ABSTRACT
BACKGROUND: Extreme temperature events (ETEs), including heat wave and cold spell, have been linked to myocardial infarction (MI) morbidity; however, their effects on MI mortality are less clear. Although ambient fine particulate matter (PM2.5) is suggested to act synergistically with extreme temperatures on cardiovascular mortality, it remains unknown if and how ETEs and PM2.5 interact to trigger MI deaths. METHODS: A time-stratified case-crossover study of 202 678 MI deaths in Jiangsu province, China, from 2015 to 2020, was conducted to investigate the association of exposure to ETEs and PM2.5 with MI mortality and evaluate their interactive effects. On the basis of ambient apparent temperature, multiple temperature thresholds and durations were used to build 12 ETE definitions. Daily ETEs and PM2.5 exposures were assessed by extracting values from validated grid datasets at each subject's geocoded residential address. Conditional logistic regression models were applied to perform exposure-response analyses and estimate relative excess odds due to interaction, proportion attributable to interaction, and synergy index. RESULTS: Under different ETE definitions, the odds ratio of MI mortality associated with heat wave and cold spell ranged from 1.18 (95% CI, 1.14-1.21) to 1.74 (1.66-1.83), and 1.04 (1.02-1.06) to 1.12 (1.07-1.18), respectively. Lag 01-day exposure to PM2.5 was significantly associated with an increased odds of MI mortality, which attenuated at higher exposures. We observed a significant synergistic interaction of heat wave and PM2.5 on MI mortality (relative excess odds due to interaction >0, proportion attributable to interaction >0, and synergy index >1), which was higher, in general, for heat wave with greater intensities and longer durations. We estimated that up to 2.8% of the MI deaths were attributable to exposure to ETEs and PM2.5 at levels exceeding the interim target 3 value (37.5 µg/m3) of World Health Organization air quality guidelines. Women and older adults were more vulnerable to ETEs and PM2.5. The interactive effects of ETEs or PM2.5 on MI mortality did not vary across sex, age, or socioeconomic status. CONCLUSIONS: This study provides consistent evidence that exposure to both ETEs and PM2.5 is significantly associated with an increased odds of MI mortality, especially for women and older adults, and that heat wave interacts synergistically with PM2.5 to trigger MI deaths but cold spell does not. Our findings suggest that mitigating both ETE and PM2.5 exposures may bring health cobenefits in preventing premature deaths from MI.
Subject(s)
Air Pollutants , Air Pollution , Myocardial Infarction , Humans , Female , Aged , Particulate Matter/adverse effects , Particulate Matter/analysis , Temperature , Air Pollutants/adverse effects , Air Pollutants/analysis , Cross-Over Studies , Air Pollution/adverse effects , Air Pollution/analysis , China/epidemiology , Environmental Exposure/adverse effects , Environmental Exposure/analysis , MortalityABSTRACT
The continuous decline of human semen quality during the past decades has drawn much concern globally. Previous studies have suggested a link between abnormal BMI and semen quality decline, but the results remain inconsistent. This systematic review and meta-analysis aimed to evaluate the association between body mass index (BMI) and semen quality. We searched PubMed, Embase, and Web of Science for eligible studies from inception to April 17, 2022. We considered men with BMI < 25.0 kg/m2 as the reference and calculated the pooled weighted mean difference of men with overweight (BMI 25.0-29.9 kg/m2), obesity (BMI ≥ 30.0 kg/m2), class I obesity (BMI 30.0-34.9 kg/m2), and class II/III obesity (BMI ≥ 35.0 kg/m2). A total of 5070 articles were identified, of which 50 studies were included (71,337 subjects). Compared with men with BMI < 25.0 kg/m2, men with obesity had an average reduction of 0.24 ml in semen volume, 19.56 × 106 in total sperm number, 2.21% in total motility, 5.95% in progressive motility, and 1.08% in normal forms, respectively, while men with overweight had an average reduction of 0.08 ml in semen volume and 2.91% in progressive motility, respectively. The reduction of semen quality was more pronounced among men with obesity than that among men with overweight. Moreover, significant reductions in semen quality were identified in men with different classes of obesity, which were more pronounced in men with class II/III obesity than that in men with class I obesity. Across men from the general population, infertile or subfertile men, and suspiciously subfertile men, we identified significant semen quality reductions in men with obesity/overweight. In conclusion, obesity and overweight were significantly associated with semen quality reductions, suggesting that maintaining normal weight may help prevent semen quality decline.
