Ambient fine particulate matter pollution (PM2.5) is one leading cause of disease burden, but no study has quantified the association between daily PM2.5 exposure and life expectancy. We aimed to ...assess the potential benefits in life expectancy by attaining the daily PM2.5 standards in 72 cities of China during 2013-2016.
We applied a two-stage approach for the analysis. At the first stage, we used a generalized additive model (GAM) with a Gaussian link to examine the city-specific short-term association between daily PM2.5 and years of life lost (YLL); at the second stage, a random-effects meta-analysis was used to generate the regional and national estimations. We further estimated the potential gains in life expectancy (PGLE) by assuming that ambient PM2.5 has met the Chinese National Ambient Air Quality Standard (NAAQS, 75 μg/m3) or the ambient air quality guideline (AQG) of the World Health Organization (WHO) (25 μg/m3). We also calculated the attributable fraction (AF), which denoted the proportion of YLL attributable to a higher-than-standards daily mean PM2.5 concentration. During the period from January 18, 2013 to December 31, 2016, we recorded 1,226,849 nonaccidental deaths in the study area. We observed significant associations between daily PM2.5 and YLL: each 10 μg/m3 increase in three-day-averaged (lag02) PM2.5 concentrations corresponded to an increment of 0.43 years of life lost (95% CI: 0.29-0.57). We estimated that 168,065.18 (95% CI: 114,144.91-221,985.45) and 68,684.95 (95% CI: 46,648.79-90,721.11) years of life lost can be avoided by achieving WHO's AQG and Chinese NAAQS in the study area, which corresponded to 0.14 (95% CI: 0.09-0.18) and 0.06 (95% CI: 0.04-0.07) years of gain in life expectancy for each death in these cities. We observed differential regional estimates across the 7 regions, with the highest gains in the Northwest region (0.28 years of gain 95% CI: 0.06-0.49) and the lowest in the North region (0.08 95% CI: 0.02-0.15). Furthermore, using WHO's AQG and Chinese NAAQS as the references, we estimated that 1.00% (95% CI: 0.68%-1.32%) and 0.41% (95% CI: 0.28%-0.54%) of YLL could be attributable to the PM2.5 exposure at the national level. Findings from this study were mainly limited by the unavailability of data on individual PM2.5 exposure.
This study indicates that significantly longer life expectancy could be achieved by a reduction in the ambient PM2.5 concentrations. It also highlights the need to formulate a stricter ambient PM2.5 standard at both national and regional levels of China to protect the population's health.
We aimed to investigate the associations between air pollutants and the risk of admission and multiple readmission events for cardiovascular disease (CVD).
A total of 285 009 participants free of CVD ...at baseline from the UK Biobank were included in this analysis. Four major cardiovascular admission events were identified during the follow-up: chronic ischaemic heart disease (CIHD), cerebrovascular disease, atrial fibrillation and heart failure. We used Prentice, Williams and Peterson-Total Time model to examine the association between ambient air pollution and first admission, as well as multiple readmissions for these CVDs.
During a median follow-up of 12 years, 17 176 (6.03%) participants were hospitalised with CVDs, and 6203 (36.11%) patients with CVD had subsequent readmission events for CVDs. We observed significant associations between air pollution and both first admission and readmission for CVDs, with generally stronger associations on readmission for cardiovascular events. For example, the adjusted HRs for the first admission and subsequent readmission for cerebrovascular disease were 1.130 (95% CI 1.070 to 1.194) and 1.270 (95% CI 1.137 to 1.418) for each IQR increase of particulate matter with a diameter ≤2.5 µm. The corresponding HRs for CIHD were 1.060 (95% CI 1.008 to 1.114) and 1.120 (95% CI 1.070 to 1.171). Sex stratified analyses showed that the associations were generally more pronounced among females than males.
This study provides evidence that ambient air pollutants might play an important role in both first admission and readmission for cardiovascular events. In addition, patients with pre-existing CVDs may be more vulnerable to air pollution compared with healthy population.
