Systemic Inflammation (C-Reactive Protein) in Older Chinese Adults Is Associated with Long-Term Exposure to Ambient Air Pollution
Ontology highlight
ABSTRACT:
SUBMITTER: Elbarbary M
PROVIDER: S-EPMC8004276 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:The objective of this study is to examine associations between short-term exposure to ambient air pollution and circulating biomarkers of systemic inflammation in participants from the Framingham Offspring and Third Generation cohorts in the greater Boston area.We included 3996 noncurrent smoking participants (mean age, 53.6 years; 54% women) who lived within 50 km from a central air pollution monitoring site in Boston, MA, and calculated the 1- to 7-day moving averages of fine particulate matter (diameter<2.5 µm), black carbon, sulfate, nitrogen oxides, and ozone before the examination visits. We used linear mixed effects models for C-reactive protein and tumor necrosis factor receptor 2, which were measured up to twice for each participant; we used linear regression models for interleukin-6, fibrinogen, and tumor necrosis factor ?, which were measured once. We adjusted for demographics, socioeconomic position, lifestyle, time, and weather. The 3- to 7-day moving averages of fine particulate matter (diameter<2.5 µm) and sulfate were positively associated with C-reactive protein concentrations. A 5 µg/m3 higher 5-day moving average fine particulate matter (diameter<2.5 µm) was associated with 4.2% (95% confidence interval: 0.8, 7.6) higher circulating C-reactive protein. Positive associations were also observed for nitrogen oxides with interleukin-6 and for black carbon, sulfate, and ozone with tumor necrosis factor receptor 2. However, black carbon, sulfate, and nitrogen oxides were negatively associated with fibrinogen, and sulfate was negatively associated with tumor necrosis factor ?.Higher short-term exposure to relatively low levels of ambient air pollution was associated with higher levels of C-reactive protein, interleukin-6, and tumor necrosis factor receptor 2 but not fibrinogen or tumor necrosis factor ? in individuals residing in the greater Boston area.
| S-EPMC5570664 | biostudies-other
Project description:Abstract Extensive evidence suggests that ambient air pollution contributes to a higher risk of hospital admissions for cerebrovascular diseases; however, its association with admissions for sequelae of stroke remains unclear. A time‐stratified case‐crossover study was conducted among 31,810 older adults who were admitted to hospital for sequelae of stroke in Guangzhou, China during 2016–2019. For each subject, daily residential exposure to fine particulate matter (PM2.5), inhalable particulate matter (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3) was extracted from a validated grid data set. Conditional logistic regression models were used for exposure‐response analyses. In single‐pollutant models, each interquartile range (IQR) increase of lag 04‐day exposure to CO (IQR: 0.25 mg/m3) and lag 3‐day exposure to O3 (69.6 μg/m3) was significantly associated with a 4.53% (95% confidence interval: 1.67%, 7.47%) and 5.63% (1.92%, 9.48%) increase in odds of hospital admissions for sequelae of stroke, respectively. These associations did not significantly vary across age or sex. With further adjustment for each of the other pollutants in 2‐pollutant models, the association for CO did not change significantly, while the association for O3 disappeared. We estimated that 7.72% of the hospital admissions were attributable to CO exposures. No significant or consistent association was observed for exposure to PM2.5, PM10, SO2, or NO2. In conclusion, short‐term exposure to ambient CO, even at levels below the WHO air quality guideline, was significantly associated with an increased odds of hospital admissions for sequelae of stroke, which may lead to considerable excess hospital admissions. Key Points Short‐term exposure to ambient carbon monoxide (CO) was significantly associated with an increased odds of hospital admissions for sequelae of stroke Ambient CO exposure may contribute to considerable excess hospital admissions for sequelae of stroke Our findings provide useful clues for the public to help prevent hospital admissions for sequelae of stroke by considering the effect of CO exposure
| S-EPMC9696746 | biostudies-literature
Project description:BACKGROUND:Health effects of air pollution on anaemia have been scarcely studied worldwide. We aimed to explore the associations of long-term exposure to ambient air pollutants with anaemia prevalence and haemoglobin levels in Chinese older adults. METHODS:We used two-level linear regression models and modified Poisson regression with robust error variance to examine the associations of particulate matter (PM) and nitrogen dioxide (NO2) on haemoglobin concentrations and the prevalence of anaemia, respectively, among 10,611 older Chinese adults enrolled in World Health Organization (WHO) Study on global AGEing and adult health (SAGE) China. The average community exposure to ambient air pollutants (PM with an aerodynamic diameter of 10 ?m or less (PM10), 2.5 ?m or less (PM2.5), 1 ?m or less (PM1) and nitrogen dioxide (NO2)) for each participant was estimated using a satellite-based spatial statistical model. Haemoglobin levels were measured for participants from dried blood spots. The models were controlled for confounders. RESULTS:All the studied pollutants were significantly associated with increased anaemia prevalence in single pollutant model (e.g., the prevalence ratios associated with an increase in inter quartile range in three years moving average PM10 (1.05; 95% CI: 1.02-1.09), PM2.5 (1.11; 95% CI: 1.06-1.16), PM1 (1.13; 95% CI: 1.06-1.20) and NO2 (1.42; 95% CI: 1.34-1.49), respectively. These air pollutants were also associated with lower concentrations of haemoglobin: PM10 (-0.53; 95% CI: -0.67, -0.38); PM2.5 (-0.52; 95% CI: -0.71, -0.33); PM1 (-0.55; 95% CI: -0.69, -0.41); NO2 (-1.71; 95% CI: -1.85, -1.57) respectively. CONCLUSIONS:Air pollution exposure was significantly associated with increased prevalence of anaemia and decreased haemoglobin levels in a cohort of older Chinese adults.