ABSTRACT
Benefiting from the unique photoluminescence behavior of the lanthanide(III) ions and organic ligands, a lanthanide(III) metal-organic framework (Ln-MOF) material can simultaneously demonstrate photoluminescence of lanthanide(III) cations and organic molecules and endow its superior applications of fluorescence sensing behaviors. Herein, we present a europium(III) MOF material {[Eu2(BPTA)·(CH3COO)2·3DMA]·0.5DMA·3H2O}n (1) (where H4BPTA is 3,3',5,5'-biphenyltetracarboxylic acid) for photoluminescence performance of quantitatively sensing the inflammatory marker neopterin (Neo). The obtained 1 comprises Eu2(COO)4 paddlewheel secondary building units, which could be bridged by BPTA4- ligands to extend a 2D framework. The fluorescence titration indicates 1 can achieve simultaneous fluorescence behavior of Eu3+ ions and Neo via on-off ratiometric effects and thus could be exploited as the ratiometric fluorescence sensor matrix. Such a fluorescence phenomenon of 1 as a ratiometric sensor for quantitative detection of Neo via an on-off ratiometric effect is never observed in MOF chemistry. Moreover, naked-eye visible color variations of the fluorescence for 1 could be observed from red to blue with increasing concentrations of Neo, confirmed by fluorescent test strips as well as portable fluorescent hydrogels. And 1 also shows a low detection limit of 15.11 nM. A synergetic contribution of the competitive absorption, fluorescence resonance energy-transfer, and photoinduced electron-transfer mechanisms between Neo and the framework of 1 realizes the on-off ratiometric fluorescence behavior for Neo detection, supported by the UV-vis spectral overlap experiment and DFT calculations.
ABSTRACT
A case-crossover study among 511,767 cardiovascular disease (CVD) deaths in Jiangsu province, China, during 2015-2021 was conducted to assess the association of exposure to ambient ozone (O3) and heat wave with CVD mortality and explore their possible interactions. Heat wave was defined as extreme high temperature for at least two consecutive days. Grid-level heat waves were defined by multiple combinations of apparent temperature thresholds and durations. Residential O3 and heat wave exposures were assessed using grid data sets (spatial resolution: 1 km × 1 km for O3; 0.0625° × 0.0625° for heat wave). Conditional logistic regression models were applied for exposure-response analyses and evaluation of additive interactions. Under different heat wave definitions, the odds ratios (ORs) of CVD mortality associated with medium-level and high-level O3 exposures ranged from 1.029 to 1.107 compared with low-level O3, while the ORs for heat wave exposure ranged from 1.14 to 1.65. Significant synergistic effects on CVD mortality were observed for the O3 and heat wave exposures, which were generally greater with higher levels of the O3 exposure, higher temperature thresholds, and longer durations of heat wave exposure. Up to 5.8% of the CVD deaths were attributable to O3 and heat wave. Women and older adults were more vulnerable to the exposure to O3 and heat wave exposure. Exposure to both O3 and heat wave was significantly associated with an increased odds of CVD mortality, and O3 and heat wave can interact synergistically to trigger CVD deaths.
Subject(s)
Air Pollutants , Air Pollution , Cardiovascular Diseases , Ozone , Humans , Female , Aged , Ozone/analysis , Cardiovascular Diseases/epidemiology , Air Pollutants/analysis , Cross-Over Studies , Hot Temperature , China/epidemiology , Air Pollution/analysis , Environmental Exposure/analysis , Particulate Matter/analysisABSTRACT
BACKGROUND: Ambient fine particulate matter (PM2.5) exposure has been associated with an increased risk of gastrointestinal cancer mortality, but the attributable constituents remain unclear. OBJECTIVES: To investigate the association of long-term exposure to PM2.5 constituents with total and site-specific gastrointestinal cancer mortality using a difference-in-differences approach in Jiangsu province, China during 2015-2020. METHODS: We split Jiangsu into 53 spatial units and computed their yearly death number of total gastrointestinal, esophagus, stomach, colorectum, liver, and pancreas cancer. Utilizing a high-quality grid dataset on PM2.5 constituents, we estimated 10-year population-weighted exposure to black carbon (BC), organic carbon (OC), sulfate, nitrate, ammonium, and chloride in each spatial unit. The effect of constituents on gastrointestinal cancer mortality was assessed by controlling time trends, spatial differences, gross domestic product (GDP), and seasonal temperatures. RESULTS: Overall, 524,019 gastrointestinal cancer deaths were ascertained in 84.77 million population. Each interquartile range increment of BC (0.46 µg/m3), OC (4.56 µg/m3), and nitrate (1.41 µg/m3) was significantly associated with a 27%, 26%, and 34% increased risk of total gastrointestinal cancer mortality, respectively, and these associations remained significant in PM2.5-adjusted models and constituent-residual models. We also identified robust associations of BC, OC, and nitrate exposures with site-specific gastrointestinal cancer mortality. The mortality risk generally displayed increased trends across the total exposure range and rose steeper at higher levels. We did not identify robust associations for sulfate, ammonium, or chlorine exposure. Higher mortality risk ascribed to constituent exposures was identified in total gastrointestinal and liver cancer among women, stomach cancer among men, and total gastrointestinal and stomach cancer among low-GDP regions. CONCLUSIONS: This study offers consistent evidence that long-term exposure to PM2.5-bound BC, OC, and nitrate is associated with total and site-specific gastrointestinal cancer mortality, indicating that these constituents need to be controlled to mitigate the adverse effect of PM2.5 on gastrointestinal cancer mortality.
