Air pollution, genetic susceptibility, and the risk of atrial fibrillation: A large prospective cohort study.

To date, no study has explored the extent to which genetic susceptibility modifies the effects of air pollutants on the risk of atrial fibrillation (AF). This study was designed to investigate the separate and joint effects of long-term exposure to air pollutants and genetic susceptibility on the risk of AF events. This study included 401,251 participants without AF at baseline from UK Biobank. We constructed a polygenic risk score and categorized it into three categories. Cox proportional hazards models were fitted to assess the separate and joint effects of long-term exposure to air pollutants and genetics on the risk of AF. Additionally, we further evaluated the effect modification of genetic susceptibility. The hazard ratios and corresponding 95% confidence intervals of incident AF for per interquartile range increase in particulate matter with an aerodynamic diameter smaller than 2.5 µm (PM2.5) or 10 µm (PM10), nitrogen dioxide (NO2), and nitrogen oxide (NOx) were 1.044 (1.025, 1.063), 1.063 (1.044, 1.083), 1.061 (1.042, 1.081), and 1.039 (1.023, 1.055), respectively. For the combined effects, participants exposed to high air pollutants levels and high genetic risk had approximately 149.2% (PM2.5), 181.7% (PM10), 170.2% (NO2), and 157.2% (NOx) higher risk of AF compared to those with low air pollutants levels and low genetic risk, respectively. Moreover, the significant additive interactions between PM10 and NO2 and genetic risk on AF risk were observed, with around 16.4% and 35.1% of AF risk could be attributable to the interactive effects. In conclusion, long-term exposure to air pollutants increases the risk of AF, particularly among individuals with high genetic susceptibility.

Environmental Exposures and Pediatric Cardiology: A Scientific Statement From the American Heart Association.

Environmental toxicants and pollutants are causes of adverse health consequences, including well-established associations between environmental exposures and cardiovascular diseases. Environmental degradation is widely prevalent and has a long latency period between exposure and health outcome, potentially placing a large number of individuals at risk of these health consequences. Emerging evidence suggests that environmental exposures in early life may be key risk factors for cardiovascular conditions across the life span. Children are a particularly sensitive population for the detrimental effects of environmental toxicants and pollutants given the long-term cumulative effects of early-life exposures on health outcomes, including congenital heart disease, acquired cardiac diseases, and accumulation of cardiovascular disease risk factors. This scientific statement highlights representative examples for each of these cardiovascular disease subtypes and their determinants, focusing specifically on the associations between climate change and congenital heart disease, airborne particulate matter and Kawasaki disease, blood lead levels and blood pressure, and endocrine-disrupting chemicals with cardiometabolic risk factors. Because children are particularly dependent on their caregivers to address their health concerns, this scientific statement highlights the need for clinicians, research scientists, and policymakers to focus more on the linkages of environmental exposures with cardiovascular conditions in children and adolescents.

Mitigating climate disruption in time: A self-consistent approach for avoiding both near-term and long-term global warming.

The ongoing and projected impacts from human-induced climate change highlight the need for mitigation approaches to limit warming in both the near term (<2050) and the long term (>2050). We clarify the role of non-CO2 greenhouse gases and aerosols in the context of near-term and long-term climate mitigation, as well as the net effect of decarbonization strategies targeting fossil fuel (FF) phaseout by 2050. Relying on Intergovernmental Panel on Climate Change radiative forcing, we show that the net historical (2019 to 1750) radiative forcing effect of CO2 and non-CO2 climate forcers emitted by FF sources plus the CO2 emitted by land-use changes is comparable to the net from non-CO2 climate forcers emitted by non-FF sources. We find that mitigation measures that target only decarbonization are essential for strong long-term cooling but can result in weak near-term warming (due to unmasking the cooling effect of coemitted aerosols) and lead to temperatures exceeding 2 °C before 2050. In contrast, pairing decarbonization with additional mitigation measures targeting short-lived climate pollutants and N2O, slows the rate of warming a decade or two earlier than decarbonization alone and avoids the 2 °C threshold altogether. These non-CO2 targeted measures when combined with decarbonization can provide net cooling by 2030 and reduce the rate of warming from 2030 to 2050 by about 50%, roughly half of which comes from methane, significantly larger than decarbonization alone over this time frame. Our analysis demonstrates the need for a comprehensive CO2 and targeted non-CO2 mitigation approach to address both the near-term and long-term impacts of climate disruption.

