Effect of exposure to ambient PM2.5 pollution on the risk of respiratory tract diseases: a meta-analysis of cohort studies.
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ABSTRACT:
SUBMITTER: Liu Q
PROVIDER: S-EPMC5445216 | biostudies-other | 2017 Jan
REPOSITORIES: biostudies-other
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Project description:PURPOSE:To conduct the first epidemiologic study prospectively examining the association between particulate matter air pollution?<?2.5 µm in diameter (PM2.5) exposure and hepatocellular carcinoma (HCC) risk in the U.S. METHODS:Surveillance, Epidemiology, and End Results (SEER) provided information on HCC cases diagnosed between 2000 and 2014 from 16 population-based cancer registries across the U.S. Ambient PM2.5 exposure was estimated by linking the SEER county with a spatial PM2.5 model using a geographic information system. Poisson regression with robust variance estimation was used to calculate incidence rate ratios and 95% confidence intervals (CIs) for the association between ambient PM2.5 exposure per 10 µg/m3 increase and HCC risk adjusting for individual-level age at diagnosis, sex, race, year of diagnosis, SEER registry, and county-level information on health conditions, lifestyle, demographic, socioeconomic, and environmental factors. RESULTS:Higher levels of ambient PM2.5 exposure were associated with a statistically significant increased risk for HCC (n?=?56,245 cases; adjusted IRR per 10 µg/m3 increase?=?1.26, 95% CI 1.08, 1.47; p?<?0.01). CONCLUSIONS:If confirmed in studies with individual-level PM2.5 exposure and risk factor information, these results suggest that ambient PM2.5 exposure may be a risk factor for HCC in the U.S.
| S-EPMC5940508 | biostudies-literature
Project description:The association between air pollution and childhood respiratory disease is inconsistent. In the present study, we investigated a short-term effect of ambient air pollutants and daily childhood lower respiratory diseases (CLRD). Daily air pollutants, weather data, and CLRD data were collected from January 2014 to April 2015 (452 days) in Nanjing, China. Time-series regression and generalized additive models were used to assess the effects of air pollutants (PM10, PM2.5, NO2, SO2, O3, and CO) on CLRD. We observed that an interquartile range (IQR) increase in concentrations of PM10, NO2, and SO2 significantly increased the daily CLRD with 6 days cumulative effects (difference of estimates: 2.8%, 95% CI: 0.6-5.0%; 4.1%, 1.2-7.0%; 5.6%, 2.6-8.6%, respectively). However, no significant association was found in IQR concentrations of PM2.5, O3, and CO. Specifically, elevated PM10, PM2.5, NO2, and SO2 significantly increased the numbers of CLRD in cool season (3.6%, 1.5-5.7%; 2.4%, 0.3-4.5%; 4.9%, 2.9-7.0%; 6.3%, 3.7-9.0%, respectively). Additionally, the effect estimates of PM10, NO2, and SO2 in female and age >27 months were more pronounced than in male and age ≤27 months. This study suggested that short-term exposure to ambient PM10, NO2, and SO2 were associated with the increased CLRD numbers.
| S-EPMC5493680 | biostudies-literature
Project description:IntroductionThe health effects of ambient ozone have been investigated in many previous studies. However, the effects of long-term exposure to ambient ozone on the incidence of cardiovascular disease (CVD) remain inconclusive.ObjectivesTo estimate the associations of long-term exposure to maximum daily 8-hours average ozone (MDA8 O3) with the incidence of total CVD, heart disease, hypertension, and stroke.MethodsThis was a prospective cohort study, and the data was obtained from the China Health and Retirement Longitudinal Survey (CHARLS) implemented during 2011-2018 and the China Family Panel Studies (CFPS) implemented during 2010-2018. We applied a Cox proportional hazards regression model to evaluate the associations of MDA8 O3 with total CVD, heart disease, hypertension, and stroke risks, and the corresponding population-attributable fractions (PAF) attributable to MDA8 O3 were also calculated. All analyses were conducted by R software.ResultsThe mean MDA8 O3 concertation of all included participants in the CHARLS and CFPS were 51.03 part per billion (ppb) and 51.15 ppb, respectively. In the CHARLS including 18,177 participants, each 10 ppb increment in MDA8 O3 concentration was associated with a 31% increase [hazard ratio (HR) = 1.31, 95% confidence interval (CI): 1.22-1.42] in the risk of incident heart disease, and the corresponding population-attributable fractions (PAF) was 13.79% [10.12%-17.32%]. In the CFPS including 30,226 participants, each 10 ppb increment in MDA8 O3 concentration was associated with an increase in the risk of incident total CVD (1.07 [1.02-1.13]), and hypertension (1.10 [1.03-1.18]). The PAFs of total CVD, and hypertension attributable to MDA8 O3 were 3.53% [0.82%-6.16%], and 5.11% [1.73%-8.38%], respectively. Stratified analyses showed greater associations in males, urban areas, and Southern China.ConclusionsLong-term exposure to MDA8 O3 may increase the incidence of CVD. Therefore, the policies that control O3 and related precursors are persistently needed.