Subject(s)
Air Pollutants , Air Pollution , Ammonium Compounds , Stomach Neoplasms , Male , Female , Humans , Particulate Matter/toxicity , Particulate Matter/analysis , Air Pollutants/toxicity , Air Pollutants/analysis , Environmental Exposure/adverse effects , Nitrates/toxicity , China/epidemiology , Carbon , Soot , Sulfates , Air Pollution/adverse effectsABSTRACT
Equilibration of metal metabolism is critical for normal liver function. Most epidemiological studies have only concentrated on the influence of limited metals. However, the single and synergistic impact of multiple-metal exposures on abnormal liver function (ALF) are still unknown. A cross-sectional study involving 1493 Chinese adults residing in Shenzhen was conducted. Plasma concentrations of 13 metals, including essential metals (calcium, copper, cobalt, iron, magnesium, manganese, molybdenum, zinc, and selenium) and toxic metals (aluminum, cadmium, arsenic, and thallium) were detected by the inductively coupled plasma spectrometry (ICP-MS). ALF was ascertained as any observed abnormality from albumin, alanine transaminase, aspartate transaminase, γ-glutamyl transpeptidase, and direct bilirubin. Diverse statistical methods were used to evaluate the single and mixture effect of metals, as well as the dose-response relationships with ALF risk, respectively. Mediation analysis was conducted to evaluate the role of blood lipids in the relation of metal exposure with ALF. The average age of subjects was 59.7 years, and 56.7 % were females. Logistic regression and the least absolute shrinkage and selection operator (LASSO) penalized regression model consistently suggested that increased levels of arsenic, aluminum, manganese, and cadmium were related to elevated risk of ALF; while magnesium and zinc showed protective effects on ALF (all p-trend < 0.05). The grouped weighted quantile sum (GWQS) regression revealed that the WQS index of essential metals and toxic metals showed significantly negative or positive relationship with ALF, respectively. Aluminum, arsenic, cadmium, and manganese showed linear whilst magnesium and zinc showed non-linear dose-response relationships with ALF risk. Mediation analysis showed that LDL-c mediated 4.41 % and 14.74 % of the relationship of plasma cadmium and manganese with ALF, respectively. In summary, plasma aluminum, arsenic, manganese, cadmium, magnesium, and zinc related with ALF, and LDL-c might underlie the pathogenesis of ALF associated with cadmium and manganese exposure. This study may provide critical public health significances in liver injury prevention and scientific evidence for the establishment of environmental standard.
Subject(s)
Cholesterol, LDL , Metals , Humans , Female , Middle Aged , Male , Cross-Sectional Studies , China , Metals/blood , Metals/toxicity , Cholesterol, LDL/blood , Liver/drug effects , Aged , Environmental Exposure/statistics & numerical data , Adult , Environmental Pollutants/blood , Mediation Analysis , Arsenic/blood , Arsenic/toxicity , Chemical and Drug Induced Liver Injury/blood , Chemical and Drug Induced Liver Injury/etiologyABSTRACT
Previous studies have indicated depression was associated with environmental exposures, but evidence is limited for the association between outdoor light at night (LAN) and depression. This study aims to examine the association between long-term outdoor LAN exposure and depressive symptoms using data from the Chinese Veteran Clinical Research platform. A total of 6445 male veterans were selected from 277 veteran communities in 18 cities of China during 2009â2011. Depressive symptoms were evaluated using the Chinese version of the Center for Epidemiological Studies Depression scale. Outdoor LAN was estimated using the Global Radiance Calibrated Nighttime Lights data. The odds ratio and 95% confidence intervals of depressive symptoms at the high level of outdoor LAN exposure against the low level during the 1 years before the investigation was 1.49 (1.15, 1.92) with p-value for trend < 0.01, and those associated with per interquartile range increase in LAN exposure was 1.22 (1.06, 1.40).