Air pollutants, genetic susceptibility, and abdominal aortic aneurysm risk: a prospective study.

BACKGROUND AND AIMS: Air pollutants are important contributors to cardiovascular diseases, but associations between long-term exposure to air pollutants and the risk of abdominal aortic aneurysm (AAA) are still unknown. METHODS: This study was conducted using a sample of 449 463 participants from the UK Biobank. Hazard ratios and 95% confidence intervals for the risk of AAA incidence associated with long-term exposure to air pollutants were estimated using the Cox proportional hazards model with time-varying exposure measurements. Additionally, the cumulative incidence of AAA was calculated by using the Fine and Grey sub-distribution hazards regression model. Furthermore, this study investigated the combined effects and interactions between air pollutants exposure and genetic predisposition in relation to the risk of AAA onset. RESULTS: Long-term exposure to particulate matter with an aerodynamic diameter <2.5 µm [PM2.5, 1.21 (1.16, 1.27)], particulate matter with an aerodynamic diameter <10 µm [PM10, 1.21 (1.16, 1.27)], nitrogen dioxide [NO2, 1.16 (1.11, 1.22)], and nitrogen oxides [NOx, 1.10 (1.05, 1.15)] was found to be associated with an elevated risk of AAA onset. The detrimental effects of air pollutants persisted even in participants with low-level exposure. For the joint associations, participants with both high levels of air pollutants exposure and high genetic risk had a higher risk of developing AAA compared with those with low concentrations of pollutants exposure and low genetic risk. The respective risk estimates for AAA incidence were 3.18 (2.46, 4.12) for PM2.5, 3.09 (2.39, 4.00) for PM10, 2.41 (1.86, 3.13) for NO2, and 2.01 (1.55, 2.61) for NOx. CONCLUSIONS: In this study, long-term air pollutants exposure was associated with an increased risk of AAA incidence.

The NADH recycling enzymes TsaC and TsaD regenerate reducing equivalents for Rieske oxygenase chemistry.

Many microorganisms use both biological and nonbiological molecules as sources of carbon and energy. This resourcefulness means that some microorganisms have mechanisms to assimilate pollutants found in the environment. One such organism is Comamonas testosteroni, which metabolizes 4-methylbenzenesulfonate and 4-methylbenzoate using the TsaMBCD pathway. TsaM is a Rieske oxygenase, which in concert with the reductase TsaB consumes a molar equivalent of NADH. Following this step, the annotated short-chain dehydrogenase/reductase and aldehyde dehydrogenase enzymes TsaC and TsaD each regenerate a molar equivalent of NADH. This co-occurrence ameliorates the need for stoichiometric addition of reducing equivalents and thus represents an attractive strategy for integration of Rieske oxygenase chemistry into biocatalytic applications. Therefore, in this work, to overcome the lack of information regarding NADH recycling enzymes that function in partnership with Rieske non-heme iron oxygenases (Rieske oxygenases), we solved the X-ray crystal structure of TsaC to a resolution of 2.18 Å. Using this structure, a series of substrate analog and protein variant combination reactions, and differential scanning fluorimetry experiments, we identified active site features involved in binding NAD+ and controlling substrate specificity. Further in vitro enzyme cascade experiments demonstrated the efficient TsaC- and TsaD-mediated regeneration of NADH to support Rieske oxygenase chemistry. Finally, through in-depth bioinformatic analyses, we illustrate the widespread co-occurrence of Rieske oxygenases with TsaC-like enzymes. This work thus demonstrates the utility of these NADH recycling enzymes and identifies a library of short-chain dehydrogenase/reductase enzyme prospects that can be used in Rieske oxygenase pathways for in situ regeneration of NADH.

Genetic Susceptibility Modifies Relationships Between Air Pollutants and Stroke Risk: A Large Cohort Study.

