GI) tract by linking exposure to external stressors with conditions such as appendicitis, colorectal cancer, and inflammatory bowel disease. In general, it has been hypothesized that the main mechanism involved in PM toxicity consists of an inflammatory response and this has also been suggested for the GI tract. In the present study, we analyzed the effect of specific redox-active PM components, such as copper (Cu) and iron (Fe), in human intestinal cells focusing on ultrastructural integrity, redox homeostasis, and modulation of some mitochondrial-related markers. According to our results, exposure to Cu- and Fe-PM components and their combination induced ultrastructural alterations in the endoplasmic reticulum and in the mitochondria with an additive effect when combined. The increase in ROS and the loss of the mitochondrial mass in the cells exposed to PM indicates that mitochondria are a target of acute metal exposure. Furthermore, the gene expression and the protein levels of mitochondria dynamics markers were affected by the PM exposure. In particular, OPA1 increases at both gene and protein levels in all conditions while Mitofusin1 decreases significantly only in the presence of Fe. The increase in PINK expression is modulated by Fe, while Cu seems to affect mainly Parkin. Finally, a significant decrease in trans-epithelial resistance was also observed. In general, our study can confirm the correlation observed between pollution exposure areas and increased incidence of GI tract conditions.

The exposome encompasses all factors people encounter through life, with the skin constantly exposed. While particulate matter (PM) and sleep deprivation are known to contribute to barrier dysfunction, their combined effects remain unclear.

To evaluate the independent and combined effects of PM exposure and short-term sleep deprivation on skin barrier function.

Forty healthy Korean women (aged 24-58 years) were enrolled in this study. Forearms were divided into 4 sites: control, PM exposure, sleep deprivation, and PM plus sleep deprivation. Parameters such as trans-epidermal water loss (TEWL), hydration, elasticity, roughness, and redness were measured at baseline and post-exposure. RNA sequencing and reverse transcription-polymerase chain reaction were conducted on tape-stripped skin samples.

PM exposure significantly increased TEWL (+25.59%, p<0.01), roughness (+21.9%, p<0.01), and redness (+13.7%, p<0.0001) while reducing elasticity (-3.98%, p<0.01). Sleep deprivation modestly reduced elasticity (-1.39%, p<0.05) without affecting other parameters. Combined PM and sleep deprivation did not further exacerbate barrier dysfunction compared to PM alone. RNA sequencing revealed reduced FLG and LORICRIN expression and upregulated endoplasmic reticulum (ER) stress markers (HSP90B1, CANX) in both PM and sleep deprivation conditions.

PM exposure impaired skin barrier function, while short-term sleep deprivation alone did not significantly affect the barrier, either independently or in combination with PM. However, it was observed that the sleep deprivation-only, while not directly causing barrier damage, induced changes in ER stress-related gene expression in tape-stripped skin samples, like the PM exposure-only. This suggests that such signaling pathways could potentially exacerbate skin barrier deterioration.

The association between exposure to fine particulate matter (PM2.5) from conception to 1 year after birth and the later development of atopic dermatitis (AD) has not been completely elucidated.

To investigate the effects of PM2.5 exposure during pregnancy and infancy on the later development of AD, and to explore vulnerable time periods to identify biologic pathways that may result in AD after exposure to PM2.5.

We conducted a birth cohort study comprising 564 869 term births born between 2004 and 2013. The infants were followed-up until 5 years after birth. A satellite-based model was used to calculate PM2.5 exposure for each child. A Cox proportional hazards model combined with a distributed lag nonlinear model was created to examine the associations of AD with PM2.5, as well as the dose-response relationship.

The birth cohort comprised 76 944 infants diagnosed with AD. Increased cumulative exposure to PM2.5 from 34 weeks' gestation until birth, as well as from 33 weeks after birth, was significantly associated with a higher incidence of AD. With regard to the dose-response relationship, exposure to > 65 μg m-3 PM2.5 sharply increased the risk of AD.

Prenatal and postnatal exposure to PM2.5 was related to later development of AD. The sensitive time periods may be late gestation and early life after birth.

With accelerated urbanization, air pollution has become an environmental problem that requires urgent resolution. Intensified inflammation, atopic dermatitis, and itchy skin have been reported in humans exposed to increasing PM2.5 concentrations. PM2.5 is the particulate matter whose aerodynamic equivalent diameter is less than or equal to 2.5 μm in ambient air. Madecassoside, a pentacyclic triterpenoid active component, which is found in and extracted from the plant Centella Asiatica, possesses unique pharmacological properties, such as anti-inflammatory activity, which are used to treat skin wounds. This study investigated the effects of madecassoside in terms of pyroptosis antagonism, cell membrane repair promotion, and skin barrier repair using THP-1 and HaCaT cells stimulated with PM2.5. We measured IL-1β and LDH contents in culture supernatants of THP-1 cells. The expressions of the proteins related to cell membrane repair and skin barrier repair were detected by western blotting, quantitative reverse transcription PCR and immunofluorescence. We found that madecassoside reduced the release of the inflammatory factor IL-1β and the lytic cell death marker lactate dehydrogenase and repaired PM2.5-induced gasdermin D-mediated cell membrane damage. Further, madecassoside may have the potential to promote skin barrier repair by alleviating skin barrier-related protein damage and nuclear transfer. Therefore, madecassoside possesses anti-PM2.5 stimulating activity through repairing gasdermin D-mediated cell membrane damage and possibly protecting the skin barrier, indicating that madecassoside has good anti-inflammatory repair efficacy.

Air pollution is a widespread environmental issue, with substantial global implications for human health. Recent epidemiological studies have shown that exposure to air pollution exacerbates various inflammatory skin conditions, including atopic dermatitis, psoriasis, or acne. Furthermore, air pollutants are associated with accelerated skin aging, hair loss, and skin cancer. The aim of this review is to elucidate the current understanding of the impact of air pollution on skin health, emphasizing the underlying mechanisms involved and existing therapeutic and cosmetic interventions available to prevent or mitigate these effects. A pivotal factor in the harmful effects of air pollution is the formation of reactive oxygen species and the resulting oxidative stress. The aryl hydrocarbon receptor signaling pathway also substantially contributes to mediating the effects of air pollutants on various skin conditions. Moreover, air pollutants can disrupt the skin barrier function and trigger inflammation. Consequently, antioxidant and anti-inflammatory therapies, along with treatments designed to restore the skin barrier function, have the potential to mitigate the adverse effects of air pollutants on skin health.