Subject(s)
Depression , Veterans , Male , Humans , Cross-Sectional Studies , Depression/epidemiology , Environmental Exposure/analysis , China/epidemiologyABSTRACT
A two-dimensional (2D) mathematical model of quadratically distorted (QD) grating is established with the principles of Fraunhofer diffraction and Fourier optics. A discrete sampling method is applied for finding a numerical solution of the diffraction pattern of QD grating. An optimized working phase term, which determines the balanced energies and high efficiency of multi-plane images, can be obtained by the bisection algorithm. To confirm the analytical approach described above, the results have been compared with those obtained using a classical numerical model based on Fraunhofer diffraction theory and a fast Fourier transform (FFT) algorithm. The results show that our analytical approach allows the precise design of QD grating and improves the optical performance of simultaneous multi-plane imaging system. An optical setup based on our well-designed QD grating has been appended to the camera port of a commercial microscope, and some preliminary microscopy images have been successfully obtained. Further upgrade of our analytical model is in progress to improve the image quality and promote the applications.
ABSTRACT
To investigate the relation of smoking and microplastic inhalation, we conducted a prospective study combining population-based and experimental work. Bronchoalveolar lavage fluid (BALF) samples from 17 smokers and 15 nonsmokers were collected in Zhuhai City, China. We simulated an active smoking model to explore the contribution of smoking to inhaled microplastics. The characteristics of microplastics in BALF samples and cigarette smoke were determined using laser direct infrared spectroscopy. We compared the differences between smokers and nonsmokers as well as between cigarette smoke and control groups. Microplastics were identified positive in all BALF samples. Smokers had higher concentrations of total microplastics (25.86 particles/g), polyurethane (11.34 particles/g), and silicone (1.15 particles/g) than nonsmokers. In the cigarette smoking simulation model, higher concentrations of total microplastics (9.99 particles/L), polyurethane (4.66 particles/L), and silicone (2.78 particles/L) were present in the cigarette smoke than those in the control group. We confirmed and extended the evidence on the presence of microplastics in the lower respiratory tract. These findings also provide new evidence on the relation between cigarette smoking and microplastic inhalation.
Subject(s)
Microplastics , Plastics , Polyurethanes , Prospective Studies , Respiratory System , SmokingABSTRACT
Microplastics (MPs) are abundant in air, but evidence of their deposition in the respiratory tract is limited. We conducted a prospective case series to investigate the deposition of microplastics in bronchoalveolar lavage fluid (BALF) and determine the internal dose of MPs via inhalation. Eighteen never-smokers aged 32-74 years who underwent fiberoptic bronchoscopy with BALF were recruited from Zhuhai, China. Control samples were obtained by performing the same procedure using isotonic saline instead of BALF. Laser direct infrared spectroscopy combined with scanning electron microscopy detected the presence and characteristics of MPs and quantitatively analyzed the microplastic in BALF and control samples. Concentrations of total and specific MPs in BALF and control samples were compared using the Wilcox test. Thirteen types of MPs were observed in 18 BALF samples. Polyethylene (PE, 86.1%) was the most abundant in BALF, followed by poly(ethylene terephthalate) (PET, 7.5%) and polypropylene (PP, 1.9%). Compared with the control samples, BALF had significantly higher concentrations of PE (median [IQR] of BALF: 0.38 [8.05] N/g), PET (0.26 [0.54] N/g), polyurethane (0.16 [0.24] N/g), PP (0.16 [0.11] N/g), and total MPs (0.91 [6.58] N/g). The presence of MPs in BALF provides novel evidence that MPs penetrate deep into the respiratory tract.
Subject(s)
Microplastics , Water Pollutants, Chemical , Humans , Bronchoalveolar Lavage Fluid/chemistry , Plastics , Smokers , Polypropylenes , Environmental MonitoringABSTRACT
Fine particulate matter (PM2.5) chemical composition has strong and diverse impacts on the planetary environment, climate, and health. These effects are still not well understood due to limited surface observations and uncertainties in chemical model simulations. We developed a four-dimensional spatiotemporal deep forest (4D-STDF) model to estimate daily PM2.5 chemical composition at a spatial resolution of 1 km in China since 2000 by integrating measurements of PM2.5 species from a high-density observation network, satellite PM2.5 retrievals, atmospheric reanalyses, and model simulations. Cross-validation results illustrate the reliability of sulfate (SO42-), nitrate (NO3-), ammonium (NH4+), and chloride (Cl-) estimates, with high coefficients of determination (CV-R2) with ground-based observations of 0.74, 0.75, 0.71, and 0.66, and average root-mean-square errors (RMSE) of 6.0, 6.6, 4.3, and 2.3 µg/m3, respectively. The three components of secondary inorganic aerosols (SIAs) account for 21% (SO42-), 20% (NO3-), and 14% (NH4+) of the total PM2.5 mass in eastern China; we observed significant reductions in the mass of inorganic components by 40-43% between 2013 and 2020, slowing down since 2018. Comparatively, the ratio of SIA to PM2.5 increased by 7% across eastern China except in Beijing and nearby areas, accelerating in recent years. SO42- has been the dominant SIA component in eastern China, although it was surpassed by NO3- in some areas, e.g., Beijing-Tianjin-Hebei region since 2016. SIA, accounting for nearly half (â¼46%) of the PM2.5 mass, drove the explosive formation of winter haze episodes in the North China Plain. A sharp decline in SIA concentrations and an increase in SIA-to-PM2.5 ratios during the COVID-19 lockdown were also revealed, reflecting the enhanced atmospheric oxidation capacity and formation of secondary particles.
