Mechanistic insights into hormesis induced by erythromycin in the marine alga Thalassiosira weissflogii.

Erythromycin (ERY) is a typical macrolide antibiotic with large production and extensive use on a global scale. Detection of ERY in both freshwaters and coaster seawaters, as well as relatively high ecotoxicity of ERY have been documented. Notably, hormesis has been reported on several freshwater algae under ERY stress, where growth was promoted at relatively lower exposures but inhibited at higher treatment levels. On the contrary, there is limited information of ERY toxicity in marine algae, hampering the risk assessment on ERY in the coaster waters. The presence of hormesis may challenge the current concept of dose-response adopted in chemical risk assessment. Whether and how exposure to ERY can induce dose-dependent toxicity in marine algae remain virtually unknown, especially at environmentally relevant concentrations. The present study used a model marine diatom Thalassiosira weissflogii (T. weissflogii) to reveal its toxicological responses to ERY at different biological levels and decipher the underlying mechanisms. Assessment of multiple apical endpoints shows an evident growth promotion following ERY exposure at an environmentally relevant concentration (1 µg/L), associated with increased contents reactive oxygen species (ROS) and chlorophyll-a (Chl-a), activated signaling pathways related to ribosome biosynthesis and translation, and production of total soluble protein. By contrast, growth inhibition in the 750 and 2500 µg/L treatments was attributed to reduced viability, increased ROS formation, reduced content of total soluble protein, inhibited photosynthesis, and perturbed signaling pathways involved in xenobiotic metabolism, ribosome, metabolism of amino acid, and nitrogen metabolism. Measurements of multiple apical endpoints coupled with de novo transcriptomics analysis applied in the present study, a systems biology approach, can generate detailed mechanistic information of chemical toxicity including dose-response and species sensitivity difference used in environmental risk assessment.

Low-level ambient sulfur dioxide exposure and genetic susceptibility associated with incidence of idiopathic pulmonary fibrosis: A national prospective cohort study.

BACKGROUND: The association between long-term air pollution exposure and the development of idiopathic pulmonary fibrosis (IPF) has been established, but the evidence regarding the effect of low levels of air pollution, especially ambient sulfur dioxide (SO2), is limited. Besides, the combined effect and interaction between genetic susceptibility and ambient SO2 on IPF remain uncertain. METHODS: This study retrieved data from 402,042 participants who were free of IPF at baseline in the UK Biobank. The annual mean concentration of ambient SO2 was estimated for each participant based on their residential addresses using a bilinear interpolation method. Cox proportional hazard models were used to examine the relationship between ambient SO2 and incident IPF. We further generated a polygenic risk score (PRS) for IPF and estimated the combined effects of genetic susceptibility and ambient SO2 on incident IPF. RESULTS: After a median follow-up of 11.78 years, 2562 cases of IPF were identified. The results indicated that each 1 µg/m3 increase in ambient SO2 was associated with a hazard ratio (HR) (95% confidence interval [CI]) of 1.67 (1.58, 1.76) for incident IPF. The study found statistically significant synergistic additive interaction between genetic susceptibility and ambient SO2. Individuals with high genetic risk and high ambient SO2 exposure had a higher risk of developing IPF (HR = 7.48, 95% CI:5.66, 9.90). CONCLUSION: The study suggests that long-term exposure to ambient SO2, even at concentrations lower than current air quality guidelines set by the Word Health Organization and European Union, may be an important risk factor for IPF. This risk is more pronounced among people with a high genetic risk. Therefore, these findings emphasize the need to consider the potential health effects of SO2 exposure and the necessity for stricter air quality standards.

Dynamic association of ambient air pollution with incidence and mortality of pulmonary hypertension: A multistate trajectory analysis.