Urban air pollutants, mainly represented by PM containing organic and inorganic substances, can penetrate the human skin and trigger oxidative stress, potentially causing skin barrier damage and aging. κ-Carrageenan oligosaccharides as degradation products of natural sulfated polysaccharide have a great potential for skin moisturization as well as improving oxidative stress and inflammation. In this study, κ-carrageenan tetrasaccharide was obtained by enzymatic digestion of κ-carrageenan, and its role in alleviating particulate matter-induced inflammatory response in HaCaT keratinocyte cell line and skin barrier dysfunction was evaluated. The results showed that particulate matter significantly increased the cellular levels of the pollutant metal ions, stimulated ROS production and cellular inflammatory response, and inhibited enzyme precursors for ceramide synthesis and interfered with lipid synthesis. In contrast, κ-carrageenan tetrasaccharide treatment can downregulate pro-inflammatory factors by chelating metal ions to reduce ROS levels and revert the action of PM on STAT3 and PI3K/AKT pathways and PPAR-γ expression. The beneficial roles of κ-carrageenan tetrasaccharide in protection of dehydration and inflammation suggest that it can be used as a cosmetic ingredient for skincare.

Particulate matter (PM) has been recognized as a significant environmental contaminant with substantial effects on human health, although the impact of PM pollution on the skin microbiota is less understood. In this study, 78 skin microbiota samples from volunteers were obtained during periods of haze and non-haze in the spring and winter. The diversity, composition, and co-occurrence networks of the skin bacterial community were revealed using high-throughput sequencing. Acinetobacter sp. XSB125 and Pseudomonas sp. XSB6 were isolated and cocultured with PM collected during haze days. Significant seasonal variations were observed in the skin bacterial community, with winter samples showing greater diversities than spring samples. Supervised partial least squares discriminant analysis indicated that PM pollution influenced the skin bacterial community composition. Stronger interactions were detected in the network structure of the skin bacterial community during haze days. Differential and random forest analyses revealed that Acinetobacter and Pseudomonas, which are important resistant opportunistic pathogens, were significantly enriched during haze days in winter. To confirm the increases in Acinetobacter and Pseudomonas during haze days, an Acinetobacter strain and a Pseudomonas strain were isolated and cultured with the PM we collected during haze days. In vitro experiments confirmed that PM promoted the growth of the Acinetobacter and Pseudomonas strains. Function analysis revealed increased metabolic function and enrichment of antibiotic resistance- and pathogenicity-related functions during haze days, including the beta-lactamase gene and attachment invasion locus protein. These findings reveal the complex interplay between PM pollution and the skin microbiota, highlighting the need for further research into mitigation strategies to protect the public health from PM exposure.

Climate change affects global temperature, meteorological variables, plant aerobiology, air pollution exposure and a host of other factors that individually have been implicated in the inception and/or exacerbation of allergic disease like asthma and allergic rhinitis. It is unknown how climate change will impact allergic disease prevalence and morbidity in the future.

Pollen seasons are lengthening with variable effects on pollen peak concentrations and allergenicity. Air pollution exposure is linked with enhance susceptibility to allergic inflammation induced by pollen and with enhanced susceptibility to infection with a morbidity/mortality from respiratory viruses, including SARS-CoV-2. The available literature largely supports the association between climate change and three of the most salient factors for allergic respiratory disease prevalence and morbidity: changes in allergen exposure, pollution exposure, and viral respiratory infection. More research is needed to understand the complex interactions between these factors and individual-level variables that influence disease susceptibility.

Airborne fine-dust pollution poses a significant threat to both respiratory and skin health; however, the skin's wound-healing process in response to such exposure remains underexplored. Therefore, this study examined the effect of fine-dust-model compounds, specifically polycyclic aromatic hydrocarbons (PM10-PAHs) and trace-metal-containing particles (PM10-Trace), on the wound-healing process using human skin equivalents reconstructed with collagen-based biomaterials and human skin cells. Our findings revealed that fine-dust exposure significantly delayed wound closure by 2-3 times compared with unexposed controls, impairing re-epithelialization. Live imaging of wound-healing dynamics revealed that trace-metal-containing particles had a more pronounced inhibitory effect than polycyclic aromatic hydrocarbons. Furthermore, fine-dust exposure elevated protease-activated receptor-1 (PAR1) expression by up to 161%, indicating significant physiological disruption. Additionally, fine-dust exposure triggered inflammation and oxidative stress, leading to structural and functional damage in the reconstructed skin. These results provide critical insights into how airborne pollutants disrupt skin repair mechanisms and highlight the need for targeted strategies to mitigate their harmful effects.

Air pollution-related skin damage has heightened the demand for natural protective agents. Hizikia fusiformis, a brown seaweed rich in fucoidan and bioactive fatty acids (α-linolenic acid, eicosatetraenoic acid, and palmitic acid), possesses antioxidant and anti-inflammatory properties. This study investigated the protective effects of H. fusiformis ethanol extract (HFE) against particulate matter (PM)-induced oxidative stress, inflammation, and apoptosis in human keratinocytes. Antioxidant activity was assessed using DPPH and hydroxyl radical scavenging assays, while PM-induced cytotoxicity, ROS generation, inflammatory markers, and apoptotic pathways were evaluated using the WST-8 assay, DCFH2-DA, qPCR, western blotting, and Hoechst staining. HFE significantly reduced ROS levels, enhanced antioxidant enzyme activity, and mitigated PM-induced cytotoxicity. These effects were mediated by fucoidan and fatty acids, which modulated inflammatory pathways (NF-κB and MAPK), stabilized membranes, and inhibited apoptosis (Bcl-2, Bax, and caspase-3). Collectively, these findings highlight HFE's potential as a natural anti-pollution skincare ingredient, supporting further in vivo studies and formulation development.

Aerosols can affect human health through mechanisms like inflammation, oxidative stress, immune dysregulation, and respiratory impairment. In high-pollution areas, airborne particles may promote the transmission of pathogens such as Mycobacterium tuberculosis. This study investigates the spatiotemporal distribution of tuberculosis, its association with air pollution, and potential sources in the geographically unique Kashgar region of Xinjiang, encircled by mountains and desert.