Subject(s)
Air Pollutants , Air Pollution , Deep Learning , Inorganic Chemicals , Air Pollutants/analysis , Reproducibility of Results , Respiratory Aerosols and Droplets , Particulate Matter/analysis , Inorganic Chemicals/analysis , China , Seasons , Environmental Monitoring/methods , Aerosols/analysis , Air Pollution/analysisABSTRACT
BACKGROUND: Accumulating studies have reported that chronic exposure to ambient fine particulate matter (PM2.5) can lead to adverse effects on lung cancer mortality; however, such chronic effects are less clear for mortality from other site-specific cancers. OBJECTIVE: To explore the causal effect of long-term PM2.5 exposure on mortality from all-site and a variety of site-specific cancers in Jiangsu province, China during 2015-2020 using a difference-in-differences analysis. METHODS: For each of 53 county-based spatial units in Jiangsu province, we calculated annual death counts for all-site cancer and 23 site-specific cancers. Using a validated high-resolution PM2.5 grid dataset, long-term PM2.5 exposure of a spatial unit within a given year was evaluated as the average of population-weighted annual concentrations during recent 10 years. Conditional Poisson regression models were employed to evaluate exposure-response associations adjusting for spatial and temporal variables, seasonal temperatures, relative humidity, and gross domestic product (GDP). RESULTS: During the study period, we identified 947,337 adult cancer deaths in Jiangsu province. Each 1 µg/m3 increment in PM2.5 exposure was significantly associated with a 2.7% increase in the risk of all-site cancer mortality. PM2.5-mortality associations were also observed in cancer of lip, oral cavity and pharynx, stomach, colorectum, pancreas, lung, bone and joints, ovary, prostate, and lymphoma (all adjusted P < 0.05), with the relative risks ranging from 1.028 (95% confidence interval [CI]: 1.011, 1.046) for stomach cancer to 1.201 (95% CI: 1.120, 1.308) for bone and joints cancers. Exposure-response curves showed that these associations were close to linearity, though most of them had increasing slopes at high exposure levels. Overall, women and subjects in low GDP regions were more vulnerable to PM2.5 exposures. CONCLUSIONS: Long-term exposure to ambient PM2.5 contributes to a higher risk of mortality from multiple site-specific cancers.
Subject(s)
Air Pollutants , Air Pollution , Lung Neoplasms , Male , Adult , Humans , Female , Particulate Matter/analysis , Air Pollutants/toxicity , China , Risk , Lung Neoplasms/chemically induced , Environmental Exposure/analysis , Air Pollution/analysisABSTRACT
BACKGROUND: Previous studies have suggested an association between non-optimum ambient temperature and decreased semen quality. However, the effect of exposure to heat waves on semen quality remains unclear. METHODS: Volunteers who intended to donate sperm in Guangdong provincial human sperm bank enrolled. Heat waves were defined by temperature threshold and duration, with a total of 9 definitions were employed, specifying daily mean temperature exceeding the 85th, 90th, or 95th percentile for at least 2, 3, or 4 consecutive days. Residential exposure to heat waves during 0-90 days before ejaculation was evaluated using a validated gridded dataset on ambient temperature. Association and potential windows of susceptibility were evaluated and identified using linear mixed models and distributed lag non-linear models. RESULTS: A total of 2183 sperm donation volunteers underwent 8632 semen analyses from 2018 to 2019. Exposure to heat wave defined as daily mean temperature exceeding the 95th percentile for at least 4 consecutive days (P95-D4) was significantly associated with a 0.11 (95% confidence interval [CI]: 0.03, 0.18) ml, 3.36 (1.35, 5.38) × 106/ml, 16.93 (7.95, 25.91) × 106, and 2.11% (1.4%, 2.83%) reduction in semen volume, sperm concentration, total sperm number, and normal forms, respectively; whereas exposure to heat wave defined as P90-D4 was significantly associated with a 1.98% (1.47%, 2.48%) and 2.08% (1.57%, 2.58%) reduction in total motility and progressive motility, respectively. Sperm count and morphology were susceptible to heat wave exposure during the early stage of spermatogenesis, while sperm motility was susceptible to exposure during the late stage. CONCLUSION: Heat wave exposure was significantly associated with a reduction in semen quality. The windows of susceptibility during 0-90 days before ejaculation varied across sperm count, motility, and morphology. Our findings suggest that reducing heat wave exposure before ejaculation may benefit sperm donation volunteers and those attempting to conceive.