Previous studies have demonstrated associations of perfluoroalkyl substances (PFASs), a group of highly persistent chemicals ubiquitous in wildlife and humans, with hypertension, but the ...relationships are mixed. Furthermore, academic literature on the relationship between isomers of PFASs and blood pressure (BP) and hypertension in populations from a higher pollution area is scant. We studied 1612 Chinese adults, ages 22–96years old, from Shenyang, China, utilizing high performance liquid chromatography-mass spectrometry to analyze isomers of perfluorooctanesulfonate (PFOS), perfluorooctanoate (PFOA), and other PFASs in blood serum. We used a mercury sphygmomanometer to measure BP. Hypertension was defined as a mean systolic BP (SBP) of at least 140mmHg, and/or diastolic BP (DBP) of at least 90mmHg, and/or use of antihypertensive medications. The results showed that increased serum concentrations of all (both branched and linear) isomers of PFASs were associated with higher prevalence of hypertension. Adjusted odds ratios for hypertension per ln-unit (ng/mL) increase in PFASs ranged from 1.10 (95%CI: 1.04, 1.17) for perfluorobutanoic acid (PFBA) to 1.26 (95%CI: 1.12, 1.42) for 3+4+5m PFOS, and the estimated increases in mean SBP and DBP ranged from 0.80mmHg (95%CI: 0.25, 1.34) for PFBA to 4.51mmHg (95%CI: 3.52, 5.51) for 3+4+5m PFOS, and from 0.51mmHg (95%CI: 0.01, 1.01) for perfluorodecanesulfonate (PFDS) to 2.48 (1.80, 3.16) for perfluorononanoic acid (PFNA), respectively. Compared with linear PFASs isomers, we identified more and stronger associations among branched PFASs isomers and blood pressure. Furthermore, females exhibited consistently stronger effects than males. In conclusion, this study is the first of its kind to show that not only PFASs positively associated with elevated blood pressure, but also that branched PFAS isomers are more frequently associated with blood pressure than linear PFAS isomers.
Branched PFASs isomers show greater impact on blood pressure than linear PFASs. Display omitted
•Few studies explored the associations between isomeric PFASs and blood pressure in human.•Branched PFASs isomers show greater impact on blood pressure than linear PFASs.•More associations of PFASs with hypertension were found in females than in males.
Epidemiological studies have reported significant association between ambient fine particulate matter air pollution (PM2.5) and mortality, however, few studies have investigated the relationship of ...mortality with PM2.5 and associated mortality burden in China, especially in a multicity setting.
We investigated the PM2.5-mortality association in six cities of the Pearl River Delta region from 2013 to 2015. We used generalized additive Poisson models incorporating penalized smoothing splines to control for temporal trend, temperature, and relative humidity. We applied meta-analyses using random-effects models to pool the effect estimates in the six cities. We also examined these associations in stratified analyses by sex, age group, education level and location of death. We further estimated the mortality burden (attributable fraction and attributable mortality) due to ambient PM2.5 exposures.
During the study period, a total of 316,305 deaths were recorded in the study area. The analysis revealed a significant association between PM2.5 and mortality. Specifically, a 10μg/m3 increase in 4-day averaged (lag03) PM2.5 concentration corresponded to a 1.76% (95% confidence interval (CI): 1.47%, 2.06%) increase in total mortality, 2.19% (95% CI: 1.80%, 2.59%) in cardiovascular mortality, and 1.68% (95% CI: 1.00%, 2.37%) in respiratory mortality. The results were generally robust to model specifications and adjustment of gaseous air pollutants. We estimated that 0.56% (95% CI: 0.47%, 0.66%) and 3.79% (95% CI: 3.14%, 4.45%) of all-cause mortalities were attributable to PM2.5 using China's and WHO's air quality standards as the reference, corresponding to 1661 (95% CI: 1379, 1946) and 11,176 (95% CI: 9261, 13,120) attributable premature mortalities, respectively.
This analysis adds to the growing body of evidence linking PM2.5 with daily mortality, and mortality burdens, particularly in one Chinese region with high levels of air pollution.
•We observed a significant association between PM2.5 and mortality.•A 10μg/m3 increase in PM2.5 corresponded to 1.76% all cause mortality increase.•About 3.79% of all-cause mortalities were attributable to PM2.5.
Most studies on the short-term health effects of air pollution have been conducted on a daily time scale, while hourly associations remain unclear.
We collected the hourly data of emergency ambulance ...calls (EACs), ambient air pollution, and meteorological variables from 2014 to 2016 in Luoyang, a central Chinese city in Henan Province. We used a generalized additive model to estimate the hourly effects of ambient air pollutants (PM2.5, PM10, SO2, and NO2) on EACs for all natural causes and cardiovascular and respiratory morbidity, with adjustment for potential confounding factors. We further examined the effect modification by temperature, relative humidity, wind speed, and atmospheric pressure using stratified analyses.