BACKGROUND: The extent to which genetic susceptibility modifies the associations between air pollutants and the risk of incident stroke is still unclear. This study was designed to investigate the separate and joint associations of long-term exposure to air pollutants and genetic susceptibility on stroke risk. METHODS: The participants of this study were recruited by the UK Biobank between 2006 and 2010. These participants were followed up from the enrollment until the occurrence of stroke events or censoring of data. Hazard ratios (HRs) and 95% CIs for stroke events associated with long-term exposure to air pollutants were estimated by fitting both crude and adjusted Cox proportional hazards models. Additionally, the polygenic risk score was calculated to estimate whether the polygenic risk score modifies the associations between exposure to air pollutants and incident stroke. RESULTS: A total of 502 480 subjects were included in this study. After exclusion, 452 196 participants were taken into the final analysis. During a median follow-up time of 11.7 years, 11 334 stroke events were observed, with a mean age of 61.60 years, and men accounted for 56.2% of the total cases. Long-term exposures to particulate matter with an aerodynamic diameter smaller than 2.5 µm (adjusted HR, 1.70 [95% CI, 1.43-2.03]) or particulate matter with an aerodynamic diameter smaller than 10 µm (adjusted HR, 1.50 [95% CI, 1.36-1.66]), nitrogen dioxide (adjusted HR, 1.10 [95% CI, 1.07-1.12]), and nitrogen oxide (adjusted HR, 1.04 [95% CI, 1.02-1.05]) were pronouncedly associated with increased risk of stroke. Meanwhile, participants with high genetic risk and exposure to high air pollutants had ≈45% (31%, 61%; particulate matter with an aerodynamic diameter smaller than 2.5 µm), 48% (33%, 65%; particulate matter with an aerodynamic diameter smaller than 10 µm), 51% (35%, 69%; nitrogen dioxide), and 39% (25%, 55%; nitrogen oxide) higher risk of stroke compared with those with low genetic risk and exposure to low air pollutants, respectively. Of note, we observed additive and multiplicative interactions between genetic susceptibility and air pollutants on stroke events. CONCLUSIONS: Chronic exposure to air pollutants was associated with an increased risk of stroke, especially in populations at high genetic risk.

Prediagnostic serum concentrations of per- and polyfluoroalkyl substances and risk of papillary thyroid cancer in the Finnish Maternity Cohort.

Human exposure to per- and polyfluoroalkyl substances (PFAS) occurs globally through contaminated food, dust, and drinking water. Studies of PFAS and thyroid cancer have been limited. We conducted a nested case-control study of prediagnostic serum levels of 19 PFAS and papillary thyroid cancer (400 cases, 400 controls) in the Finnish Maternity Cohort (pregnancies 1986-2010; follow-up through 2016), individually matched on sample year and age. We used conditional logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) for log2 transformed and categorical exposures, overall and stratified by calendar period, birth cohort, and median age at diagnosis. We adjusted for other PFAS with Spearman correlation rho = 0.3-0.6. Seven PFAS, including perfluoroctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), N-ethyl-perfluorooctane sulfonamidoacetic acid (EtFOSAA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), and perfluorohexane sulfonic acid (PFHxS) were detected in >50% of women. These PFAS were not associated with risk of thyroid cancer, except for PFHxS, which was inversely associated (OR log2 = 0.82, 95% CI: 0.70-0.97). We observed suggestive but imprecise increased risks associated with PFOA, PFOS, and EtFOSAA for those diagnosed at ages <40 years, whereas associations were null or inverse among those diagnosed at 40+ years (P-interaction: .02, .08, .13, respectively). There was little evidence of other interactions. These results show no clear association between PFAS and papillary thyroid cancer risk. Future work would benefit from evaluation of these relationships among those with higher exposure levels and during periods of early development when the thyroid gland may be more susceptible to environmental harms.

Ambient Air Pollution and Depressed Mood in the National Longitudinal Study of Adolescent to Adult Health (Add Health) Wave IV.

Depression is a major contributor to the global burden of disease. There is limited understanding of how environmental exposures may contribute to depression etiology. We used Wave IV of the National Longitudinal Study of Adolescent to Adult Health (Add Health) to examine associations between low-level ambient air pollution exposure and depressed mood in a generally healthy population of over 10,000 24-32 year olds. Annual mean PM2.5 levels in the 2008-2009 study were close to the current U.S. standard. In fully adjusted quasi-binomial logistic regression models, there were no meaningful associations between IQR increases in air pollutant and change in depressed mood status regardless of specific pollutant or moving average lags. In interaction effects models, an IQR increase in lag day 0-30 PM2.5 resulted in 1.20 (95% CI, 1.02-1.41) times higher likelihood of having depressed mood, but only for persons with chronic lung disease (interaction P=0.04); the association was null for participants without chronic lung disease (OR 0.98, 95% CI, 0.91, 1.05). Our findings suggest that among persons with a lifetime history of chronic lung disease, greater exposure to even low-level PM2.5, PM10, and sulfate may be associated with modest increases in the likelihood of having depressed mood.