Kriging interpolation and time series observation were used to analyze spatiotemporal trends and identify hot and cold spots of tuberculosis (TB) incidence and air quality in Xinjiang from 2011 to 2023. Kruskal-Wallis and multiple comparisons were applied to assess regional differences. Meteorological clustering and trajectory analysis identified pollutant pathways and potential source areas, with hypotheses proposed for TB transmission routes.

The interaction between tuberculosis, the geographic environment, and aerosols in Xinjiang reveals a consistent spatial distribution of air quality index (AQI) and TB incidence, with overlapping hotspots and cold spots. The incidence rate of tuberculosis is "n/100,000."Southern Xinjiang, shows higher TB incidence (235.31 ± 92.44) and poorer air quality (AQI: 64.19 ± 11.73) compared to Northern Xinjiang (TB: 83.82 ± 21.43, AQI: 53.90 ± 6.48). Significant regional differences in TB incidence (p < 0.0001) were confirmed, with post-hoc analyses indicating higher TB rates and worse air quality in Southern Xinjiang. Trajectory and concentration-weighted trajectory (WCWT) analysis identified dust from the Taklimakan Desert as a major contributor to PM2.5 and PM10 pollution, with values exceeding 150 μg/m3 for PM2.5 and 400 μg/m3 for PM10 in key areas like Aksu and Kashgar. The Kunlun and Tianshan mountain ranges serve as barriers that trap migrating dust, while meteorological patterns indicate that dust-laden trajectories extend further into the mountainous areas. This phenomenon exacerbates the spread of tuberculosis (TB) in the high-risk regions of southern Xinjiang.

The study highlights a distinct interaction between TB, the geographic environment, and aerosols in southern Xinjiang. Poor air quality and elevated TB incidence overlap, particularly in Kashgar. Here, dust from the Taklimakan Desert, trapped by the Kunlun and Tianshan mountains, intensifies PM2.5 and PM10 pollution, further contributing to TB transmission in high-risk areas.

Air pollution, particularly fine particulate matter (PM2.5), has been associated with various health issues, but its effects on skin health, specifically skin redness, remain underexplored. This study aims to examine the relationship between PM2.5 exposure and skin redness, with a focus on the role of sebum production in different age groups. A total of 472 participants from two communities in Taiwan in two age groups (20-59 years, n=240; over 60 years, n=232) were included in the study. PM2.5 exposure levels were estimated using land use regression models based on participants' residential addresses. Skin redness area was assessed using the VISIA Imaging System. Linear regression analyses were conducted to examine the association between PM2.5 and redness area, adjusting for demographic, lifestyle, and ultraviolet exposure. Results showed a significant positive association between PM2.5 levels and redness area in both age groups. In the 20-59 age group, each unit increase in PM2.5 corresponded to a 1.70-unit increase in redness area (95% CI: 0.32 - 3.07, p < 0.01), while in the over-60 group, the increase was 2.63 units (95% CI: 1.19 - 4.08, p < 0.001). Additionally, porphyrins showed a positive association with redness area among the 20-59 age group (p < 0.05), while no significant association was found in the over-60 group. This study suggests a linkage between PM2.5 exposure and skin redness area, indicating that air pollution may be a contributing factor to skin health issues. The findings suggest that the interaction between lipophilic and carcinogenic substances in PM2.5 and porphyrins could elevate redness area levels and potentially increase the risk of chronic skin conditions and skin cancer.

Climate change will continue to impact allergic diseases in direct and indirect ways. Rising global temperatures are contributing to increased duration of pollen seasons, altered aeroallergen production and potency of allergens, and changes in the geographic distribution of allergenic plants that drive increased human exposure to aeroallergens and increased allergic disease morbidity. Climate change is inextricably linked with air pollution, the latter of which was shown to act as an adjuvant for allergic inflammatory processes promoting allergic sensitization. Pollutant exposure is also linked with higher prevalence of childhood asthma and exacerbation of existing asthma and allergic disease. Increased exposure, or co-exposure, to aeroallergens and air pollution as a result of climate change will result in higher rates of sensitization, and incident allergic disease remains uncertain. Vulnerable populations, including children, the elderly, and marginalized groups, are likely to be disproportionately affected. This review summarizes the current knowledge of the effects of climate change on aeroallergens, and by extension, allergic disease. Addressing these health challenges requires a comprehensive understanding of the interaction between climate change, allergens, pollution and public health, alongside proactive measures to mitigate these effects.

Atopic dermatitis (AD) is a paradigmatic prevalent, long-lasting, and inflammatory skin condition with a diverse range of clinical manifestations. The etiology and clinical symptoms of AD are influenced by complex pathophysiological processes, which involve a strong genetic component, epidermal dysfunction, and immunological dysregulation, and a strong influence of other physiological and environmental factors. The FDA has approved targeted and well-tolerated immunomodulators including biologics like dupilumab and crisaborole, and small molecules such as baricitinib, as novel therapies for AD. They effectively treat AD but are too expensive for most patients. The review provides an update on the state of knowledge of AD pathogenesis, discusses the available diagnostic and scoring indices, and provides a scientific foundation for treatment methods for AD. This review also presents data on clinical efficacy of innovative treatments' considering recent guidelines, emphasizing the newest medications and ongoing trials. Finally, the new implication of artificial intelligence (AI) in AD management is explored, where AI can speed up diagnosis and therapy. The PubMed, Google Scholar, and ScienceDirect databases were used for this review.

Cutaneous tissue is one of the main targets of outdoor stressors, and nowadays, the effect of pollution on skin conditions and premature skin ageing has been well correlated, although the exact effect that different pollutants have on the skin has not been well defined, especially when compared to other stressors. Among the air pollutants, UV radiation and particulate matter (PM) have been found among the most aggressive in terms of skin damage, inducing oxinflammatory responses, promoting degradation of extracellular matrix (ECM) components, and compromising the cutaneous defensive barrier. Topical application of technologies able to prevent oxidative damage is still one of the best approaches to protect our skin, and considering the well-known antioxidant network, application of an antioxidant mixture is more recommended than a single compound. In the present study, human skin explants were exposed every day for 4 days to diesel particles (DEE) or to UV after the daily pre-treatment with a topical application of a commercially available antioxidant mixture (AOX Mix), containing 15% ascorbic acid, 0.5% ferulic acid and 1% tocopherol. Oxidative stress markers such as 4-hydroxynonenal, skin barrier proteins such as involucrin, filaggrin, claudin-1 and desmocollin-1, resilience markers such as elastin and tropoelastin, and the levels of Type I and Type III collagens were assessed. Topical application was able to prevent most of the damage induced by the outdoor stressors, confirming that daily protection is needed to prevent cutaneous premature ageing.