| S-EPMC7246731 | biostudies-literature
Project description:BackgroundStudies have identified relationships between air pollution and birth weight, but have been inconsistent in identifying individual pollutants inversely associated with birth weight or elucidating susceptibility of the fetus by trimester of exposure. We examined effects of prenatal ambient pollution exposure on average birth weight and risk of low birth weight in full-term births.MethodsWe estimated average ambient air pollutant concentrations throughout pregnancy in the neighborhoods of women who delivered term singleton live births between 1996 and 2006 in California. We adjusted effect estimates of air pollutants on birth weight for infant characteristics, maternal characteristics, neighborhood socioeconomic factors, and year and season of birth.Results3,545,177 singleton births had monitoring for at least one air pollutant within a 10 km radius of the tract or ZIP Code of the mother's residence. In multivariate models, pollutants were associated with decreased birth weight; -5.4 grams (95% confidence interval -6.8 g, -4.1 g) per ppm carbon monoxide, -9.0 g (-9.6 g, -8.4 g) per pphm nitrogen dioxide, -5.7 g (-6.6 g, -4.9 g) per pphm ozone, -7.7 g (-7.9 g, -6.6 g) per 10 microg/m3 particulate matter under 10 microm, -12.8 g (-14.3 g, -11.3 g) per 10 microg/m3 particulate matter under 2.5 microm, and -9.3 g (-10.7 g, -7.9 g) per 10 microg/m3 of coarse particulate matter. With the exception of carbon monoxide, estimates were largely unchanged after controlling for co-pollutants. Effect estimates for the third trimester largely reflect the results seen from full pregnancy exposure estimates; greater variation in results is seen in effect estimates specific to the first and second trimesters.ConclusionsThis study indicates that maternal exposure to ambient air pollution results in modestly lower infant birth weight. A small decline in birth weight is unlikely to have clinical relevance for individual infants, and there is debate about whether a small shift in the population distribution of birth weight has broader health implications. However, the ubiquity of air pollution exposures, the responsiveness of pollutant levels to regulation, and the fact that the highest pollution levels in California are lower than those regularly experienced in other countries suggest that precautionary efforts to reduce pollutants may be beneficial for infant health from a population perspective.
| S-EPMC2919523 | biostudies-literature
Project description:ObjectiveTo study the association between ambient air pollutants and serum C-reactive protein (CRP) concentration in 1,392 type 2 diabetic patients in Pune, India.Research design and methodsA cross-sectional study was conducted that linked daily time series of ambient air pollution data (obtained from central monitoring sites) and plasma CRP concentration in type 2 diabetic patients from the Wellcome Trust Genetic (WellGen) Study, recruited between March 2005 and May 2007. Air pollution effects on CRP concentration were investigated with delays (lags) of 0-7 days and multiday averaging spans of 7, 14, and 30 days before blood collection adjusted for age, sex, BMI, hemoglobin, fasting plasma glucose, treatment with agents with anti-inflammatory action, season, air temperature, and relative humidity.ResultsMedian CRP concentration was 3.49 mg/L. For 1 SD increase in SO(2) and oxides of nitrogen (NO(x)) concentrations in ambient air, a day before blood collection (lag(1)), we observed a significant increase in CRP (9.34 and 7.77%, respectively). The effect was higher with lag(2) (12.42% for SO(2) and 11.60% for NO(x)) and wore off progressively thereafter. We also found a significant association with multiday averaging times of up to 30 and 7 days for SO(2) and NO(x), respectively. No significant associations were found between particulate matter with an aerodynamic profile ≤10 µm (PM(10)) and CRP concentration except in summer. The association was significantly higher among patients with a shorter duration of diabetes, and in those not on statin and thiazolidinedione treatment.ConclusionsWe demonstrate, for the first time, a possible contribution of ambient air pollution to systemic inflammation in Indian type 2 diabetic patients. This may have implications for vascular complications of diabetes.