Large-scale genome-wide association studies reveal the genetic causal etiology between air pollutants and autoimmune diseases.

BACKGROUND: Epidemiological evidence links a close correlation between long-term exposure to air pollutants and autoimmune diseases, while the causality remained unknown. METHODS: Two-sample Mendelian randomization (TSMR) was used to investigate the role of PM10, PM2.5, NO2, and NOX (N = 423,796-456,380) in 15 autoimmune diseases (N = 14,890-314,995) using data from large European GWASs including UKB, FINNGEN, IMSGC, and IPSCSG. Multivariable Mendelian randomization (MVMR) was conducted to investigate the direct effect of each air pollutant and the mediating role of common factors, including body mass index (BMI), alcohol consumption, smoking status, and household income. Transcriptome-wide association studies (TWAS), two-step MR, and colocalization analyses were performed to explore underlying mechanisms between air pollution and autoimmune diseases. RESULTS: In TSMR, after correction of multiple testing, hypothyroidism was causally associated with higher exposure to NO2 [odds ratio (OR): 1.37, p = 9.08 × 10-4] and NOX [OR: 1.34, p = 2.86 × 10-3], ulcerative colitis (UC) was causally associated with higher exposure to NOX [OR: 2.24, p = 1.23 × 10-2] and PM2.5 [OR: 2.60, p = 5.96 × 10-3], rheumatoid arthritis was causally associated with higher exposure to NOX [OR: 1.72, p = 1.50 × 10-2], systemic lupus erythematosus was causally associated with higher exposure to NOX [OR: 4.92, p = 6.89 × 10-3], celiac disease was causally associated with lower exposure to NOX [OR: 0.14, p = 6.74 × 10-4] and PM2.5 [OR: 0.17, p = 3.18 × 10-3]. The risky effects of PM2.5 on UC remained significant in MVMR analyses after adjusting for other air pollutants. MVMR revealed several common mediators between air pollutants and autoimmune diseases. Transcriptional analysis identified specific gene transcripts and pathways interconnecting air pollutants and autoimmune diseases. Two-step MR revealed that POR, HSPA1B, and BRD2 might mediate from air pollutants to autoimmune diseases. POR pQTL (rs59882870, PPH4=1.00) strongly colocalized with autoimmune diseases. CONCLUSION: This research underscores the necessity of rigorous air pollutant surveillance within public health studies to curb the prevalence of autoimmune diseases.

Wastewater contaminants in a fractured bedrock aquifer and their potential use as enteric virus indicators.

Domestic wastewater is a source of persistent organic pollutants and pathogens to the aquatic environment, including groundwater aquifers. Wastewater contaminants include a variety of personal care products, pharmaceuticals, endocrine disrupters, bacteria, and viruses. Groundwater from 22 wells completed in a semi-confined to confined, fractured Silurian dolostone aquifer in southern Wellington County, Ontario, Canada, was analyzed for 14 organic wastewater contaminants (4 artificial sweeteners, 10 pharmaceuticals) as well as E. coli, total coliforms, and 6 human enteric viruses. Enteric viruses were detected in 8.6% of 116 samples, and at least one organic wastewater contaminant was detected in 82% of the wells (in order of decreasing detection frequency: acesulfame, ibuprofen, sulfamethoxazole, triclosan, carbamazepine, and saccharin). Virus indicator metrics [positive and negative predictive values (PPV, NPV), sensitivity, specificity] were calculated at the sample and well level for the organic wastewater compounds, E. coli, and total coliforms. Fecal bacteria were not good predictors of virus presence (PPV = 0%-8%). Of the potential chemical indicators, triclosan performed the best at the sample level (PPV = 50%, NPV = 100%), and ibuprofen performed the best at the well level (PPV = 60%, NPV = 67%); however, no samples had triclosan or ibuprofen concentrations above their practical quantification limits. Therefore, none of the compounds performed sufficiently well to be considered reliable for assessing the potential threat of enteric viruses in wastewater-impacted groundwater in this bedrock aquifer. Future studies need to evaluate the indicator potential of persistent organic wastewater contaminants in different types of aquifers, especially in fractured rock where heterogeneity is strong.IMPORTANCEAssessing the potential risk that human enteric viruses pose in groundwater aquifers used for potable water supply is complicated by several factors, including: (i) labor-intensive methods for the isolation and quantification of viruses in groundwater, (ii) the temporal variability of these viruses in domestic wastewater, and (iii) their potentially rapid transport in the subsurface, especially in fractured rock aquifers. Therefore, aquifer risk assessment would benefit from the identification of suitable proxy indicators of enteric viruses that are easier to analyze and less variable in wastewater sources. Traditional fecal indicators (e.g., E. coli and coliforms) are generally poor indicators of enteric viruses in groundwater. While many studies have examined the use of pharmaceutical and personal care products as tracers of domestic wastewater and fecal pollution in the environment, there is a paucity of data on the potential use of these chemical tracers as enteric virus indicators, especially in groundwater.