Exposure to particulate matter (PM) in the air harms human health. Most studies on particulate matter's (PM) effects have primarily focused on respiratory and cardiovascular diseases. Recently, IL-32θ, one of the IL-32 isoforms, has been demonstrated to modulate cancer development and inflammatory responses. This study revealed that one-point mutated IL-32θ (A94V) plays an important role in attenuating skin inflammation. IL-32θ (A94V) inhibited PM-induced COX-2, a pro-inflammatory cytokine GM-CSF and CYP1A1 in PM-exposed human keratinocytes HaCaT cells. IL-32θ (A94V) modulating effects were mediated via down-regulating ERK/p38/NF-κB/ AP-1 and AhR/ARNT signaling pathways. Our study indicates that PM triggers skin inflammation by upregulating COX-2, GM-CSF and CYP1A1 expression. IL-32θ (A94V) suppresses the expressions of COX-2, GM-CSF, and CYP1A1 by blocking the nuclear translocation of NF-κB and AP-1, as well as inhibiting the activation of the AhR/ARNT signaling pathway. Our findings offer valuable insights into developing therapeutic strategies and potential drugs to mitigate PM-induced skin inflammation by inhibiting the ERK/p38/NF-κB/AP-1 and AhR/ARNT signaling pathways.

Keratinocytes are susceptible to airborne particulate matter (PM) exposure, resulting in human skin barrier dysfunction. Therefore, it is important to find useful reagents to resolve skin damages caused by PM. Here, we explored the protective effect of 7S MaR1, a specialized pro-resolving mediator derived from docosahexaenoic acid, on skin inflammation and the oxidative stress induced by PM with a diameter 10 μm or less (PM10) in human keratinocyte HaCaT cells. Interestingly, PM10-induced ROS generation was modulated by 7S MaR1 via the recovery of ROS scavenger genes. 7S MaR1 reduced PM10-induced IL-6 expression via modulating the p38/ERK/NF-κB signaling pathways. These results demonstrate that PM10 induces inflammatory cytokines, which can lead to skin diseases. In addition, 7S MaR1 can resolve inflammation caused by PM10-induced oxidative stress and inflammatory cytokines. [BMB Reports 2024; 57(11): 490-496].

Exposure to airborne particulate <10 μm (PM10) adversely affects the ocular surface. This study tested PM10 on epithelial barrier integrity in immortalized human corneal epithelial cells (HCE-2) and mouse cornea, and whether antioxidant SKQ1 is restorative. HCE-2 were exposed to 100 μg/ml PM10 ± SKQ1 for 24 h. An Electric Cell-Substrate Impedance Sensing (ECIS) system monitored the impact of PM10. RT-PCR, western blotting and immunofluorescence measured levels of barrier and associated proteins, stanniocalcin 2 (STC2), and a kit measured total calcium. In vivo, female C57BL/6 mice were exposed to either control air or PM10 (±SKQ1) in a whole-body exposure chamber, and barrier associated proteins tested. Tight junction and mucins proteins in the cornea were tested. In HCE-2, PM0 vs control significantly reduced mRNA and protein levels of tight junction and adherence proteins, and mucins. ECIS data demonstrated that PM10 vs control cells exhibited a significant decrease in epithelial barrier strength at 4000 Hz indicated by reduced impedance and resistance. PM10 also upregulated STC2 protein and total calcium levels. In vivo, PM10 vs control reduced zonula occludens 1 and mucins. SKQ1 pre-treatment reversed PM10 effects both in vitro and in vivo. In conclusion, PM10 exposure reduced tight junction and mucin proteins, and compromised the seal between cells in the corneal epithelium leading to decreased epithelial barrier strength. This effect was reversed by SKQ1. Since the corneal epithelium forms the first line of defense against air pollutants, including PM10, preserving its integrity using antioxidants such as SKQ1 is crucial in reducing the occurrence of ocular surface disorders.

Limited evidence was available on ambient air pollution and pediatric atopic dermatitis (AD). The study aimed to evaluate the associations between short-term exposure to air pollutants and outpatient visits for pediatric AD. From 2016-2018, we collected data on six criteria air pollutants (PM2.5, PM10, NO2, SO2, CO and O3) and daily outpatient visits for pediatric AD in 66 hospitals, covering all districts in Shanghai, China. The over-dispersed Poisson generalized additive model (GAM) was applied to fit the associations of criteria air pollutants with hospital visits. Two-pollutant models were fitted and stratified analyses by sex, age and season were conducted. We identified 477,833 outpatient visits for pediatric AD. Each interquartile range (IQR) increase in PM2.5 (IQR: 30.9 μg/m3), PM10 (8.9 μg/m3), NO2 (25.5 μg/m3), SO2 (5.8 μg/m3) and CO (0.283 mg/m3) on the concurrent day was significantly associated with increments of 2.08 % (95 % CI: 0.53 %, 3.65 %), 2.53 % (95 % CI: 0.87 %, 4.22 %), 8.14 % (95 % CI: 6.24 %, 10.08 %), 5.67 % (95 % CI: 3.58 %, 7.80 %), and 2.27 % (95 % CI: 0.70 %, 3.87 %) in pediatric AD outpatient visits, respectively. The effects of NO2 remained robust after adjustment for other air pollutants. The exposure-response curves for PM2.5 and PM10 were steeper for moderate-lower concentrations, with a flatten curves at high concentration; nearly linear relationships were found for NO2. Higher associations of NO2 exposure on AD were detected in children under 6 years old (p=0.01); and we observed larger effect of air pollutants in cool seasons (p<0.001 for PM2.5, PM10, NO2 and CO; p=0.043 for SO2). This study indicated that short-term exposure to air pollution could increase risk of outpatient visits for pediatric AD.