| S-EPMC3579327 | biostudies-literature
Project description:Air pollutants (AP) play a role in subclinical inflammation, and are associated with cardiovascular morbidity and mortality. Metabolic syndrome (MetS) is inflammatory and precedes cardiovascular morbidity and type 2 diabetes. Thus, a positive association between AP and MetS may be hypothesized. We explored this association, (taking into account, pathway-specific MetS definitions), and its potential modifiers in Swiss adults. We studied 3769 participants of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults, reporting at least four-hour fasting time before venepuncture. AP exposures were 10-year mean residential PM10 (particulate matter <10μm in diameter) and NO2 (nitrogen dioxide). Outcomes included MetS defined by World Health Organization (MetS-W), International Diabetes Federation (MetS-I) and Adult Treatment Panel-III (MetS-A) using four- and eight-hour fasting time limits. We also explored associations with individual components of MetS. We applied mixed logistic regression models to explore these associations. The prevalence of MetS-W, MetS-I and MetS-A were 10%, 22% and 18% respectively. Odds of MetS-W, MetS-I and MetS-A increased by 72% (51-102%), 31% (11-54%) and 18% (4-34%) per 10μg/m3 increase in 10-year mean PM10. We observed weaker associations with NO2. Associations were stronger among physically-active, ever-smokers and non-diabetic participants especially with PM10 (p<0.05). Associations remained robust across various sensitivity analyses including ten imputations of missing observations and exclusion of diabetes cases. The observed associations between AP exposure and MetS were sensitive to MetS definitions. Regarding the MetS components, we observed strongest associations with impaired fasting glycemia, and positive but weaker associations with hypertension and waist-circumference-based obesity. Cardio-metabolic effects of AP may be majorly driven by impairment of glucose homeostasis, and to a less-strong extent, visceral adiposity. Well-designed prospective studies are needed to confirm these findings.
| S-EPMC4478007 | biostudies-literature
Project description:This study aimed to investigate whether long-term exposure to airborne hydrocarbons, including volatile organic compounds, increases the risk of developing retinal vein occlusion (RVO) among the population of Taiwan. A retrospective cohort study involving 855,297 people was conducted. Cox proportional hazards regression analysis fitted the multiple pollutant models for two targeted pollutants, including total hydrocarbons (THC), nonmethane hydrocarbons (NMHC) were used, and the risk of RVO was estimated. The chi-squared test and one-way analysis of variance were used to test differences in demographics and comorbidity distribution among tertiles of the targeted pollutants. Before controlling for multiple pollutants, hazard ratios for the overall population were 19.88 (95% CI: 17.56-22.50) at 0.51-ppm increases in THC and 4.33 (95% CI: 3.97-4.73) at 0.27-ppm increases in NMHC. The highest adjusted hazard ratios for different multiple pollutant models of each targeted pollutant were statistically significant (all p values were ?0.05) for all patients at 29.67 (95% CI: 25.57-34.42) for THC and 16.24 (95% CI: 14.14-18.65) for NMHC. Our findings suggest that long-term exposure to THC and NMHC contribute to RVO development.
| S-EPMC6759191 | biostudies-literature
Project description:PurposeLong-term exposure to ambient fine particle (PM2.5) concentrations has been associated with an increased rate or risk of neurodegenerative conditions, but individual PM sources have not been previously examined in relation to neurodegenerative diseases.MethodsUsing the Statewide Planning and Research Cooperative System database, we studied 63,287 hospital admissions with a primary diagnosis of either Alzheimer's disease, dementia, or Parkinson's disease for New York State residents living within 15 miles from six PM2.5 monitoring sites. In addition to PM2.5 concentrations, we studied seven specific PM2.5 sources: secondary sulfate, secondary nitrate, biomass burning, diesel, spark-ignition emissions, pyrolyzed organic rich, and road dust. We estimated the rate of neurodegenerative hospital admissions associated with increased concentration of PM2.5 and individual PM2.5 sources average concentrations in the previous 0-29, 0-179, and 0-364 days.ResultsIncreases in ambient PM2.5 concentrations were not consistently associated with increased hospital admissions rates. Increased source-specific PM2.5 concentrations were associated with both increased (e.g., secondary sulfates and diesel emissions) and decreased rates (e.g., secondary nitrate and spark-ignition vehicular emissions) of neurodegenerative admissions.ConclusionsWe did not observe clear associations between overall ambient PM2.5 concentrations or source-apportioned ambient PM2.5 contributions and rates of neurologic disease hospitalizations.