BACKGROUND: There is little evidence regarding the association between ambient air pollution and incidence and the mortality of pulmonary hypertension (PH). METHODS: We included 494,750 participants at baseline in the UK Biobank study. Exposures to PM2.5, PM10, NO2, and NOx were estimated at geocoded participants' residential addresses, utilizing pollution data provided by UK Department for Environment, Food and Rural Affairs (DEFRA). The outcomes were the incidence and mortality of PH. We used multivariate multistate models to investigate the impacts of various ambient air pollutants on both incidence and mortality of PH. RESULTS: During a median follow-up of 11.75 years, 2517 participants developed incident PH, and 696 died. We observed that all ambient air pollutants were associated with increased incidence of PH with different magnitudes, with adjusted hazard ratios (HRs) [95% confidence intervals (95% CIs)] for each interquartile range (IQR) increase of 1.73 (1.65, 1.81) for PM2.5, 1.70 (1.63, 1.78) for PM10, 1.42 (1.37, 1.48) for NO2, and 1.35 (1.31, 1.40) for NOx. Furthermore, PM2.5, PM10, NO2 and NO2 influenced the transition from PH to death, and the corresponding HRs (95% CIs) were 1.35 (1.25, 1.45), 1.31 (1.21, 1.41), 1.28 (1.20, 1.37) and 1.24 (1.17, 1.32), respectively. CONCLUSION: The results of our study indicate that exposure to various ambient air pollutants might play key but differential roles in both the incidence and mortality of PH.

Strengthened public awareness of one health to prevent zoonosis spillover to humans.

The COVID-19 outbreak has forced the world to rethink the interconnected health of humans and nature, i.e. One Health (OH). However, the current sector-technology-based solutions have a high cost. We propose a human-oriented One Health (HOH) concept to restrain the unsustainable behaviors of natural resource exploitation and consumption, which may trigger original zoonosis spillover from an imbalanced natural ecosystem. HOH can complement a nature-based solution (NBS), where the former refers to the unknown part of nature, while the latter is based on already known natural knowledge. Additionally, a systemic analysis of popular Chinese social media during the pandemic outbreak (January 1-March 31, 2020) revealed that the wide public was influenced by OH thought. In the post-pandemic era, it is time to deepen public awareness of HOH to guide the world onto a more sustainable track and prevent more serious zoonosis spillover in the future.

Exposure to Air Pollution during Pre-Hypertension and Subsequent Hypertension, Cardiovascular Disease, and Death: A Trajectory Analysis of the UK Biobank Cohort.

BACKGROUND: The associations between air pollution exposure and morbidity and mortality of cardiovascular diseases (CVDs) have been widely reported; however, evidence on such associations across different dynamic disease trajectories remain unknown. OBJECTIVE: We examined whether ambient air pollution during the prehypertension (pre-HTN) stage could aggravate the progression from hypertension (HTN) to CVD, and consequent death. METHODS: A total of 168,010 adults with pre-HTN (120-139 mmHg systolic blood pressure or 80-89 mmHg diastolic blood pressure) from the UK Biobank were included in this analysis. We used a multistate model to explore the associations between five air pollutants (PM2.5, PM2.5 absorbance, PM10, NO2, and NOx) and the risk of six disease transitions (from pre-HTN to HTN, from pre-HTN to CVD, from pre-HTN to death, from HTN to CVD, from HTN to death, and from CVD to death). Mediation analyses were further conducted to explore the role of intermediate diseases in the dynamic progression of CVDs. RESULTS: During a median follow-up of 12 y, 13,743 (8.18%) of participants with pre-HTN developed HTN, whereas 12,825 (7.63%) and 4,467 (2.66%) directly developed CVD or died, respectively. Air pollution was positively associated with the dynamic disease progression. For example, a per-interquartile range increase of PM2.5 was significantly associated with the hazard ratios (HRs) of 1.105 [95% confidence intervals (CI): 1.083, 1.127], 1.045 (95% CI: 1.022, 1.068), and 1.086 (95% CI: 1.047, 1.126) in the transition from pre-HTN to HTN, CVD, and death, respectively. Higher levels of air pollution were associated with increased transition probability of disease progression. Mediation analyses indicated that intermediate diseases subsequently significantly mediated air pollutant-associated risk to develop more serious disease. CONCLUSIONS: This study provides evidence that air pollution might play a role in the early stages of CVD progression. Controlling air pollution might be an effective measure to prevent CVD progression and reduce the disease burden of CVD. https://doi.org/10.1289/EHP10967.