Butin is a naturally occurring compound with a wide range of medicinal properties, including anti-inflammatory, anti-arthritic, and antioxidant properties. Particulate matter 2.5 (PM2.5) and ultraviolet B (UVB) radiation contribute to skin cell damage via the induction of oxidative stress.

This study sought to assess the protective effects of butin against damage triggered by PM2.5 and UVB in human HaCaT keratinocytes. Assessments were performed to evaluate cell viability, apoptosis, and cellular component damage.

Butin exhibited its protective ability via the inhibition of PM2.5-induced reactive oxygen species generation, lipid peroxidation, DNA damage, protein carbonylation, and mitochondrial damage. Butin reduced the PM2.5-induced c-Fos and phospho-c-Jun protein levels as well as mitogen-activated protein kinase. Furthermore, butin mitigated PM2.5- and UVB-induced apoptosis.

Butin had the potential as a pharmaceutical candidate for treating skin damage caused by PM2.5 and UVB exposure.

Background/Objectives: The external environment constantly influences human health through many factors, including air quality, access to green spaces, exposure to pollutants, and climate change. Contamination poses a substantial threat to human well-being; conversely, environmental factors also positively impact health. The purpose of this study is to provide a comprehensive review of the complex relationship between various environmental factors and human health. While individual studies have explored specific aspects, a broader integrative understanding is lacking. Methods: Through databases (PubMed, Cochrane, Copernicus), 4888 papers were identified, with 166 selected for detailed analysis. Results: We summarized recent research, identifying multiple associations between environmental factors such as air pollution, climate change, solar radiation, and meteorological conditions and their impact on various health outcomes, including respiratory, cardiovascular, metabolic and gastrointestinal, renal and urogenital, neurological and psychological health, infectious and skin diseases, and major cancers. We use chord diagrams to illustrate these links. We also show the interaction between different environmental factors. Findings begin with exploring the direct impact of environmental factors on human health; then, the interplay and combined effects of environmental factors, elucidating their (often indirect) interaction and collective contribution to human health; and finally, the implications of climate change on human health. Conclusions: Researchers and policymakers need to consider that individuals are exposed to multiple pollutants simultaneously, the "multipollutant exposure phenomenon". It is important to study and regulate environmental factors by considering the combined impact of various pollutants rather than looking at each pollutant separately. We emphasize actionable recommendations and solutions.

Atopic dermatitis (AD) is a complex disease characterized by dry, pruritic skin and significant atopic and psychological sequelae. Although AD has always been viewed as multifactorial, early research was dominated by overlapping genetic determinist views of either innate barrier defects leading to inflammation or innate inflammation eroding skin barrier function. Since 1970, however, the incidence of AD in the United States has increased at a pace that far exceeds genetic drift, thus suggesting a modern, environmental etiology. Another implicated factor is Staphylococcus aureus; however, a highly contagious microorganism is unlikely to be the primary etiology of a noncommunicable disease. Recently, the roles of the skin and gut microbiomes have received greater attention as potentially targetable drivers of AD. Here too, however, dysbiosis on a population scale would require induction by an environmental factor. In this review, we describe the evidence supporting the environmental hypothesis of AD etiology and detail the molecular mechanisms of each of the AD-relevant toxins. We also outline how a pollution-focused paradigm demands earnest engagement with environmental injustice if the field is to meaningfully address racial and geographic disparities. Identifying specific toxins and their mechanisms can also inform in-home and national mitigation strategies.

Exposure to Particulate matter 2.5 (PM2.5) accelerates aging, causing declines in tissue and organ function, and leading to diseases such as cardiovascular, neurodegenerative, and musculoskeletal disorders. PM2.5 is a major environmental pollutant and an exogenous pathogen in air pollution that is now recognized as an accelerator of human aging and a predisposing factor for several age-related diseases. In this paper, we seek to elucidate the mechanisms by which PM2.5 induces cellular senescence, such as genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, and mitochondrial dysfunction, and age-related diseases. Our goal is to increase awareness among researchers within the field of the toxicity of environmental pollutants and to advocate for personal and public health initiatives to curb their production and enhance population protection. Through these endeavors, we aim to promote longevity and health in older adults.

Epidemiological evidence suggests that particulate matter (PM) exposure can trigger or worsen atopic dermatitis (AD); however, the underlying mechanisms remain unclear. Recently, pregnane X receptor (PXR), a xenobiotic receptor, was reported to be related to skin inflammation in AD.

This study aimed to explore the effects of PM on AD and investigate the role of PXR in PM-exposed AD.

In vivo and in vitro AD-like models were employed, using BALB/c mice, immortalized human keratinocytes (HaCaT), and mouse CD4 + T cells.

Topical application of PM significantly increased dermatitis score and skin thickness in AD-like mice. PM treatment increased the mRNA and protein levels of type 17 inflammatory mediators, including interleukin (IL)-17A, IL-23A, IL-1β, and IL-6, in AD-like mice and human keratinocytes. PM also activated PXR signaling, and PXR knockdown exacerbated PM-induced type 17 inflammation in human keratinocytes and mouse CD4 + T cells. In contrast, PXR activation by rifampicin (a human PXR agonist) reduced PM-induced type 17 inflammation. Mechanistically, PXR activation led to a pronounced inhibition of the nuclear factor kappa B (NF-κB) pathway.

In summary, PM exposure induces type 17 inflammation and PXR activation in AD. PXR activation reduces PM-induced type 17 inflammation by suppressing the NF-κB signaling pathway. Thus, PXR represents a promising therapeutic target for controlling the PM-induced AD aggravation.

Particulate matter (PM) is a harmful air pollutant composed of chemicals and metals which affects human health by penetrating both the respiratory system and skin, causing oxidative stress and inflammation. This review investigates the association between PM and skin disease, focusing on the underlying molecular mechanisms and specific disease pathways involved. Studies have shown that PM exposure is positively associated with skin diseases such as atopic dermatitis, psoriasis, acne, and skin aging. PM-induced oxidative stress damages lipids, proteins, and DNA, impairing cellular functions and triggering inflammatory responses through pathways like aryl hydrocarbon receptor (AhR), NF-κB, and MAPK. This leads to increased production of inflammatory cytokines and exacerbates skin conditions. PM exposure exacerbates AD by triggering inflammation and barrier disruption. It disrupts keratinocyte differentiation and increases pro-inflammatory cytokines in psoriasis. In acne, it increases sebum production and inflammatory biomarkers. It accelerates skin aging by degrading ECM proteins and increasing MMP-1 and COX2. In conclusion, PM compromises skin health by penetrating skin barriers, inducing oxidative stress and inflammation through mechanisms like ROS generation and activation of key pathways, leading to cellular damage, apoptosis, and autophagy. This highlights the need for protective measures and targeted treatments to mitigate PM-induced skin damage.

