Dataset Information

Age-Period-Cohort Analysis of Type 2 Diabetes Mortality Attributable to Particulate Matter Pollution in China and the U.S.

ABSTRACT: Aim:We aimed to assess and compare secular trends in type 2 diabetes mortality attributable to particulate matter pollution in China and U.S. Methods:We performed an age-period-cohort (APC) analysis to estimate the independent effects of age, period, and cohort on mortality of type 2 diabetes attributable to particulate matter pollution. We collected age-standardized and age-specific mortality rates (1990-2017) from the Global Burden of Disease 2017 Study for China and the U.S. Results:During the period 1990-2017, the age-standardized mortality rates of type 2 diabetes attributable to particulate matter pollution in China showed a general increasing trend, while that in U.S. showed an increase before 2002 and subsequently a decrease. The age effect increased markedly in China compared with the U.S. The period effect showed a substantially increase in China while that in the U.S. increased during 1990-2007 and tended to be stable during 2007-2017. The cohort effect peaked in birth cohort born in 1902-1906 in both China and U.S. and declined consistently in the cohort born in 1992-1996. Conclusions:The age-standardized mortality rates of type 2 diabetes attributable to particulate matter pollution, the age, and period effect in China have been increasing in both sexes from 1990 to 2017. The overall mortality in the U.S. began to decrease since 2003, and the period effect showed a tendency to stabilize. Consequently, it is necessary to educate the nation with the correct knowledge and adopting policies on pollutant emission and techniques to reduce air pollution in China.

SUBMITTER: Liu X

PROVIDER: S-EPMC7306083 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Age-Period-Cohort Analysis of Type 2 Diabetes Mortality Attributable to Particulate Matter Pollution in China and the U.S.

Liu Xiaoxue X Zhou Maigeng M Yu Chuanhua C Zhang Zhi-Jiang ZJ

Journal of diabetes research 20200611

<h4>Aim</h4>We aimed to assess and compare secular trends in type 2 diabetes mortality attributable to particulate matter pollution in China and U.S.<h4>Methods</h4>We performed an age-period-cohort (APC) analysis to estimate the independent effects of age, period, and cohort on mortality of type 2 diabetes attributable to particulate matter pollution. We collected age-standardized and age-specific mortality rates (1990-2017) from the Global Burden of Disease 2017 Study for China and the U.S.<h4 ...[more]

PMID: 32626775

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Project description:Using daily fine particulate matter (PM2.5) composition data from the 2000-2005 U.S. EPA Chemical Speciation Network (CSN) for over 200 sites, we applied multivariate methods to identify and quantify the major fine particulate matter (PM2.5) source components in the U.S. Novel aspects of this work were: (1) the application of factor analysis (FA) to multi-city daily data, drawing upon both spatial and temporal variations of chemical species; and, (2) the exclusion of secondary components (sulfates, nitrates and organic carbon) from the source identification FA to more clearly discern and apportion the PM2.5 mass to primary emission source categories. For the quantification of source-related mass, we considered two approaches based upon the FA results: 1) using single key tracers for sources identified by FA in a mass regression; and, 2) applying Absolute Principal Component Analysis (APCA). In each case, we followed a two-stage mass regression approach, in which secondary components were first apportioned among the identified sources, and then mass was apportioned to the sources and to other secondary mass not explained by the individual sources. The major U.S. PM2.5 source categories identified via FA (and their key elements) were: Metals Industry (Pb, Zn); Crustal/Soil Particles (Ca, Si); Motor Vehicle Traffic (EC, NO2); Steel Industry (Fe, Mn); Coal Combustion (As, Se); Oil Combustion (V, Ni); Salt Particles (Na, Cl) and Biomass Burning (K). Nationwide spatial plots of the source-related PM2.5 impacts were confirmatory of the factor interpretations: ubiquitous sources, such as Traffic and Soil, were found to be spread across the nation, more unique sources (such as Steel and Metals Processing) being highest in select industrialized cities, Biomass Burning was highest in the U.S. Northwest, while Residual Oil combustion was highest in cities in the Northeastern U.S. and in cities with major seaports. The sum of these source contributions and the secondary PM2.5 components agreed well with the U.S. PM2.5 observed during the study period (mean=14.3 ug/m3; R2= 0.91). Apportionment regression analyses using single-element tracers for each source category gave results consistent with the APCA estimates. Comparisons of nearby sites indicated that the PM2.5 mass and the secondary aerosols were most homogenous spatially, while traffic PM2.5 and its tracer, EC, were among the most spatially representative of the source-related components. Comparison of apportionment results to a previous analysis of the 1979-1982 IP Network revealed similar and correlated major U.S. source category factors, albeit at lower levels than in the earlier period, suggesting a consistency in the U.S. spatial patterns of these source-related exposures over time, as well. These results indicate that applying source apportionment methods to the nationwide CSN can be an informative avenue for identifying and quantifying source components for the subsequent estimation of source-specific health effects, potentially contributing to more efficient regulation of PM2.5.