| S-EPMC7796937 | biostudies-literature
Project description:BackgroundDespite accumulating evidence of an association between air pollution and renal disease, studies on the association between long-term exposure to air pollution and renal function are still contradictory. This study aimed to investigate this association in a large population with relatively low exposure and with improved estimation of renal function as well as renal injury biomarkers.MethodsWe performed a cross-sectional analysis in the middle-aged general population participating in the Swedish CardioPulmonary bioImaging Study (SCAPIS; n = 30 154). Individual 10-year exposure to total and locally emitted fine particulate matter (PM2.5), inhalable particulate matter (PM10), and nitrogen oxides (NOx) were modelled using high-resolution dispersion models. Linear regression models were used to estimate associations between exposures and estimated glomerular filtration rate (eGFR, combined creatinine and cystatin C) and serum levels of renal injury biomarkers (KIM-1, MCP-1, IL-6, IL-18, MMP-2, MMP-7, MMP-9, FGF-23, and uric acid), with consideration of potential confounders.ResultsMedian long-term PM2.5 exposure was 6.2 µg/m3. Almost all participants had a normal renal function and median eGFR was 99.2 mL/min/1.73 m2. PM2.5 exposure was associated with 1.3% (95% CI 0.6, 2.0) higher eGFR per 2.03 µg/m3 (interquartile range, IQR). PM2.5 exposure was also associated with elevated serum matrix metalloproteinase 2 (MMP-2) concentration, with 7.2% (95% CI 1.9, 12.8) higher MMP-2 per 2.03 µg/m3. There was a tendency towards an association between PM10 and higher levels of uric acid, but no associations were found with the other biomarkers. Associations with other air pollutants were null or inconsistent.ConclusionIn this large general population sample at low exposure levels, we found a surprising association between PM2.5 exposure and a higher renal filtration. It seems unlikely that particle function would improve renal function. However, increased filtration is an early sign of renal injury and may be related to the relatively healthy population at comparatively low exposure levels. Furthermore, PM2.5 exposure was associated with higher serum concentrations of MMP-2, an early indicator of renal and cardiovascular pathology.
| S-EPMC11313149 | biostudies-literature
Project description:BackgroundAir pollution is a major risk factor for planetary health and has long been suspected of predisposing humans to respiratory diseases induced by pathogens like influenza viruses. However, epidemiological evidence remains elusive due to lack of longitudinal data from large cohorts.ObjectiveOur aim is to quantify the short-term association of influenza incidence with exposure to ambient air pollutants in Chinese cities.MethodsBased on air pollutant data and influenza surveillance data from 82 cities in China over a period of 5 years, we applied a two-stage time series analysis to assess the association of daily incidence of reported influenza cases with six common air pollutants [particulate matter with aerodynamic diameter ≤2.5μm (PM2.5), particulate matter with aerodynamic diameter ≤10μm (PM10), NO2, SO2, CO, and O3], while adjusting for potential confounders including temperature, relative humidity, seasonality, and holiday effects. We built a distributed lag Poisson model for one or multiple pollutants in each individual city in the first stage and conducted a meta-analysis to pool city-specific estimates in the second stage.ResultsA total of 3,735,934 influenza cases were reported in 82 cities from 2015 to 2019, accounting for 72.71% of the overall case number reported in the mainland of China. The time series models for each pollutant alone showed that the daily incidence of reported influenza cases was positively associated with almost all air pollutants except for ozone. The most prominent short-term associations were found for SO2 and NO2 with cumulative risk ratios of 1.094 [95% confidence interval (CI): 1.054, 1.136] and 1.093 (95% CI: 1.067, 1.119), respectively, for each 10 μg/m3 increase in the concentration at each of the lags of 1-7 d. Only NO2 showed a significant association with the daily incidence of influenza cases in the multipollutant model that adjusts all six air pollutants together. The impact of air pollutants on influenza was generally found to be greater in children, in subtropical cities, and during cold months.DiscussionIncreased exposure to ambient air pollutants, particularly NO2, is associated with a higher risk of influenza-associated illness. Policies on reducing air pollution levels may help alleviate the disease burden due to influenza infection. https://doi.org/10.1289/EHP12146.
| S-EPMC10711743 | biostudies-literature