Ambient air pollution, bone mineral density and osteoporosis: Results from a national population-based cohort study.

Evidence concerning the associations of ambient air pollution exposure with bone mineral density and osteoporosis has been mixed. We conducted cross-sectional and prospective analysis of the associations between air pollution exposure and osteoporosis using data from UK Biobank study. Estimated bone mineral density (eBMD) of each participant at baseline survey was calculated using quantitative ultrasound data, and incident osteoporosis cases were identified during the follow-up period according to health-related records. Air pollution concentrations were assessed using land use regression models. We fitted multivariable linear and logistic regression models to estimate the associations of air pollution with eBMD and osteoporosis prevalence at baseline. We applied cox proportional hazard regression models to assess the relationships between air pollution and osteoporosis incidence. Among the 341,311 participants at baseline, higher air pollution exposure was associated with lower eBMD levels and increased odds of osteoporosis prevalence. For example, an IQR increase in PM2.5, PM2.5 absorbance, PM10, NO2 and NOx levels were associated with 0.0018 (95% CI: 0.0012, 0.0023) to 0.0052 (95% CI: 0.0046, 0.0058) g/cm2 decrease in eBMD. A total of 330,988 participants without osteoporosis were followed up for an average of 12.0 years. We identified 8105 incident osteoporosis cases (456 cases with pathological fracture and 7634 cases without pathological fracture) during the follow-up. The hazard ratios for an interquartile range increase in PM2.5, PM2.5 absorbance, PM10, NO2 and NOx were 1.09 (95% CI: 1.06, 1.12), 1.04 (95% CI: 1.02, 1.07), 1.04 (95% CI: 1.01, 1.07), 1.07 (95% CI: 1.04, 1.10), and 1.06 (95% CI: 1.03, 1.09), respectively. Our study suggests that ambient air pollution might be a risk factor of decreased bone mineral density and osteoporosis incidence.

Screening of structural and functional alterations in duckweed (Lemna minor) induced by per- and polyfluoroalkyl substances (PFASs) with FTIR spectroscopy.

As a class of common emerging pollutants, per- and polyfluoroalkyl substances (PFASs) and their alternatives have been widely detected in various environmental matrices, exhibiting a great threat to the ecological environment and human health. Nevertheless, changes in biomolecular structure and function of duckweed caused by PFASs and their alternatives remain unknown thus far. Herein, the effects of four PFASs, including two common legacy PFASs (perfluorooctane sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA)) and two PFASs alternatives (perfluorobutane sulfonic acid (PFBS) and 1H,1H,2H, 2H-perfluorooctane sulfonic acid (6:2 FTS)) on duckweed (Lemna minor) at biochemical level were investigated with Fourier transform infrared spectroscopy (FTIR). Although no obvious inhibitions were observed in the growth of L. minor with PFASs exposure at three levels of 1 µg L-1, 100 µg L-1, and 10 mg L-1, significant structural and functional alterations were induced at the biochemical level. In response to PFASs exposure, lipid peroxidation, proteins aggregation and α-helix to ß-sheet transformation of the protein conformation, as well as changes of DNA conformations were detected. Moreover, alterations in lipid, protein, and DNA were proved to be concentration-related and compound-specific. Compared to the two legacy PFASs (PFOS and PFOA), alternative ones exhibited greater effects on the biological macromolecules of L. minor. The findings of this study firstly reveal structural and functional alterations in L. minor induced by PFASs exposure, providing further understanding of their toxicity effects.

Improving cleaner production of human activities to mitigate total petroleum hydrocarbons accumulation in coastal environment.

The marine coast is an important ecological transitional boundary but easily suffers from human intervention. Total petroleum hydrocarbons (TPHs) are ubiquitous along the coast. However, the influence of anthropogenic and natural factors on TPHs distribution remains unclear. This study sampled surficial sediment (N = 243) from the coasts of the largest peninsula-Leizhou Peninsula, in Southern China. We found that land-based discharge, sea traffic, and sediment type significantly (p < 0.05) drive the accumulation of TPHs. We observed that TPHs increased by 1.036 µg · g-1 (exp[αi] = exp. [0.0355]) of its original value with the addition of one more boat on the wharf. Although the average TPHs were at a moderate level (124.68, ND-1536.14, µg · g-1) and risk, 'Blue Carbon' ecosystems, i.e., mangroves (224.84, ND - 1441.13, µg · g-1, p < 0.001) were more severely polluted. Cleaner production policy should be applied to mitigate TPHs discharging trend from coastal areas.