Structural and Electronic Factors Controlling the Efficiency and Rate of Intersystem Crossing to the Triplet State in Thiophene Polycyclic Derivatives.

Thiophene polycyclic derivatives are widely used in organic light-emitting diodes, photovoltaics, and medicinal chemistry applications. Understanding the electronic and structural factors controlling their intersystem crossing rates is paramount for these applications to be successful. This study investigates the photophysical, electronic structure, and excited state dynamics of 1,2-benzodiphenylene sulfide, benzo[b]naphtho[1,2-d]thiophene, and benzo[b]naphtho[2,3-d]thiophene in polar aprotic and non-polar solvents. Steady-state absorption and emission spectroscopy, femtosecond transient absorption spectroscopy, and DFT and TD-DFT calculations are employed. Low fluorescence quantum yields of 1.2 to 2.7% are measured in acetonitrile and cyclohexene, evidencing that the primary relaxation pathways in these thiophene derivatives are nonradiative. Linear interpolation of internal coordinates calculations predict that an S-C bond elongation reaction coordinate facilitates the efficient intersystem crossing to the T1 state. Excitation of 1,2-benzodiphenylene sulfide and benzo[b]naphtho[1,2-d]thiophene at 350 nm or benzo[b]naphtho[2,3-d]thiophene at 365 nm, populates the lowest-energy 1ππ* state, which relaxes to the 1ππ* minimum in tens of picoseconds or intersystem crosses to the triplet manifold in ca. 500 ps to 1.1 ns depending on the position at which the benzene rings are added. Excitation at 266 nm does not affect the intersystem crossing rates. Laser photodegradation experiments demonstrate that the thiophene polycyclic derivatives are highly photostable.

Treatment of agricultural wastewater using microalgae: A review.

The rapid development of agriculture has led to a large amount of wastewater, which poses a great threat to environmental safety. Microalgae, with diverse species, nutritional modes and cellular status, can adapt well in agricultural wastewater and absorb nutrients and remove pollutants effectively. Besides, after treatment of agricultural wastewater, the accumulated biomass of microalgae has broad applications, such as fertilizer and animal feed. This paper reviewed the current progresses and further perspectives of microalgae-based agricultural wastewater treatment. The characteristics of agricultural wastewater have been firstly introduced; Then the microalgal strains, cultivation modes, cellular status, contaminant metabolism, cultivation systems and biomass applications of microalgae for wastewater treatment have been summarized; At last, the bottlenecks in the development of the microalgae treatment methods, as well as recommendations for optimizing the adaptability of microalgae to wastewater in terms of wastewater pretreatment, microalgae breeding, and microalgae-bacterial symbiosis systems were discussed. This review would provide references for the future developments of microalgae-based agricultural wastewater treatment.

Establishment and validation of a prediction model for gestational diabetes.