ABSTRACT
This study examined the associations of long-term exposure to ambient fine particulate matter (PM2.5) compositions/ozone with methylation of peripheral brain-derived neurotrophic factor (BDNF) promoters. A total of 101 participants were recruited from a cohort in Shijiazhuang, Hebei province, China. They underwent baseline and follow-up surveys in 2011 and 2015. DNA methylation levels were detected by bisulfite-PCR amplification and pyrosequencing. Participants' three-year average levels of PM2.5 compositions and ozone were estimated. Bayesian kernel machine regression (BKMR) models were used to examine the joint effects of pollutants on methylation levels. Exposure to PM2.5 compositions and ozone mixtures at the 75th percentile was associated with increased methylation levels at CpG2 of BDNF promoter (203%, 95% CI: 89, 316) than the lowest level of exposure, and sulfate dominated the effect in the BKMR models.Our findings provide clues to the epigenetic mechanisms for the associations of PM2.5 compositions and ozone with BDNF.
ABSTRACT
BACKGROUND: Pneumonia is a major contributor to hospital admission for patients with chronic obstructive pulmonary disease (COPD). However, evidence for acute effects of ambient air pollution exposure on pneumonia hospital admission among patients with COPD is scarce. We aimed to examine the association between short-term exposure to ambient air pollution and pneumonia hospital admission among patients with COPD. METHODS: We enrolled COPD cases aged ≥ 60 years old and further filtered those who were admitted into hospitals from pneumonia during 2016-2019 in Guangdong province, China for main analysis. A time-stratified case-crossover design was applied to investigate the association and conditional logistic regression model was used for data analysis. We performed inverse distance weighting method to estimate daily individual-level exposure on particulate matter with an aerodynamic diameter ≤ 2.5 µm (PM2.5), particulate matter with an aerodynamic diameter ≤ 10 µm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3) based on personal residential addresses. RESULTS: We included 6473 pneumonia hospital admissions during the study period. Each interquartile range (IQR) increase in PM2.5 (lag 2; IQR, 22.1 µg/m3), SO2 (lag 03; IQR, 4.2 µg/m3), NO2 (lag 03; IQR, 21.4 µg/m3), and O3 (lag 04; IQR, 57.9 µg/m3) was associated with an odds ratio in pneumonia hospital admission of 1.043 (95% CI: 1.004-1.083), 1.081 (95% CI: 1.026-1.140), 1.045 (95% CI: 1.005-1.088), and 1.080 (95% CI: 1.018-1.147), respectively. Non-linear trends for PM2.5, PM10, and SO2 were observed in the study. Sex, age at hospital admission, and season at hospital admission did not modify the associations. CONCLUSIONS: We found significantly positive associations of short-term exposure to PM2.5, SO2, NO2, and O3 with pneumonia hospital admission among COPD patients. It provides new insight for comprehensive pneumonia prevention and treatment among COPD patients.
Subject(s)
Air Pollutants , Air Pollution , Pneumonia , Pulmonary Disease, Chronic Obstructive , Air Pollutants/adverse effects , Air Pollutants/analysis , Air Pollution/adverse effects , Air Pollution/analysis , Cross-Over Studies , Hospitals , Humans , Middle Aged , Pneumonia/chemically induced , Pneumonia/diagnosis , Pneumonia/epidemiology , Pulmonary Disease, Chronic Obstructive/chemically induced , Pulmonary Disease, Chronic Obstructive/diagnosis , Pulmonary Disease, Chronic Obstructive/epidemiologyABSTRACT
BACKGROUND: Short-term exposure to ambient air pollution has been linked to increased risk of stroke mortality, but its adverse effects on mortality from specific types of stroke including ischemic stroke and hemorrhagic stroke remain poorly understood. METHODS: Using the China National Mortality Surveillance System, we conducted a time-stratified case-crossover study among 412,567 stroke deaths in Jiangsu province, China during 2015-2019. Residential daily PM2.5 , PM10 , SO2 , NO2 , CO, and O3 exposure concentrations were extracted from the ChinaHighAirPollutants dataset for each subject. Conditional logistic regression models were performed to conduct exposure-response analyses. RESULTS: Each 10 µg/m3 increase of PM2.5 , PM10 , SO2 , NO2 , CO, and O3 was respectively associated with a 1.44%, 0.93%, 5.55%, 2.90%, 0.148%, and 0.54% increase in odds of mortality from ischemic stroke, which was significantly stronger than that from hemorrhagic stroke (percent change in odds: 0.74%, 0.51%, 3.11%, 1.15%, 0.090%, and 0.10%). The excess fraction of ischemic stroke mortality associated with PM2.5 , PM10 , SO2 , NO2 , CO, and O3 exposure was 6.90%, 6.48%, 8.21%, 8.61%, 9.67%, and 4.76%, respectively, which was also significantly higher than that of hemorrhagic stroke mortality (excess fraction: 3.49%, 3.48%, 4.69%, 3.48%, 5.86%, and 0.88%). These differences in adverse effects generally remained across sex, age, and season. CONCLUSIONS: Short-term exposure to ambient air pollution was significantly associated with increased risk of both ischemic and hemorrhagic stroke mortality and posed considerable excess mortality. Our results suggest that air pollution exposure may lead to substantially greater adverse effects on mortality from ischemic stroke than that from hemorrhagic stroke.