Histone Deacetylase Inhibitor Panobinostat Benefits the Therapeutic Efficacy of Oncolytic Herpes Simplex Virus Combined with PD-1/PD-L1 Blocking in Glioma and Squamous Cell Carcinoma Models.

BACKGROUND: Combination therapy has been widely explored for oncolytic virus (OV), as it can be met with tumor resistance. The HDAC inhibitor (HDACi) panobinostat is a potent pan-deacetylase inhibitor which blocks multiple cancer-related pathways and reverses epigenetic events in cancer progression. METHODS: In this study, oncolytic activity in vitro and antitumor therapeutic efficacy in vivo when combined with oHSV and panobinostat were investigated. RESULTS: (1) Treatment with panobinostat enhanced oHSV propagation and cytotoxicity in human glioma A172 and squamous cell carcinoma SCC9 cells. (2) Combined treatment with oHSV and panobinostat enhanced virus replication mediated by the transcriptional downregulation of IFN-ß- and IFN-responsive antiviral genes in human glioma A172 and squamous cell carcinoma SCC9 cells. (3) Panobinostat treatment induced upregulation of PD-L1 expression in both glioma and squamous cell carcinoma cells. (4) A significantly enhanced therapeutic efficacy was shown in vivo for the murine glioma CT-2A and squamous cell carcinoma SCC7 models when treated with a combination of oHSV, including PD-1/PD-L1 blockade and HDAC inhibition. CONCLUSIONS: Consequently, these data provide some new clues for the clinical development of combination therapy with OVs, epigenetic modifiers, and checkpoint blockades for glioma and squamous cell carcinoma.

Ambient air pollution associated with incidence and dynamic progression of type 2 diabetes: a trajectory analysis of a population-based cohort.

BACKGROUND: Though the association between air pollution and incident type 2 diabetes (T2D) has been well documented, evidence on the association with development of subsequent diabetes complications and post-diabetes mortality is scarce. We investigate whether air pollution is associated with different progressions and outcomes of T2D. METHODS: Based on the UK Biobank, 398,993 participants free of diabetes and diabetes-related events at recruitment were included in this analysis. Exposures to particulate matter with a diameter ≤ 10 µm (PM10), PM2.5, nitrogen oxides (NOx), and NO2 for each transition stage were estimated at each participant's residential addresses using data from the UK's Department for Environment, Food and Rural Affairs. The outcomes were incident T2D, diabetes complications (diabetic kidney disease, diabetic eye disease, diabetic neuropathy disease, peripheral vascular disease, cardiovascular events, and metabolic events), all-cause mortality, and cause-specific mortality. Multi-state model was used to analyze the impact of air pollution on different progressions of T2D. Cumulative transition probabilities of different stages of T2D under different air pollution levels were estimated. RESULTS: During the 12-year follow-up, 13,393 incident T2D patients were identified, of whom, 3791 developed diabetes complications and 1335 died. We observed that air pollution was associated with different progression stages of T2D with different magnitudes. In a multivariate model, the hazard ratios [95% confidence interval (CI)] per interquartile range elevation in PM2.5 were 1.63 (1.59, 1.67) and 1.08 (1.03, 1.13) for transitions from healthy to T2D and from T2D to complications, and 1.50 (1.47, 1.53), 1.49 (1.36, 1.64), and 1.54 (1.35, 1.76) for mortality risk from baseline, T2D, and diabetes complications, respectively. Generally, we observed stronger estimates of four air pollutants on transition from baseline to incident T2D than those on other transitions. Moreover, we found significant associations between four air pollutants and mortality risk due to cancer and cardiovascular diseases from T2D or diabetes complications. The cumulative transition probability was generally higher among those with higher levels of air pollution exposure. CONCLUSIONS: This study indicates that ambient air pollution exposure may contribute to increased risk of incidence and progressions of T2D, but to diverse extents for different progressions.