AIM: To develop a visual prediction model for gestational diabetes (GD) in pregnant women and to establish an effective and practical tool for clinical application. METHODS: To establish a prediction model, the modelling set included 1756 women enrolled in the Zunyi birth cohort, the internal validation set included 1234 enrolled women, and pregnant women in the Wuhan cohort were included in the external validation set. We established a demographic-lifestyle factor model (DLFM) and a demographic-lifestyle-environmental pollution factor model (DLEFM) based on whether the women were exposed to environmental pollutants. The least absolute shrinkage and selection lasso-logistic regression analyses were used to identify the independent predictors of GD and construct a nomogram for predicting its occurrence. RESULTS: The DLEFM regression analysis showed that a family history of diabetes (odd ratio [OR] 2.28; 95% confidence interval [CI] 1.05-4.71), a history of GD in pregnant women (OR 4.22; 95% CI 1.89-9.41), being overweight or obese before pregnancy (OR 1.71; 95% CI 1.27-2.29), a history of hypertension (OR 2.61; 95% CI 1.41-4.72), sedentary time (h/day) (OR 1.16; 95% CI 1.08-1.24), monobenzyl phthalate (OR 1.95; 95% CI 1.45-2.67) and Q4 mono-ethyl phthalate concentration (OR 1.85; 95% CI 1.26-2.73) were independent predictors. The area under the receiver operating curves for the internal validation of the DLEFM and the DLFM constructed using these seven factors was 0.827 and 0.783, respectively. The calibration curve of the DLEFM was close to the diagonal line. The DLEFM was thus the more optimal model, and the one which we chose. CONCLUSIONS: A nomogram based on preconception factors was constructed to predict the occurrence of GD in the second and third trimesters. It provided an effective tool for the early prediction and timely management of GD.

Path analysis reveals combined winter climate and pollution effects on the survival of a marine top predator.

Marine ecosystems are experiencing growing pressure from multiple threats caused by human activities, with far-reaching consequences for marine food webs. Determining the effects of multiple stressors is complex, in part, as they can affect different aspects of biological organisation (behaviour, individual traits and demographic rates). Determining the combined effects of stressors, through different biological pathways, is key to predict the consequences for the viability of populations threatened by global change. Due to their position in the food chain, top predators such as seabirds are considered more sensitive to environmental changes. Climate change is affecting the prey resources available for seabirds, through bottom-up effects, while organic pollutants can bioaccumulate in food chains with the greatest impacts on top predators. However, knowledge of their combined effects on population dynamics is scarce. Using a path analysis, we quantify the effects of climate change and pollution on the survival of adult great black-backed gulls, both directly and through effects of individuals' body mass. Warmer ocean temperatures in gulls' winter foraging areas in the North Sea were correlated with higher survival, potentially explained by shifts in prey availability associated with global climate change. We also found support for indirect negative effects of organochlorines, highly toxic pollutants to seabirds, on survival, which acted, in part, through a negative effect on body mass. The results from this path analysis highlight how, even for such long-lived species where variance in survival tends to be limited, two stressors still have had a marked influence on adult survival and illustrate the potential of path models to improve predictions of population variability under multiple stressors.

The immunotoxicity mechanism of hemocytes in Chlamys farreri incubated with noradrenaline and benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide alone or in combination.

Benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE) is the active intermediate metabolite of benzo[a]pyrene (B[a]P) and is considered the ultimate immunotoxicant. The neuroendocrine immunoregulatory network of bivalves is affected under pollutant stress. Besides, bivalves are frequently affected by pollutants in marine environments, yet the combined effects of neuroendocrine factors and detoxification metabolites on bivalves under pollutant stress and the signal pathways that mediate this immunoregulation are not well understood. Therefore, we incubated the hemocytes of Chlamys farreri with the neuroendocrine factor noradrenaline (NA) and the B[a]P detoxification metabolite BPDE, alone or in combination, to examine the immunotoxic effects of NA and BPDE on the hemocytes in C. farreri. Furthermore, the effects of NA and BPDE on the hemocyte signal transduction pathway were investigated by assessing potential downstream targets. The results revealed that NA and BPDE, alone or in combination, resulted in a significant decrease in phagocytic activity, bacteriolytic activity and the total hemocyte count. In addition, the immunotoxicity induced by BPDE was further exacerbated by co-treatment with NA, and the two showed synergistic effects. Analysis of signaling pathway factors showed that NA activated G proteins by binding to α-AR, which transmitted information to the Ca2+-NF-κB signaling pathway to regulate the expression of phagocytosis-associated proteins and regulated cytokinesis through the cAMP signaling pathway. BPDE could activate PTK and affect phagocytosis and cytotoxicity proteins through Ca2+-NF-κB signal pathway, also affect the regulation of phagocytosis and cytotoxicity by inhibiting the AC-cAMP-PKA pathway to down-regulate the expression of NF-κB and CREB. In addition, BPDE and NA may affect the immunity of hemocytes by down-regulating phagocytosis-related proteins through inhibition of the lectin pathway, while regulating the expression of cytotoxicity-related proteins through the C-type lectin. In summary, immune parameters were suppressed through Ca2+ and cAMP dependent pathways exposed to BPDE and the immunosuppressive effects were enhanced by the neuroendocrine factor NA.