Subject(s)
Air Pollutants , Air Pollution , Hemorrhagic Stroke , Ischemic Stroke , Stroke , Air Pollutants/adverse effects , Air Pollutants/analysis , Air Pollution/adverse effects , Air Pollution/analysis , China/epidemiology , Cross-Over Studies , Environmental Exposure/adverse effects , Environmental Exposure/analysis , Humans , Ischemia , Nitrogen Dioxide/adverse effects , Nitrogen Dioxide/analysis , Particulate Matter/adverse effects , Particulate Matter/analysis , Stroke/epidemiologyABSTRACT
BACKGROUND: Whether ambient temperature exposure contributes to death from asthma remains unknown to date. We therefore conducted a case-crossover study in China to quantitatively evaluate the association and burden of ambient temperature exposure on asthma mortality. METHODS: Using data from the National Mortality Surveillance System in China, we conducted a time-stratified case-crossover study of 15 888 individuals who lived in Hubei and Jiangsu province, China and died from asthma as the underlying cause in 2015-2019. Individual-level exposures to air temperature and apparent temperature on the date of death and 21 days prior were assessed based on each subject's residential address. Distributed lag nonlinear models based on conditional logistic regression were used to quantify exposure-response associations and calculate fraction and number of deaths attributable to non-optimum ambient temperatures. RESULTS: We observed a reverse J-shaped association between air temperature and risk of asthma mortality, with a minimum mortality temperature of 21.3 °C. Non-optimum ambient temperature is responsible for substantial excess mortality from asthma. In total, 26.3% of asthma mortality were attributable to non-optimum temperatures, with moderate cold, moderate hot, extreme cold and extreme hot responsible for 21.7%, 2.4%, 2.1% and 0.9% of asthma mortality, respectively. The total attributable fraction and number was significantly higher among adults aged less than 80 years in hot temperature. CONCLUSIONS: Exposure to non-optimum ambient temperature, especially moderate cold temperature, was responsible for substantial excess mortality from asthma. These findings have important implications for planning of public-health interventions to minimize the adverse respiratory damage from non-optimum ambient temperature.
Subject(s)
Asthma , Cold Temperature , Adult , Asthma/epidemiology , China/epidemiology , Cross-Over Studies , Hot Temperature , Humans , Mortality , TemperatureABSTRACT
AIMS: To study the association between short-term exposure to air pollutants and mortality of Chronic Ischemic Heart Disease (CIHD). METHODS: Using a case-crossover design, we investigated 148,443 CIHD deaths from 2015 to 2020 in Jiangsu Province, China. Exposure to six ambient pollutants, including PM10, PM2.5, NO2, CO, SO2, and O3, was assessed by extracting daily concentrations from validated 10 km × 10 km pollutant grids at each subject's residential address. A conditional logistic regression approach was used to explore the exposure-response relationship with adjustment for temperature and relative humidity. We calculated the Population Attributable Fractions (PAFs) and the attributable deaths number of CIHD. RESULTS: An increase of 10 µg/m3 in PM10 and PM2.5 exposure was associated with a 1.16% (95% CI: 0.85-1.48%) and 1.80% (1.36-2.24%) increase in CIHD mortality, respectively. A threshold value of 123 µg/m3 was identified for the association between O3 exposure and CIHD mortality. Controlling for PM2.5, each increase of 10 µg/m3 in O3 (>threshold) was statistically significantly associated with a 0.94% (0.19-1.71%) increase in CIHD mortality, however there was no association between NO2, SO2, CO exposure and CIHD mortality. Reducing PM2.5, PM10 and O3 to the WHO air quality guidelines would prevent 6.16% (95% CI: 4.70-7.58%), 4.30% (3.18-5.43%) and 1.29% (0.48-4.20%) of CIHD deaths, respectively. During the warm season, mortality and PAFs of CIHD associated with PM2.5, PM10, and O3 were significantly higher. CONCLUSIONS: Short-term exposure to ambient PM2.5, PM10, and O3 might trigger deaths from CIHD. These findings indicate that the premature deaths of CIHD patients can be alleviated by reducing exposure to polluted air.