Associations between conjunctivitis and ambient PM2.5 and physical activity: A nationwide prospective cohort study.

BACKGROUND: Currently, there is no evidence of fine particulate matter pollution (PM2.5) altering the relationship between physical activity (PA) and the risk of conjunctivitis. METHODS: Based on the UK Biobank study, we included 308,507 participants aged 40-69 years at baseline (2006 to 2010) and prospectively followed up for conjunctivitis diagnosis till 2020. Annual concentrations of PM2.5 in 2010 were estimated for each participant using Land Use Regression models. PA levels during work and leisure time were reported via the International Physical Activity Questionnaire at baseline. We used Cox proportional hazards models to examine the associations of PM2.5 and PA with incident conjunctivitis, as well as their interaction at both multiplicative and additive scales. RESULTS: During the 11.6 years of follow up, we identified 4002 incident conjunctivitis cases. High-PA (≥3000 metabolic equivalent of task [MET]-mins/week) was associated with lower risk of conjunctivitis (hazard ratio [HR]: 0.79, 95% confidence interval [CI]: 0.73-0.86) compared to low-PA (0 to <600 MET-mins/week), while every 1 µg/m3 increment in PM2.5 was associated with a 16% higher risk of conjunctivitis (HR = 1.16, 95% CI: 1.09-1.23). We did not observe statistically significant interactions between PM2.5 and PA on their associations with conjunctivitis. CONCLUSION: Habitual PA and PM2.5 exposure were oppositely related to incident conjunctivitis. The benefits of PA remain in people irrespective of exposure to air pollution.

How does bivalve size influence microplastics accumulation?

Microplastics (wasted plastic particles < 5 mm in diameter) are ubiquitously distributed in the marine environment. Filter-feeding and low trophic level bivalves are vulnerable to microplastics accumulation from the surrounding depositional environment, thereby threatening both ecological health and human food safety. Microplastics had been detected in lots of coastal Bivalvia species. However, the influence of biological morphology on the mechanism of microplastics accumulation is not clear. There is also a knowledge gap of which species are preferred for commercial consumption, which creates loopholes in risk identification for food safety. A survey on a commercial popular eaten but under-researched hard clam (Meretrix meretrix; Linnaeus, 1758) from a famous fishery port city in southern China was carried out to comprehensively analyze shell size influence on microplastics accumulation in bivalves and consequently, human intake risk via bivalve consumption. Detected microplastics count in per individual (MCI) was 24.64 ± 19.11 items · individual-1, and microplastics count per gram (MCG; wet weight with shell) was 0.66 ± 0.54 items · g-1. When the shell width grew by 1 mm, MCI increased by 1.01 times, but MCG decreased by 0.97 times. Dominant microplastics characteristics found in this study was fiber and fragment. Sizes ranged from 25 to 150 µm, and dark colors (black, red, and blue) were found. The mostly common polymers were polyethene (PE, 40%), polyethylene terephthalate (PET, 23%), and polypropylene (PP, 18%). Estimated annual intake (EAI) risk of microplastics via hard clam consumption by residents was 6652.26 ± 5327.28 items · year -1 · person -1. The microplastics in bivalves and EAI was relatively high. When shell width grew by 1 mm, EAI decreased by 0.97 times. Therefore, eating a fixed amount of larger hard clams with a relatively low amount of microplastics can reduce EAI risk for consumers. A systematic investigation of emission sources along main coast, where bivalve production is prominent will be useful for food safety control in this region.

Population attributable fraction of lung cancer due to genetic variants, modifiable risk factors, and their interactions: a nationwide prospective cohort study.