| S-EPMC11331174 | biostudies-literature
Project description:Smoking, sex, air pollution, lifestyle, and diet may act independently or in concert with each other to contribute to the different outcomes of lung cancer (LC). This study aims to explore their associations with the carcinogenesis of LC, which will be useful for formulating further preventive strategies. This retrospective, longitudinal follow-up cohort study was carried out by connecting to the MJ Health Database, Taiwan Cancer Registry database, and Taiwan cause of death database from 2000 to 2015. The studied subjects were persons attending the health check-ups, distributed throughout the main island of Taiwan. Cox proportional hazards regression models were used to investigate the risk factors associated with LC development and mortality after stratifying by smoking status, with a special emphasis on ambient two-year average PM2.5 exposure, using a satellite-based spatiotemporal model at a resolution of 1 km2, and on dietary habit including consumption of fruits and vegetables. After a median follow-up of 12.3 years, 736 people developed LC, and 401 people died of LC-related causes. For never smokers, the risk of developing LC (aHR: 1.32, 95%CI: 1.12-1.56) and dying from LC-related causes (aHR: 1.28, 95%CI: 1.01-1.63) rises significantly with every 10 μg/m3 increment of PM2.5 exposure, but not for ever smokers. Daily consumption of more than two servings of vegetables and fruits is associated with lowering LC risk in ever smokers (aHR: 0.68, 95%CI: 0.47-0.97), and preventing PM2.5 exposure is associated with lowering LC risk for never smokers.
| S-EPMC8656990 | biostudies-literature
Project description:Study questionTo what extent are ambient concentrations of particulate matter <2.5 microns (PM2.5), nitrogen dioxide (NO2) and ozone (O3) associated with risk of self-reported physician-diagnosed uterine leiomyomata (UL)?Summary answerIn this large prospective cohort study of Black women, ambient concentrations of O3, but not PM2.5 or NO2, were associated with increased risk of UL.What is known alreadyUL are benign tumors of the myometrium that are the leading cause of gynecologic inpatient care among reproductive-aged women. Black women are clinically diagnosed at two to three times the rate of white women and tend to exhibit earlier onset and more severe disease. Two epidemiologic studies have found positive associations between air pollution exposure and UL risk, but neither included large numbers of Black women.Study design, size, durationWe conducted a prospective cohort study of 21 998 premenopausal Black women residing in 56 US metropolitan areas from 1997 to 2011.Participants/material, setting, methodsWomen reported incident UL diagnosis and method of confirmation (i.e. ultrasound, surgery) on biennial follow-up questionnaires. We modeled annual residential concentrations of PM2.5, NO2 and O3 throughout the study period. We used Cox proportional hazards regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for a one-interquartile range (IQR) increase in air pollutant concentrations, adjusting for confounders and co-pollutants.Main results and the role of chanceDuring 196 685 person-years of follow-up, 6238 participants (28.4%) reported physician-diagnosed UL confirmed by ultrasound or surgery. Although concentrations of PM2.5 and NO2 were not appreciably associated with UL (HRs for a one-IQR increase: 1.01 (95% CI: 0.93, 1.10) and 1.05 (95% CI: 0.95, 1.16), respectively), O3 concentrations were associated with increased UL risk (HR for a one-IQR increase: 1.19, 95% CI: 1.07, 1.32). The association was stronger among women age <35 years (HR: 1.26, 95% CI: 0.98, 1.62) and parous women (HR: 1.28, 95% CI: 1.11, 1.48).Limitations, reasons for cautionOur measurement of air pollution is subject to misclassification, as monitoring data are not equally spatially distributed and we did not account for time-activity patterns. Our outcome measure was based on self-report of a physician diagnosis, likely resulting in under-ascertainment of UL. Although we controlled for several individual- and neighborhood-level confounding variables, residual confounding remains a possibility.Wider implications of the findingsInequitable burden of air pollution exposure has important implications for racial health disparities, and may be related to disparities in UL. Our results emphasize the need for additional research focused on environmental causes of UL.Study funding/competing interest(s)This research was funded by the National Cancer Institute (U01-CAA164974) and the National Institute of Environmental Health Sciences (R01-ES019573). L.A.W. is a fibroid consultant for AbbVie, Inc. and accepts in-kind donations from Swiss Precision Diagnostics, Sandstone Diagnostics, FertilityFriend.com and Kindara.com for primary data collection in Pregnancy Study Online (PRESTO). M.J. declares consultancy fees from the Health Effects Institute (as a member of the review committee). The remaining authors declare they have no actual or potential competing financial interests.Trial registration numberN/A.