The paper explains how nano exposure is assessed in the construction field and focuses on the production of fire-resistant insulation panels with nanoclay. Utilizing the commercial ANSYS CFX® software, a preliminary theoretical simulation was conducted on nano exposure in the workplace, which revealed that particle dispersion is primarily driven by diffusion. Panel post-processing through drilling results in the highest inhalation exposure, followed by mixing and grinding activities. Compared to a state of 'no activity', each activity resulted in an exposure increase by a factor of min. 1000. An overall assessment suggests that the use of nanoparticles in construction materials may not significantly heighten workers' exposure to nanopowders when considering particle concentration alone as opposed to using traditional micro-scale materials. However, the issue persists when it comes to blending powders or performing finishing tasks on panels, with concentration levels being significantly higher for drilling, grinding, and mixing powders at 2.4 times above the standard reference value (40,000 particles/cm3); this is unacceptable, even for brief durations. Examination of dermal contact with gloves and masks worn by workers revealed no nanoparticle penetration. Safety measures were proposed for workers based on decision trees to enhance their safety. Ten categories of protection strategies have been devised to combat the impact of nanoparticles, which are tailored to specific technical situations, but they must be modified for various types of nanoparticles despite potential shared health implications.

Human skin ageing is closely related to the ageing of the whole organism, and it's a continuous multisided process that is influenced not only by genetic and physiological factors but also by the cumulative impact of environmental factors. Currently, there is a scientific community need for developing skin models representing ageing processes to (i) enhance understanding on the mechanisms of ageing, (ii) discover new drugs for the treatment of age-related diseases, and (iii) develop effective dermo-cosmetics. Bioengineers worldwide are trying to reproduce skin ageing in the laboratory aiming to better comprehend and mitigate the senescence process. This review provides details on the main ageing molecular mechanisms and procedures to obtain in vitro aged skin models.

Air pollution, a global health concern, has been associated with adverse effects on human health. In particular, particulate matter (PM), which is a major contributor to air pollution, impacts various organ systems including the skins. In fact, PM has been suggested as a culprit for accelerating skin aging and pigmentation. In this study, using single-cell RNA sequencing, IL-24 was found to be highly upregulated among the differentially expressed genes commonly altered in keratinocytes and fibroblasts of ex vivo skins exposed to PM. It was verified that PM exposure triggered the expression of IL-24 in keratinocytes, which subsequently led to a decrease in type I procollagen expression and an increase in MMP1 expression in fibroblasts. Furthermore, long-term treatment of IL-24 induced cellular senescence in fibroblasts. Through high-throughput screening, we identified chemical compounds that inhibit the IL-24-STAT3 signaling pathway, with lovastatin being the chosen candidate. Lovastatin not only effectively reduced the expression of IL24 induced by PM in keratinocytes but also exhibited a capacity to restore the decrease in type I procollagen and the increase in MMP1 caused by IL-24 in fibroblasts. This study provides insights into the significance of IL-24, illuminating mechanisms behind PM-induced skin aging, and proposes IL-24 as a promising target to mitigate PM-associated skin aging.

Airborne particulate matter (PM) contains polycyclic aromatic hydrocarbons (PAHs) as primary toxic components, causing oxidative damage and being associated with various inflammatory skin pathologies such as premature aging, atopic dermatitis, and psoriasis. Coffee cherry pulp (CCS) extract, rich in chlorogenic acid, caffeine, and theophylline, has demonstrated strong antioxidant properties. However, its specific anti-inflammatory effects and ability to protect macrophages against PAH-induced inflammation remain unexplored. Thus, this study aimed to evaluate the anti-inflammatory properties of CCS extract on RAW 264.7 macrophage cells exposed to atmospheric PAHs, compared to chlorogenic acid (CGA), caffeine (CAF), and theophylline (THP) standards. The CCS extract was assessed for its impact on the production of nitric oxide (NO) and expression of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). Results showed that CCS extract exhibited significant antioxidant activities and effectively inhibited protease and lipoxygenase (LOX) activities. The PAH induced the increase in intracellular reactive oxygen species, NO, TNF-α, IL-6, iNOS, and COX-2, which were markedly suppressed by CCS extract in a dose-dependent manner, comparable to the effects of chlorogenic acid, caffeine, and theophylline. In conclusion, CCS extract inhibits PAH-induced inflammation by reducing pro-inflammatory cytokines and reactive oxygen species (ROS) production in RAW 264.7 cells. This effect is likely due to the synergistic effects of its bioactive compounds. Chlorogenic acid showed strong antioxidant and anti-inflammatory activities, while caffeine and theophylline enhanced anti-inflammatory activity. CCS extract did not irritate the hen's egg chorioallantoic membrane. Therefore, CCS extract shows its potential as a promising cosmeceutical ingredient for safely alleviating inflammatory skin diseases caused by air pollution.

The skin is the layer of tissue that covers the largest part of the body in vertebrates, and its main function is to act as a protective barrier against external environmental factors, such as microorganisms, ultraviolet light and mechanical damage. Due to its important function, investigating the factors that lead to skin aging and age-related diseases, as well as understanding the biology of this process, is of high importance. Indeed, it has been reported that several external and internal stressors contribute to skin aging, similar to the aging of other tissues. Moreover, during aging, senescent cells accumulate in the skin and express senescence-associated factors, which act in a paracrine manner on neighboring healthy cells and tissues. In this review, we will present the factors that lead to skin aging and cellular senescence, as well as ways to study senescence in vitro and in vivo. We will further discuss the adverse effects of the accumulation of chronic senescent cells and therapeutic agents and tools to selectively target and eliminate them.