BACKGROUND: Genetic variants and modifiable risk factors (including environmental exposure and lifestyle) greatly contribute to the development of lung cancer. The population attributable fraction (PAF) of these risk factors, especially their interactive effects, has not been well quantified. METHODS: A total of 398,577 participants were included in this analysis. There were 2504 incident lung cancer cases identified over an average 10.4-year follow-up. We applied Cox proportional hazards models to examine the associations between risk factors and incident lung cancer. We further developed a polygenic risk score and evaluated whether environmental factors modified the effect of genetic risk on incident lung cancer. Furthermore, we calculated the PAF for each risk factor, as well as their gene-environment additive interaction, and then combined them to create a weighted PAF that takes into consideration participants with overlapping risk factors. RESULTS: Our analysis showed that smoking was the leading risk factor for lung cancer with a PAF of 63.73%. We observed additive interactions between smoking, PM2.5, NOx, and genetic risk, with PAFs of 17.85% (smoking-high genetic risk interaction), 10.79% (smoking-intermediate genetic risk interaction), 5.30% (NOx-high genetic risk interaction), 6.55% (PM2.5-high genetic risk interaction), and 4.99% (PM2.5-intermediate genetic risk interaction). We estimated that 73.46% of lung cancer cases could be attributable to potentially modifiable risk factors after adjusting for the correlation between them. CONCLUSION: High genetic risk and several modifiable factors may increase the risk of incident lung cancer. Participants with a high genetic risk may be more vulnerable to developing lung cancer if exposed to smoking and/or high air pollution. Our findings provide evidence that the majority of incident lung cancer cases could be prevented by eliminating modifiable risk factors.

Comparison of 19 major infectious diseases during COVID-19 epidemic and previous years in Zhejiang, implications for prevention measures.

BACKGROUND: The global pandemic of coronavirus disease 2019 (COVID-19) has attracted great public health efforts across the world. Few studies, however, have described the potential impact of these measures on other important infectious diseases. METHODS: The incidence of 19 major infectious diseases in Zhejiang Province was collected from the National Notifiable Infectious Disease Surveillance System from January 2017 to October 2020. The entire epidemic control phase was divided into three stages. The government deployed the first level response from 24 January to 2 March (the most rigorous measures). When the outbreak of COVID-19 was under control, the response level changed to the second level from 3 to 23 March, and then the third level response was implemented after 24 March. We compared the epidemiological characteristics of 19 major infectious diseases during different periods of the COVID-19 epidemic and previous years. RESULTS: A total of 1,814,881 cases of 19 infectious diseases were reported in Zhejiang from January 2017 to October 2020, resulting in an incidence rate of 8088.30 cases per 1,000,000 person-years. After the non-pharmaceutical intervention, the incidence of 19 infectious diseases dropped by 70.84%, from 9436.32 cases per 1,000,000 person-years to 2751.51 cases per 1,000,000 person-years, with the large decrease in the first response period of influenza. However, we observed that the daily incidence of severe fever with thrombocytopenia syndrome (SFTS) and leptospirosis increased slightly (from 1.11 cases per 1,000,000 person-years to 1.82 cases per 1,000,000 person-years for SFTS and 0.30 cases per 1,000,000 person-years to 1.24 cases per 1,000,000 person-years for leptospirosis). There was no significant difference in the distribution of epidemiological characteristic of most infectious diseases before and during the implementation of COVID-19 control measures. CONCLUSION: Our study summarizes the epidemiological characteristics of 19 infectious diseases and indicates that the rigorous control measures for COVID-19 are also effective for majority of infectious diseases.

Risk/benefit tradeoff of habitual physical activity and air pollution on chronic pulmonary obstructive disease: findings from a large prospective cohort study.

BACKGROUND: The combined health impact of physical activity (PA) and air pollution on chronic obstructive pulmonary disease (COPD) remains unclear. We investigated the joint effects of habitual PA and long-term fine particulate matter (PM2.5) exposure on COPD incidence in a prospective population-based cohort. METHODS: A prospective cohort study was conducted using data from the UK Biobank. Incidence of COPD was ascertained through linkage to the UK National Health Services register. Annual mean PM2.5 concentration was obtained using land use regression model. PA was measured by questionnaire and wrist-worn accelerometer. Cox proportional hazard models were applied to examine the associations between PM2.5, PA, and COPD. Additive and multiplicative interactions were examined. RESULTS: A total of 266,280 participants free of COPD at baseline were included in data analysis with an average follow-up of 10.64 years, contributing to around 2.8 million person-years. Compared with participants with low level of PA, those with higher PA levels had lower risks of COPD incidence [hazard ratio (HR): 0.769, 95% CI: 0.720, 0.820 for moderate level; HR: 0.726, 95% CI: 0.679, 0.776 for high level]. By contrast, PM2.5 was associated with increased risk of COPD (HR per interquartile range increment: 1.065, 95% CI: 1.032, 1.099). Limited evidence of interaction between habitual PA and PM2.5 exposure was found. Similar results were found for accelerometer-measured PA. CONCLUSIONS: Our study suggests that habitual PA could reduce risk of COPD incidence, and such protective effects were not affected by ambient PM2.5 pollution exposure.