Porous rod-shaped Fe2O3/Ag/BP: a novel substrate for highly sensitive SERS detection of persistent organic pollutants.

A surface enhanced Raman scattering (SERS) substrate of porous rod-shaped ferric oxide (Fe2O3) combined with silver nanoparticles (Ag NPs) and black phosphorus (Fe2O3/Ag/BP) was fabricated to detect the persistent organic pollutants (POPs) at low concentration. The organic pollutant Rhodamine 6G (R6G) was used as the probe molecule to study the performances of Fe2O3/Ag/BP, and 4-chlorobiphenyl (PCB-3) was the target of detection. The limit of detection (LOD) of R6G based on this novel SERS substrate Fe2O3/Ag/BP was as low as 1.0 × 10-15M, which was five orders of magnitude lower than that of Fe2O3/Ag (10-10M). The enhancement factor (EF) of Fe2O3/Ag/BP was 6.44 × 108, which was 3.1 times higher than that of porous rod-shaped Fe2O3/Ag (2.08 × 108). The Raman signal of R6G based on Fe2O3/Ag/BP had a good homogeneity, and the relative standard deviation (RSD) of Raman signal intensities of R6G at 1643 cm-1was only 5.97%. Furthermore, the Fe2O3/Ag/BP substrate exhibited a recyclability through the photocatalytic degradation of R6G. The LOD of PCB-3 based on Fe2O3/Ag/BP was 10-9M. Besides, Fe2O3/Ag/BP had a high SERS activity even it was kept in a centrifuge tube without requiring complicated treatment. These results highlight the potential application of Fe2O3/Ag/BP for ultra-trace detection of POPs in the environment.

Biomarkers of Airway Disease, Barrett's and Underdiagnosed Reflux Noninvasively (BAD-BURN) in World Trade Center exposed firefighters: a case-control observational study protocol.

BACKGROUND: Particulate matter exposure (PM) is a cause of aerodigestive disease globally. The destruction of the World Trade Center (WTC) exposed first responders and inhabitants of New York City to WTC-PM and caused obstructive airways disease (OAD), gastroesophageal reflux disease (GERD) and Barrett's Esophagus (BE). GERD not only diminishes health-related quality of life but also gives rise to complications that extend beyond the scope of BE. GERD can incite or exacerbate allergies, sinusitis, bronchitis, and asthma. Disease features of the aerodigestive axis can overlap, often necessitating more invasive diagnostic testing and treatment modalities. This presents a need to develop novel non-invasive biomarkers of GERD, BE, airway hyperreactivity (AHR), treatment efficacy, and severity of symptoms. METHODS: Our observational case-cohort study will leverage the longitudinally phenotyped Fire Department of New York (FDNY)-WTC exposed cohort to identify Biomarkers of Airway Disease, Barrett's and Underdiagnosed Reflux Noninvasively (BAD-BURN). Our study population consists of n = 4,192 individuals from which we have randomly selected a sub-cohort control group (n = 837). We will then recruit subgroups of i. AHR only ii. GERD only iii. BE iv. GERD/BE and AHR overlap or v. No GERD or AHR, from the sub-cohort control group. We will then phenotype and examine non-invasive biomarkers of these subgroups to identify under-diagnosis and/or treatment efficacy. The findings may further contribute to the development of future biologically plausible therapies, ultimately enhance patient care and quality of life. DISCUSSION: Although many studies have suggested interdependence between airway and digestive diseases, the causative factors and specific mechanisms remain unclear. The detection of the disease is further complicated by the invasiveness of conventional GERD diagnosis procedures and the limited availability of disease-specific biomarkers. The management of reflux is important, as it directly increases risk of cancer and negatively impacts quality of life. Therefore, it is vital to develop novel noninvasive disease markers that can effectively phenotype, facilitate early diagnosis of premalignant disease and identify potential therapeutic targets to improve patient care. TRIAL REGISTRATION: Name of Primary Registry: "Biomarkers of Airway Disease, Barrett's and Underdiagnosed Reflux Noninvasively (BADBURN)". Trial Identifying Number: NCT05216133 . Date of Registration: January 31, 2022.