Project description:BackgroundIt remains unclear whether in utero and childhood exposure to air pollution affects pubertal development, particularly age of menarche in girls.ObjectiveThe aim of this study was to determine whether residential ambient particulate matter (PM) exposure in utero and during childhood is associated with age of menarche.MethodsWe studied 5,201 girls in the Growing Up Today Study 2 (2004-present) who were 10-17 y of age at enrollment (47.7% premenarchal; 52.3% postmenarchal). Exposure to three size fractions of PM [fine PM with aerodynamic diameter ≤2.5μm (PM2.5), PM with aerodynamic diameters between 2.5μm and 10μm (PM2.5-10), and PM with aerodynamic diameter 10μm (PM10)] was assigned based on maternal residential address, updated every 2 y, using nationwide spatiotemporal models. We estimated average PM exposure in utero, and time-varying windows: annual average exposure in the prior 1 and 2 y and cumulative average from birth. Age of menarche was self-reported on three surveys administered in 2004, 2006, and 2008. We calculated hazard ratios (HR) for menarche for an interquartile range (IQR) increase in PM exposure using Cox proportional hazard models adjusting for potential confounders.ResultsGirls attained menarche at 12.3 y of age on average. In the adjusted model, higher residential exposure to ambient PM2.5 during all time windows was associated with earlier age of menarche. The HRs of menarche for each IQR (4 μg/m3) increase in exposure to PM2.5 during the in utero period, 1 y prior to menarche, and throughout childhood were 1.03 [95% confidence interval (CI): 1.00, 1.06], 1.06 (95% CI: 1.02, 1.10) and 1.06 (95% CI: 1.02, 1.10), respectively. Effect estimates for PM10 exposure were similar, albeit attenuated, for all time windows. PM2.5-10 exposure was not associated with age of menarche.DiscussionAmong a large, nationwide, prospective cohort of U.S. girls, higher exposure to PM2.5 and PM10 in utero and throughout childhood was associated with an earlier age of menarche. Our results suggest that PM2.5 and PM10 may have endocrine-disrupting properties that could lead to altered timing of menarche. https://doi.org/10.1289/EHP12110.

Project description:BackgroundEpigenetic age, as defined by DNA methylation, may be influenced by air pollution exposure.ObjectiveTo evaluate the relationship between NO2, particulate matter (PM), PM components and accelerated epigenetic age.MethodsIn a sample of non-Hispanic white women living in the contiguous U.S. (n = 2747), we estimated residential exposure to PM2.5, PM10 and NO2 using a model incorporating land-use regression and kriging. Predictive k-means was used to assign participants to clusters representing different PM2.5 component profiles. We measured DNA methylation (DNAm) in blood using the Illumina's Infinium HumanMethylation450 BeadChip and calculated DNAm age using the Hannum, Horvath and Levine epigenetic clocks. Age acceleration was defined based on residuals after regressing DNAm age on chronological age. We estimated associations between interquartile range (IQR) increases in pollutants and age acceleration using linear regression. For PM2.5, we stratified by cluster membership. We examined epigenome-wide associations using robust linear regression models corrected with false discovery rate q-values.ResultsNO2 was inversely associated with age acceleration using the Hannum clock (β = -0.24, 95% CI: -0.47, -0.02). No associations were observed for PM10. For PM2.5, the association with age acceleration varied by PM2.5 component cluster. For example, with the Levine clock, an IQR increase in PM2.5 was associated with an over 6-year age acceleration in a cluster that has relatively high fractions of crustal elements relative to overall PM2.5 (β = 6.57, 95% CI: 2.68, 10.47), and an almost 2-year acceleration in a cluster characterized by relatively low sulfur fractions (β = 1.88, 95% CI: 0.51, 3.25). In a cluster distinguished by lower relative nitrate concentrations, PM2.5 was inversely associated with age acceleration (β = -1.33, 95% CI: -2.43, -0.23). Across the epigenome, NO2 was associated with methylation at 2 CpG sites.ConclusionAir pollution was associated with epigenetic age, a marker of mortality and disease risk, among certain PM2.5 component profiles.

Dataset Information

Age-Period-Cohort Analysis of Type 2 Diabetes Mortality Attributable to Particulate Matter Pollution in China and the U.S.

Publications

Age-Period-Cohort Analysis of Type 2 Diabetes Mortality Attributable to Particulate Matter Pollution in China and the U.S.

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