In the single-pollutant models, PM2.5, PM10, SO2, and NO2 were associated with an immediate increase in all-cause morbidity at 0, 0, 12, 10 h, separately, after exposure to these pollutants (excess risks: 0.19% (95% confidence interval (CI): 0.03%, 0.35%), 0.13% (95% CI: 0.02%, 0.24%), 0.28% (95% CI: 0.01%, 0.54%) and 0.52% (95% CI: 0.06%, 0.99%), respectively). These effects remained generally stable in two-pollutant models. SO2 and NO2 were significantly associated with an immediate increase in risk of cardiovascular morbidity, but the effects on respiratory morbidity were relatively more delayed. The stratified analyses suggested that temperature could modify the association between PM2.5 and EACs, humidity and atmospheric pressure could modify the association between SO2 and EACs.
Our study provides new evidence that higher concentrations of PM2.5, PM10, SO2, and NO2 may have transiently acute effects on all-cause morbidity and subacute effects on respiratory morbidity. SO2 and NO2 may also have immediate effects on cardiovascular morbidity. Findings of this study have important implications for the formation of hourly air quality standards.
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•Short-term exposure to air pollutants may have acute and subacute health effects.•SO2 and NO2 may have immediate effects on cardiovascular morbidity.•Temperature, humidity, and atmospheric pressure were important effect modifiers.
•Ambient exposure to PM2.5 and PMc were associated with mortality from IHD and COPD.•Exposure to PM2.5 exerted larger effects on mortality of IHD and COPD than PMc.•Substantial mortality burden of ...IHD and COPD could be attributable to PM2.5 exposure.
Both inhalable particles (PM10) and fine particles (PM2.5) are regulated in various countries mainly due to their adverse health effects. However, there is increasing evidence that PM2.5 might be responsible for these effects and coarse particles (PMc) plays little role in adverse health effects, if so, it might be not necessary to monitor PM10.
In this study, we conducted a time-series analysis using a generalized additive model to explore the effects of PM2.5, PMc, and PM10 on mortality from ischemic heart disease (IHD) and chronic obstructive pulmonary disease (COPD) in 96 Chinese cities during 2013–2016. The mortality number and attributable fraction were further estimated using the national air quality standard and WHO’s guideline as the reference.
We observed significant effects of PM2.5 on IHD and COPD mortality; each 10 ug/m3 increase in lag01 PM2.5 was associated with a 0.26% (95% CI: 0.17%, 0.34%) increase in IHD mortality and a 0.19% (95% CI: 0.09%, 0.29%) increase in COPD mortality. We also found significant effects of PMc and PM10 on mortality from IHD and COPD, but the magnitudes of effects were weaker than those of PM2.5. The results were robust when adjusting for co-pollutants and altering model parameters. We further estimated that about 1.27% (95% CI: 0.29%, 2.30%) of IHD mortality and 1.25% (95% CI: 0.08%, 2.46%) of COPD mortality could be attributable to PM2.5 exposure using WHO’s guideline (25 ug/m3) as a reference, corresponding to 15,337 (95% CI: 3,375, 27,842) mortalities from IHD and 5,653 (95% CI: 379, 11,152) COPD mortalities in the 96 cities. Across all of China, almost fifty thousand cases of IHD mortality and twenty thousand cases of COPD mortality might be avoidable if the PM2.5 concentration declined to the WHO guideline.
Our study indicates that short-term exposure to PM2.5 could be an important risk factor of mortality from IHD and COPD, and substantial cardiopulmonary mortality could be avoidable by reducing daily PM2.5 concentrations. It is nonnegligible to consider the role of PMc in triggering in cardiopulmonary mortality. And it could be necessary to continue monitoring PM10 in the study regions due to the adverse effects of PMc.
Several studies have investigated the short-term effects of ambient air pollutants in the development of high blood pressure and hypertension. However, little information exists regarding the health ...effects of long-term exposure. To investigate the association between residential long-term exposure to air pollution and blood pressure and hypertension, we studied 24 845 Chinese adults in 11 districts of 3 northeastern cities from 2009 to 2010. Three-year average concentration of particles with an aerodynamic diameter ≤10 µm (PM(10)), sulfur dioxide (SO(2)), nitrogen dioxides (NO(2)), and ozone (O(3)) were calculated from monitoring stations in the 11 districts. We used generalized additive models and 2-level logistic regressions models to examine the health effects. The results showed that the odds ratio for hypertension increased by 1.12 (95% confidence interval CI, 1.08-1.16) per 19 μg/m(3) increase in PM(10), 1.11 (95% CI, 1.04-1.18) per 20 μg/m(3) increase in SO(2), and 1.13 (95% CI, 1.06-1.20) per 22 μg/m(3) increase in O(3). The estimated increases in mean systolic and diastolic blood pressure were 0.87 mm Hg (95% CI, 0.48-1.27) and 0.32 mm Hg (95% CI, 0.08-0.56) per 19 μg/m(3) interquartile increase in PM(10), 0.80 mm Hg (95% CI, 0.46-1.14) and 0.31 mm Hg (95% CI, 0.10-0.51) per 20 μg/m(3) interquartile increase in SO(2), and 0.73 mm Hg (95% CI, 0.35-1.11) and 0.37 mm Hg (95% CI, 0.14-0.61) per 22 μg/m(3) interquartile increase in O(3). These associations were only statistically significant in men. In conclusion, long-term exposure to PM(10), SO(2), and O(3) was associated with increased arterial blood pressure and hypertension in the study population.