Particulate matter 2.5 (PM2.5) causes skin aging, inflammation, and impaired skin homeostasis. Hyperoside, a flavanol glycoside, has been proposed to reduce the risk of diseases caused by oxidative stress. This study evaluated the cytoprotective potential of hyperoside against PM2.5-induced skin cell damage. Cultured human HaCaT keratinocytes were pretreated with hyperoside and treated with PM2.5. Initially, the cytoprotective and antioxidant ability of hyperoside against PM2.5 was evaluated. Western blotting was further employed to investigate endoplasmic reticulum (ER) stress and cellular senescence and for evaluation of cell cycle regulation-related proteins. Hyperoside inhibited PM2.5-mediated ER stress as well as mitochondrial damage. Colony formation assessment confirmed that PM2.5-impaired cell proliferation was restored by hyperoside. Moreover, hyperoside reduced the activation of PM2.5-induced ER stress-related proteins, such as protein kinase R-like ER kinase, cleaved activating transcription factor 6, and inositol-requiring enzyme 1. Hyperoside promoted cell cycle progression in the G0/G1 phase by upregulating the PM2.5-impaired cell cycle regulatory proteins. Hyperoside significantly reduced the expression of PM2.5-induced senescence-associated β-galactosidase and matrix metalloproteinases (MMPs), such as MMP-1 and MMP-9. Overall, hyperoside ameliorated PM2.5-impaired cell proliferation, ER stress, and cellular senescence, offering potential therapeutic implications for mitigating the adverse effects of environmental pollutants on skin health.

Exposure to environmental stressors like particulate matter (PM) and ultraviolet radiation (UV) induces cutaneous oxidative stress and inflammation and leads to skin barrier dysfunction and premature aging. Metals like iron or copper are abundant in PM and are known to contribute to reactive oxygen species (ROS) production.

Although it has been suggested that topical antioxidants may be able to help in preventing and/or reducing outdoor skin damage, limited clinical evidence under real-life exposure conditions have been reported. The aim of the present study was to evaluate the ability of a topical serum containing 15% ascorbic acid, 0.5% ferulic acid, and 1% tocopherol (CF Mix) to prevent oxinflammatory skin damage and premature aging induced by PM + UV in a human clinical trial.

A 4-day single-blinded, clinical study was conducted on the back of 15 females (18-40 years old). During the 4 consecutive days, the back test zones were treated daily with or without the CF Mix, followed by with/without 2 h of PM and 5 min of UV daily exposure.

Application of the CF Mix prevented PM + UV-induced skin barrier perturbation (Involucrin and Loricrin), lipid peroxidation (4HNE), inflammatory markers (COX2, NLRP1, and AhR), and MMP9 activation. In addition, CF Mix was able to prevent Type I Collagen loss.

This is the first human study confirming multipollutant cutaneous damage and suggesting the utility of a daily antioxidant topical application to prevent pollution induced skin damage.

Air pollutants deteriorate the survival environment and endanger human health around the world. A large number of studies have confirmed that air pollution jeopardizes multiple organs, such as the cardiovascular, respiratory, and central nervous systems. Skin is the largest organ and the first barrier that protects us from the outside world. Air pollutants such as particulate matter (PM), polycyclic aromatic hydrocarbons (PAHs), volatile organic compounds (VOCs) will affect the structure and function of the skin and bring about the development of inflammatory skin diseases (atopic dermatitis (AD), psoriasis), skin accessory diseases (acne, alopecia), auto-immune skin diseases (cutaneous lupus erythematosus(CLE) scleroderma), and even skin tumors (melanoma, basal cell carcinoma (BCC), squamous-cell carcinoma (SCC)). Oxidative stress, skin barrier damage, microbiome dysbiosis, and skin inflammation are the pathogenesis of air pollution stimulation. In this review, we summarize the current evidence on the effects of air pollution on skin diseases and possible mechanisms to provide strategies for future research.

Industrialization and population growth are leading to the production of significant amounts of sewage containing hazardous xenobiotic compounds. These compounds pose a threat to human and animal health, as well as the overall ecosystem. To combat this issue, chemical, physical, and biological techniques have been used to remove these contaminants from water bodies affected by human activity. Biotechnological methods have proven effective in utilizing microorganisms and enzymes, particularly laccases, to address this problem. Laccases possess versatile enzymatic characteristics and have shown promise in degrading different xenobiotic compounds found in municipal, industrial, and medical wastewater. Both free enzymes and crude enzyme extracts have demonstrated success in the biotransformation of these compounds. Despite these advancements, the widespread use of laccases for bioremediation and wastewater treatment faces challenges due to the complex composition, high salt concentration, and extreme pH often present in contaminated media. These factors negatively impact protein stability, recovery, and recycling processes, hindering their large-scale application. These issues can be addressed by focusing on large-scale production, resolving operation problems, and utilizing cutting-edge genetic and protein engineering techniques. Additionally, finding novel sources of laccases, understanding their biochemical properties, enhancing their catalytic activity and thermostability, and improving their production processes are crucial steps towards overcoming these limitations. By doing so, enzyme-based biological degradation processes can be improved, resulting in more efficient removal of xenobiotics from water systems. This review summarizes the latest research on bacterial laccases over the past decade. It covers the advancements in identifying their structures, characterizing their biochemical properties, exploring their modes of action, and discovering their potential applications in the biotransformation and bioremediation of xenobiotic pollutants commonly present in water sources.

Atopic dermatitis, also known as atopic eczema, is a chronic inflammatory skin disease characterized by red pruritic skin lesions, xerosis, ichthyosis, and skin pain. Among the social impacts of atopic dermatitis are difficulties and detachment in relationships and social stigmatization. Additionally, atopic dermatitis is known to cause sleep disturbance, anxiety, hyperactivity, and depression. Although the pathological process behind atopic dermatitis is not fully known, it appears to be a combination of epidermal barrier dysfunction and immune dysregulation. Skin is the largest organ of the human body which acts as a mechanical barrier to toxins and UV light and a natural barrier against water loss. Both functions face significant challenges due to atopic dermatitis. The list of factors that can potentially trigger or contribute to atopic dermatitis is extensive, ranging from genetic factors, family history, dietary choices, immune triggers, and environmental factors. Consequently, prevention, early clinical diagnosis, and effective treatment may be the only resolutions to combat this burdensome disease. Ensuring safe and targeted drug delivery to the skin layers, without reaching the systemic circulation is a promising option raised by nano-delivery systems in dermatology. In this review, we explored the current understanding and approaches of atopic dermatitis and outlined a range of the most recent therapeutics and dosage forms brought by nanotechnology. This review was conducted using PubMed, Google Scholar, and ScienceDirect databases.