Linking human activity to spatial accumulation of microplastics along mangrove coasts.

Microplastics (MP) in mangrove coasts are threating ecological health and seafood safety. However, quantitative evidence on the effects of different coastal human activities on microplastic accumulation in mangrove sediments is lacking, thereby impeding the policy development of evidence-based waste management. In this study, continuous geographical sampling (N = 50) was applied to collect sediments from the largest mangrove coast, namely the Leizhou Peninsula in China. Similar worldwide research data (16 mangrove coasts) were collected from the Science Citation Index Expanded (SCIE) database of the Web of Science. The connections between human drivers and microplastic accumulation were evaluated by spatial comparison, multi-correspondence analysis, and multiple differences analysis. The microplastic abundance fluctuated widely along the mangrove coasts (average value was 51.24, ranged from 6.40 to 255.57 items·kg-1 dry weight; coefficient of variation = 97%) with a globally lower-middle concentration in sediments of the Leizhou Peninsula. Densely populated urban residents and the floating population of tourists largely contributed to the high abundance of microplastics in mangrove sediments, of which large-sized (1-5 mm) white foams were the dominant type. Although suburbs had less crowds, both onshore and offshore fishery production could cause high accumulation of microplastics in neighboring mangrove coasts, which were characterized by small-sized (<1 mm) fragments with fresh color. Small microplastics (80%) with fresh color (44%) were dominant. Weathering may break down more toxic particles in urban areas neighboring mangrove coasts. Larger mangrove patches could partly block ocean-based microplastics; however, coasts surrounded by more geographical barriers had intensified pollutant accumulation. It was suggested that foam packaging of commodities for urban residents and tourists in popular tourism areas should be reduced and restrictions of fishery waste plastics are needed along shores with mangroves, especially in coasts surrounded by more geographic barriers.

Global burden of chronic obstructive pulmonary disease attributable to ambient particulate matter pollution and household air pollution from solid fuels from 1990 to 2019.

We aimed to estimate the spatiotemporal trends in the global burden of chronic obstructive pulmonary disease (COPD) attributable to both household air pollution from solid fuels (HAP) and ambient particulate matter (APM) from 1990 to 2019 and compared the possible differences between the burdens attributable to APM and HAP. The number of deaths, disability-adjusted life-years (DALYs), and years of life lost (YLLs) of COPD attributable to HAP from solid fuels and APM during 1990-2019 were extracted from the Global Burden of Diseases Study 2019. The proportion of YLLs in DALYs and average YLLs per COPD death were also calculated. Subgroup analyses by sex, age, and socio-demographic index (SDI) were conducted. The estimated annual percentage change (EAPC) was used to assess the temporal trend of age-standardized rate of mortality (ASMR) and DALYs (ASDR). Over the past 30 years, we observed a clear downward trend in COPD deaths attributable to HAP and an upward trend by 97.61% in COPD deaths attributable to APM. The global COPD burden attributable to APM in 2019 was higher than those due to HAP, except in low-SDI regions. For both HAP and APM, YLLs continued to predominate in DALYs of COPD, with an average YLLs per death of more than 10 years in different regions. The ASMR was higher in males and lower in high-SDI regions. The ASMR and ASDR attributable to HAP decreased globally in all age groups during 1990-2019, while those attributable to APM increased among people older than 80 years and in regions with lower SDI. Our study reveals an increasing trend in APM-attributable COPD burden over the past three decades. Comparatively, the global burden due to HAP decreased markedly, but it was still pronounced in low-SDI regions. Continued efforts on PM mitigation are needed for COPD prevention.