Little is known about the joint mental health effects of air pollution and tobacco smoking in low- and middle-income countries.
To investigate the effects of exposure to ambient fine particulate ...matter pollution (PM
) and smoking and their combined (interactive) effects on depression.
Multilevel logistic regression analysis of baseline data of a prospective cohort study (
= 41 785). The 3-year average concentrations of PM
were estimated using US National Aeronautics and Space Administration satellite data, and depression was diagnosed using a standardised questionnaire. Three-level logistic regression models were applied to examine the associations with depression.
The odds ratio (OR) for depression was 1.09 (95% C11.01-1.17) per 10 μg/m
increase in ambient PM
, and the association remained after adjusting for potential confounding factors (adjusted OR = 1.10, 95% CI 1.02-1.19). Tobacco smoking (smoking status, frequency, duration and amount) was also significantly associated with depression. There appeared to be a synergistic interaction between ambient PM
and smoking on depression in the additive model, but the interaction was not statistically significant in the multiplicative model.
Our study suggests that exposure to ambient PM
may increase the risk of depression, and smoking may enhance this effect.
There are relatively few studies that focus on the health effects of exposure to size-specific particles on respiratory mortality in China. We aimed to examine the association between different ...particle sizes and mortality from cause-specific respiratory diseases. We used a time series model with a quasi-Poisson link to investigate the relationship between different particle sizes and mortality from respiratory diseases, chronic obstructive pulmonary diseases (COPD), pneumonia, and asthma in Shenzhen during 2014–2017. A total of 3716 mortalities due to respiratory diseases were collected. Both PM
1
and PM
2.5
were associated with mortality of overall respiratory diseases, COPD, and pneumonia. An interquartile range (IQR) increase in PM
1
at lag03 was associated with a 12.21% (95% CI: 2.59%, 22.75%) increase in respiratory mortality, and each IQR increase in PM
2.5
at lag03 corresponded to a 12.09% (95% CI: 2.52%, 22.56%) increase in respiratory mortality. PM
1-2.5
was not associated with mortality from all-cause or cause-specific respiratory diseases. This study suggests that both PM
1
and PM
2.5
may increase the risk of mortality due to respiratory diseases in Shenzhen, China.
No prior study has examined the effects of air pollution on the progression from healthy to chronic lung disease, subsequent chronic lung multimorbidity and further to death.
We used data from the UK ...Biobank of 265 506 adults free of chronic lung disease at recruitment. Chronic lung multimorbidity was defined as the coexistence of at least two chronic lung diseases, including asthma, chronic obstructive pulmonary disease and lung cancer. The concentrations of air pollutants were estimated using land-use regression models. Multistate models were applied to assess the effect of air pollution on the progression of chronic lung multimorbidity.
During a median follow-up of 11.9 years, 13 863 participants developed at least one chronic lung disease, 1055 developed chronic lung multimorbidity and 12 772 died. We observed differential associations of air pollution with different trajectories of chronic lung multimorbidity. Fine particulate matter showed the strongest association with all five transitions, with HRs (95% CI) per 5 µg/m
increase of 1.31 (1.22 to 1.42) and 1.27 (1.01 to 1.57) for transitions from healthy to incident chronic lung disease and from incident chronic lung disease to chronic lung multimorbidity, and 1.32 (1.21 to 1.45), 1.24 (1.01 to 1.53) and 1.91 (1.14 to 3.20) for mortality risk from healthy, incident chronic lung disease and chronic lung multimorbidity, respectively.
Our study provides the first evidence that ambient air pollution could affect the progression from free of chronic lung disease to incident chronic lung disease, chronic lung multimorbidity and death.
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