With the development of modern sheep raising technology, the increasing density of animals in sheep house leads to the accumulation of microbial aerosols in sheep house. It is an important prerequisite to grasp the characteristics of bacteria in aerosols in sheep house to solve the problems of air pollution and disease prevention and control in sheep house. In this study, the microorganisms present in the air of sheep houses were investigated to gain insights into the structure of bacterial communities and the prevalence of pathogenic bacteria. Samples from six sheep pens in each of three sheep farms, totaling 18, were collected in August 2022 from Ningxia province, China. A high-volume air sampler was utilized for aerosol collection within the sheep housing followed by DNA extraction for 16S rRNA sequencing. Employing high-throughput 16S rRNA sequencing technology, we conducted an in-depth analysis of microbial populations in various sheep pen air samples, enabling us to assess the community composition and diversity. The results revealed a total of 11,207 operational taxonomic units (OTUs) within the bacterial population across the air samples, encompassing 152 phyla, 298 classes, 517 orders, 853 families, 910 genera, and 482 species. Alpha diversity and beta diversity analysis indicated that differences in species diversity, evenness and coverage between different samples. At the bacterial phylum level, the dominant bacterial groups are Firmicutes, Proteobacteria, and Actinobacteria, among which Firmicutes (97.90-98.43%) is the highest. At the bacterial genus level, bacillus, Bacteroides, Fusobacterium, etc. had higher abundance, with Bacillus (85.47-89.87%) being the highest. Through an in-depth analysis of microbial diversity and a meticulous examination of pathogenic bacteria with high abundance in diverse sheep house air samples, the study provided valuable insights into the microbial diversity, abundance, and distinctive features of prevalent pathogenic bacteria in sheep house air. These findings serve as a foundation for guiding effective disease prevention and control strategies within sheep farming environments.

Cutaneous tissues is among the main target of outdoor stressors such as ozone (O3 ), particulate matter (PM), and ultraviolet radiation (UV) all involved in inducing extrinsic skin aging. Only a few reports have studied the multipollutant interaction and its effect on skin damage. In the present work, we intended to evaluate the ability of pollutants such as O3 and PM to further aggravate cutaneous UV damage. In addition, the preventive properties of a cosmeceutical formulation mixture (AOX mix) containing 15% vitamin C (L-ascorbic acid), 1% vitamin E (α-tocopherol) and 0.5% ferulic acid was also investigated. Skin explants obtained from three different subjects were exposed to 200 mJ UV light, 0.25 ppm O3 for 2 h, and 30 min of diesel engine exhaust (DEE), alone or in combination for 4 days (time point D1 and D4). The results showed a clear additive effect of O3 and DEE in combination with UV in terms of keratin 10, Desmocollin and Claudin loss. In addition, the multipollutant exposure significantly induced the inflammatory response measured as NLRP1/ASC co-localization suggesting the activation of the inflammasome machinery. Finally, the loss of Aquaporin3 was also affected by the combined outdoor stressors. Furthermore, daily topical pre-treatment with the AOX Mix significantly prevented the cutaneous changes induced by the multipollutants. In conclusion, this study is among the first to investigate the combined effects of three of the most harmful outdoor stressors on human skin and confirms that daily topical of an antioxidant application may prevent pollution-induced skin damage.

Continuous exposure of human skin to air pollution can result in a range of undesirable skin conditions. In our recent study, UV and visible light were found to increase cytotoxicity of fine particulate matter (PM2.5 ) against human keratinocytes. Since it is impossible to avoid exposure of human skin to PM2.5 , effective strategies are needed to reduce their damaging effects. l-ascorbic acid and resveratrol were tested as potential topical agents against pollution-related skin impairment. Although these agents were previously found to ameliorate PM-dependent damage, the effect of light and seasonal variation of particles were not previously studied. EPR spin-trapping, DPPH assay, and singlet oxygen phosphorescence were used to determine the scavenging activities of the antioxidants. MTT, JC-10 and iodometric assays were used to analyze the effect on PM2.5 -induced cytotoxicity, mitochondrial damage and oxidation of lipids. Live-cell imaging was employed to examine wound-healing properties of cells. Light-induced, PM2.5 -mediated oxidative damage was examined by immunofluorescent staining. Both antioxidants effectively scavenged free radicals and singlet oxygen produced by PM2.5 , reduced cell death and prevented oxidative damage to HaCaT cells. l-ascorbic acid and resveratrol, especially when applied in combination, can protect HaCaT cells against the dark and light induced toxicity of PM2.5 .

Particulate matter (PM) exposure disrupts the skin barrier, causing cutaneous inflammation that may eventually contribute to the development of various skin diseases. Herein, we introduce anti-inflammatory artificial extracellular vesicles (AEVs) fabricated through cell extrusion using the biosurfactant PEGylated mannosylerythritol lipid (P-MEL), hereafter named AEVP-MEL. The P-MEL has anti-inflammatory abilities with demonstrated efficacy in inhibiting the secretion of pro-inflammatory mediators. Mechanistically, AEVP-MEL enhanced anti-inflammatory response by inhibiting the mitogen-activated protein kinase (MAPK) pathway and decreasing the release of inflammatory mediators such as reactive oxygen species (ROS), cyclooxygenase-2 (COX-2), and pro-inflammatory cytokines in human keratinocytes. Moreover, AEVP-MEL promoted increased expression levels of skin barrier proteins (e.g., involucrin, IVL) and water-proteins (e.g., aquaporin 3, AQP3). In vivo studies revealed that repeated PM exposure to intact skin resulted in cutaneous inflammatory responses, including increased skin thickness (hyperkeratosis) and mast cell infiltration. Importantly, our data showed that the AEVP-MEL treatment significantly restored immune homeostasis in the skin affected by PM-induced inflammation and enhanced the intrinsic skin barrier function. This study highlights the potential of the AEVP-MEL in promoting skin health against PM exposure and its promising implications for the prevention and treatment of PM-related skin disorders.