Exposure Pathways and Toxicity of Microplastics in Terrestrial Insects.

The detrimental effects of plastics on aquatic organisms, including those of macroplastics, microplastics, and nanoplastics, have been well established. However, knowledge on the interaction between plastics and terrestrial insects is limited. To develop effective strategies for mitigating the impact of plastic pollution on terrestrial ecosystems, it is necessary to understand the toxicity effects and influencing factors of plastic ingestion by insects. An overview of current knowledge regarding plastic ingestion by terrestrial insects is provided in this Review, and the factors influencing this interaction are identified. The pathways through which insects interact with plastics, which can lead to plastic accumulation and microplastic transfer to higher trophic levels, are also discussed using an overview and a conceptual model. The diverse impacts of plastic exposure on insects are discussed, and the challenges in existing studies, such as a limited focus on certain plastic types, are identified. Further research on standardized methods for sampling and analysis is crucial for reliable research, and long-term monitoring is essential to assess plastic trends and ecological impacts in terrestrial ecosystems. The mechanisms underlying these effects need to be uncovered, and their potential long-term consequences for insect populations and ecosystems require evaluation.

Quantifying 209 Polychlorinated Biphenyl Congeners in Silicone Wristbands to Evaluate Differences in Exposure among Demolition Workers.

A social housing estate in Denmark was designated for demolition due to exceedance of guidance values for polychlorinated biphenyls (PCBs) in indoor air. Here, we deployed precleaned silicone wristbands (n = 46) among demolition workers of these contaminated buildings during single workdays while conducting various work tasks. We established a method to analyze all 209 PCBs in wristbands to identify prominent congeners of exposure and evaluate differences between tasks. Wristbands were extracted using microwave-assisted extraction and then concentrated for gas chromatography-tandem mass spectrometry (GC-MS/MS) analysis. Twenty-nine chromatographic peaks representing 37 congeners were detected in every wristband, and tetra-CBs were the dominant homologue group. PCB-66, -44, and -70 were the most abundant congeners measured in worker wristbands, none of which are included within the typical seven indicator or WHO 12 PCBs. Workers who cut PCB-containing sealants had wristbands with the highest PCB concentrations (geometric mean ∑209PCBs = 1963 ng/g wristband), which were followed by those handling concrete elements on the building roof. Additionally, wristbands captured a broader range of PCBs than has been previously measured in air and serum samples. Taken together, our results highlight the importance of total congener analysis in assessing current PCB exposure in demolition work and the utility of wristbands for assessing these exposures.

Associations between air pollutants and acute exacerbation of drug-resistant tuberculosis: evidence from a prospective cohort study.

BACKGROUND: Short-term exposure to air pollution may trigger symptoms of drug-resistant tuberculosis (DR-TB) through stimulating lung tissue, damaging tracheobronchial mucosa, the key anti-mycobacterium T cell immune function, and production and release of inflammatory cytokines. OBJECTIVE: To investigate the association between acute exacerbations of DR-TB and short-term residential exposure to air pollutants (PM10, PM2.5, SO2, NO2, CO and O3) based on a large prospective cohort in Anhui Province, China. METHOD: Patients were derived from a prospective cohort study of DR-TB in Anhui Province. All DR-TB patients underwent drug-susceptibility testing and prefecture-level reference laboratories confirmed their microbiologies. The case-crossover design was performed to evaluate the association between the risk of acute exacerbations of DR-TB and short-term residential exposure to air pollution. RESULTS: Short-term NO2 exposure was significantly related to an elevated risk of first-time outpatient visit due to acute exacerbations of DR-TB(relative risk:1.159, 95% confidence interval:1.011 ~ 1.329). Stratification analyses revealed that the relationship between the risk of acute exacerbations and NO2 exposure was stronger in the elderly (age ≥ 65) DR-TB patients, and in individuals with a history of TB treatment. CONCLUSIONS: NO2 Exposure was significantly associated with an elevated risk of acute exacerbation of DR-TB in Anhui Province, China.