| S-EPMC8487660 | biostudies-literature
Project description:BackgroundThe influences of air pollution exposure and temperature on respiratory diseases have become major global health concerns. This study investigated the relationship between ambient air pollutant concentrations and temperature in cold industrial cities that have the risk of hospitalization for respiratory diseases.MethodsA time-series study was conducted in Changchun, China, from 2015 to 2019 to analyse the number of daily admissions for respiratory diseases, air pollutant concentrations, and meteorological factors. Time-series decomposition was applied to analyse the trend and characteristics of the number of admissions. Generalized additive models and distributed lag nonlinear models were constructed to explore the effects of air pollutant concentrations and temperature on the number of admissions.ResultsThe number of daily admissions showed an increasing trend, and the seasonal fluctuation was obvious, with more daily admissions in winter and spring than in summer and autumn. There were positive and gradually decreasing lag effects of PM10, PM2.5, NO2, and CO concentrations on the number of admissions, whereas O3 showed a J-shaped trend. The results showed that within the 7-day lag period, 0.5°C was the temperature associated with the lowest relative risk of admission due to respiratory disease, and extremely low and high temperatures (<-18°C, >27°C, respectively) increased the risk of hospitalization for respiratory diseases by 8.3% and 12.1%, respectively.ConclusionsFrom 2015 to 2019, respiratory diseases in Changchun showed an increasing trend with obvious seasonality. The increased concentrations of SO2, NO2, CO, PM2.5, O3 and PM10 lead to an increased risk of hospitalization for respiratory diseases, with a significant lag effect. Both extreme heat and cold could lead to increases in the risk of admission due to respiratory disease.
| S-EPMC9569423 | biostudies-literature
Project description:BACKGROUND:Air pollution alters small pulmonary vessels in animal models. We hypothesised that long-term ambient air pollution exposure would be associated with differences in pulmonary vascular volumes in a population-based study. METHODS:The Multi-Ethnic Study of Atherosclerosis recruited adults in six US cities. Personalised long-term exposures to ambient black carbon, nitrogen dioxide (NO2), oxides of nitrogen (NO x ), particulate matter with a 50% cut-off aerodynamic diameter of <2.5??m (PM2.5) and ozone were estimated using spatiotemporal models. In 2010-2012, total pulmonary vascular volume was measured as the volume of detectable pulmonary arteries and veins, including vessel walls and luminal blood volume, on noncontrast chest computed tomography (TPVVCT). Peripheral TPVVCT was limited to the peripheral 2?cm to isolate smaller vessels. Linear regression adjusted for demographics, anthropometrics, smoking, second-hand smoke, renal function and scanner manufacturer. RESULTS:The mean±sd age of the 3023 participants was 69.3±9.3?years; 46% were never-smokers. Mean exposures were 0.80??g·m-3 black carbon, 14.6?ppb NO2 and 11.0??g·m-3 ambient PM2.5. Mean±sd peripheral TPVVCT was 79.2±18.2?cm3 and TPVVCT was 129.3±35.1?cm3. Greater black carbon exposure was associated with a larger peripheral TPVVCT, including after adjustment for city (mean difference 0.41 (95% CI 0.03-0.79)?cm3 per interquartile range; p=0.036). Associations for peripheral TPVVCT with NO2 were similar but nonsignificant after city adjustment, while those for PM2.5 were of similar magnitude but nonsignificant after full adjustment. There were no associations for NO x or ozone, or between any pollutant and TPVVCT. CONCLUSIONS:Long-term black carbon exposure was associated with a larger peripheral TPVVCT, suggesting diesel exhaust may contribute to remodelling of small pulmonary vessels in the general population.