Subject(s)
Air Pollutants , Myocardial Ischemia , Ozone , Particulate Matter , Air Pollutants/adverse effects , Air Pollutants/analysis , Air Pollution/adverse effects , Air Pollution/analysis , China/epidemiology , Cross-Over Studies , Environmental Exposure/adverse effects , Environmental Exposure/analysis , Humans , Myocardial Ischemia/mortality , Nitrogen Dioxide/adverse effects , Nitrogen Dioxide/analysis , Ozone/adverse effects , Ozone/analysis , Particulate Matter/adverse effects , Particulate Matter/analysisABSTRACT
This study aimed to investigate the association between air pollutants and methylation of peripheral brain-derived neurotrophic factor (BDNF) promoters. A total of 101 individuals were recruited in this panel study. BDNF promoter methylation was detected by bisulfite-PCR amplification and pyrosequencing. Participants' exposure to air pollutants was estimated using a satellite-based random forests approach. A generalized estimated equation model with natural cubic splines was employed to examine the associations between air pollutants and BDNF promoter methylation levels. The associations between air pollution and BDNF promoter methylation showed nonlinear curves with threshold effects. The threshold concentration for the association of nitrogen dioxide (NO2) with average methylation level was 59.7 µg/m3, and that for the association of particulate matter ≤ 1 µm in diameter (PM1) with CpG2 methylation level was 70.9 µg/m3. The percent change of average methylation level at the 95th percentile of NO2 against the threshold concentration was 43.25% (95%CI: 13.10%, 73.40%), and that of CpG2 methylation at the 95th percentile of PM1 was 128.29% (95%CI: 43.27%, 213.31%). Overall, long-term exposures of PM1, PM2.5, PM10, and NO2 were associated with significant changes in BDNF promoter methylation levels with threshold effects.
Subject(s)
Air Pollutants , Air Pollution , Air Pollutants/analysis , Air Pollutants/toxicity , Air Pollution/adverse effects , Air Pollution/analysis , Brain-Derived Neurotrophic Factor/genetics , China , DNA Methylation , Environmental Exposure/adverse effects , Environmental Exposure/analysis , Humans , Nitrogen Dioxide/analysis , Particulate Matter/analysis , Particulate Matter/toxicityABSTRACT
BACKGROUND: Exposure to non-optimum ambient temperature has been linked to increased risk of total cardiovascular disease (CVD) mortality; however, the adverse effects on mortality from specific types of CVD remain less understood. OBJECTIVES: To comprehensively investigate the association of ambient temperature with cause-specific CVD mortality, and to estimate and compare the corresponding mortality burden. METHODS: We conducted a time-stratified case-crossover study of 1000,014 CVD deaths in Jiangsu province, China during 2015-2019 using data from the China National Mortality Surveillance System. Residential daily 24-hour average temperature for each subject was extracted from a validated grid data at a spatial resolution of 0.0625° × 0.0625°. We fitted distributed lag non-linear models (DLNM) based on conditional logistic regression to quantitatively investigate the association of ambient temperature with total and cause-specific CVD mortality, which was used to further estimate mortality burden attributable to non-optimum ambient temperatures. RESULTS: With adjustment for relative humidity, we observed reverse J-shaped exposure-response associations of ambient temperature with total and cause-specific CVD mortality, with minimum mortality temperatures ranging from 19.5 °C to 23.0 °C. An estimated 20.3% of the total CVD deaths were attributable to non-optimum temperatures, while the attributable fraction (AF) of mortality from chronic rheumatic heart diseases, hypertensive diseases, ischemic heart diseases (IHD), pulmonary heart disease, stroke, and sequelae of stroke was 22.4%, 23.2%, 23.3%, 20.9%, 17.6% and 21.3%, respectively. For total and cause-specific CVDs, most deaths were attributable to moderate cold temperature. We observed significantly higher mortality burden from total and certain cause-specific CVDs in adults 80 years or older and those who were widowed. CONCLUSION: Exposure to ambient temperature was significantly associated with increased risk of cause-specific CVD mortality. The burden of CVD mortality attributable to non-optimum temperature was substantial especially in older and widowed adults, and significantly varied across specific types of CVD.