| S-EPMC6910868 | biostudies-literature
Project description:The effectiveness of regulatory actions designed to improve air quality is often assessed by predicting changes in public health resulting from their implementation. Risk of premature mortality from long-term exposure to ambient air pollution is the single most important contributor to such assessments and is estimated from observational studies generally assuming a log-linear, no-threshold association between ambient concentrations and death. There has been only limited assessment of this assumption in part because of a lack of methods to estimate the shape of the exposure-response function in very large study populations. In this paper, we propose a new class of variable coefficient risk functions capable of capturing a variety of potentially non-linear associations which are suitable for health impact assessment. We construct the class by defining transformations of concentration as the product of either a linear or log-linear function of concentration multiplied by a logistic weighting function. These risk functions can be estimated using hazard regression survival models with currently available computer software and can accommodate large population-based cohorts which are increasingly being used for this purpose. We illustrate our modeling approach with two large cohort studies of long-term concentrations of ambient air pollution and mortality: the American Cancer Society Cancer Prevention Study II (CPS II) cohort and the Canadian Census Health and Environment Cohort (CanCHEC). We then estimate the number of deaths attributable to changes in fine particulate matter concentrations over the 2000 to 2010 time period in both Canada and the USA using both linear and non-linear hazard function models.
| S-EPMC5093184 | biostudies-literature
Project description:Human exposure to fine particles can have significant harmful effects on the respiratory and cardiovascular system. To investigate daily exposure characteristics to PM2.5 with ambient concentrations in an urban environment, a personal exposure measurements were conducted for school children, office workers and at their residents, in the city of Taj 'Agra', India. In order to account for all the sources of particulate matter exposure, measurements on several different days during December 2013 to February 2014 were carried out. Personal environment monitors (PEM) and APM 550 were used to measure PM2.5 concentration. The research findings provide insight into possible sources and their interaction with human activities in modifying the human exposure levels.
| S-EPMC4716460 | biostudies-literature
Project description:Using a case-crossover study design and conditional logistic regression, we compared the relative odds of transmural (full-wall) myocardial infarction (MI) calculated using exposure surrogates that account for human activity patterns and the indoor transport of ambient PM(2.5) with those calculated using central-site PM(2.5) concentrations to estimate exposure to PM(2.5) of outdoor origin (exposure to ambient PM(2.5)). Because variability in human activity and indoor PM(2.5) transport contributes exposure error in epidemiologic analyses when central-site concentrations are used as exposure surrogates, we refer to surrogates that account for this variability as "refined" surrogates. As an alternative analysis, we evaluated whether the relative odds of transmural MI associated with increases in ambient PM(2.5) is modified by residential air exchange rate (AER), a variable that influences the fraction of ambient PM(2.5) that penetrates and persists indoors. Use of refined exposure surrogates did not result in larger health effect estimates (ORs=1.10-1.11 with each interquartile range (IQR) increase), narrower confidence intervals, or better model fits compared with the analysis that used central-site PM(2.5). We did observe evidence for heterogeneity in the relative odds of transmural MI with residential AER (effect-modification), with residents of homes with higher AERs having larger ORs than homes in lower AER tertiles. For the level of exposure-estimate refinement considered here, our findings add support to the use of central-site PM(2.5) concentrations for epidemiological studies that use similar case-crossover study designs. In such designs, each subject serves as his or her own matched control. Thus, exposure error related to factors that vary spatially or across subjects should only minimally impact effect estimates. These findings also illustrate that variability in factors that influence the fraction of ambient PM(2.5) in indoor air (e.g., AER) could possibly bias health effect estimates in study designs for which a spatiotemporal comparison of exposure effects across subjects is conducted.
| S-EPMC4084717 | biostudies-literature