Long-term exposure to air pollution and type 2 diabetes mellitus in a multiethnic cohort.
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ABSTRACT:
SUBMITTER: Park SK
PROVIDER: S-EPMC4339386 | biostudies-literature | 2015 Mar
REPOSITORIES: biostudies-literature
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Long-term exposure to air pollution and type 2 diabetes mellitus in a multiethnic cohort.
Park Sung Kyun SK Adar Sara D SD O'Neill Marie S MS Auchincloss Amy H AH Szpiro Adam A Bertoni Alain G AG Navas-Acien Ana A Kaufman Joel D JD Diez-Roux Ana V AV
American journal of epidemiology 20150217 5
Although air pollution has been suggested as a possible risk factor for type 2 diabetes mellitus (DM), results from existing epidemiologic studies have been inconsistent. We investigated the associations of prevalence and incidence of DM with long-term exposure to air pollution as estimated using annual average concentrations of particulate matter with an aerodynamic diameter of 2.5 μm or less (PM₂.₅) and nitrogen oxides at baseline (2000) in the Multi-Ethnic Study of Atherosclerosis. All partic ...[more]
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Project description:BACKGROUND:Malaysia has the highest rate of diabetes mellitus (DM) in the Southeast Asian region, and has ongoing air pollution and periodic haze exposure. METHODS:Diabetes data were derived from the Malaysian National Health and Morbidity Surveys conducted in 2006, 2011 and 2015. The air pollution data (NOx, NO2, SO2, O3 and PM10) were obtained from the Department of Environment Malaysia. Using multiple logistic and linear regression models, the association between long-term exposure to these pollutants and prevalence of diabetes among Malaysian adults was evaluated. RESULTS:The PM10 concentration decreased from 2006 to 2014, followed by an increase in 2015. Levels of NOx decreased while O3 increased annually. The air pollutant levels based on individual modelled air pollution exposure as measured by the nearest monitoring station were higher than the annual averages of the five pollutants present in the ambient air. The prevalence of overall diabetes increased from 11.4% in 2006 to 21.2% in 2015. The prevalence of known diabetes, underdiagnosed diabetes, overweight and obesity also increased over these years. There were significant positive effect estimates of known diabetes at 1.125 (95% CI, 1.042, 1.213) for PM10, 1.553 (95% CI, 1.328, 1.816) for O3, 1.271 (95% CI, 1.088, 1.486) for SO2, 1.124 (95% CI, 1.048, 1.207) for NO2, and 1.087 (95% CI, 1.024, 1.153) for NOx for NHMS 2006. The adjusted annual average levels of PM10 [1.187 (95% CI, 1.088, 1.294)], O3 [1.701 (95% CI, 1.387, 2.086)], NO2 [1.120 (95% CI, 1.026, 1.222)] and NOx [1.110 (95% CI, 1.028, 1.199)] increased significantly from NHMS 2006 to NHMS 2011 for overall diabetes. This was followed by a significant decreasing trend from NHMS 2011 to 2015 [0.911 for NO2, and 0.910 for NOx]. CONCLUSION:The findings of this study suggest that long-term exposure to O3 is an important associated factor of underdiagnosed DM risk in Malaysia. PM10, NO2 and NOx may have mixed effect estimates towards the risk of DM, and their roles should be further investigated with other interaction models. Policy and intervention measures should be taken to reduce air pollution in Malaysia.
| S-EPMC7119016 | biostudies-literature
Project description:BACKGROUND:Air pollution exposures have been shown to adversely impact health through a number of biological pathways associated with glucose metabolism. However, few studies have evaluated the associations between air pollution and glycosylated hemoglobin (HbA1c) levels. Further, no studies have evaluated these associations in US populations or investigated whether associations differ in diabetic as compared to non-diabetic populations. To address this knowledge gap, we investigated the associations between airborne fine particulate matter (PM2.5) and nitrogen dioxide (NO2) and HbA1c levels in both diabetic and non-diabetic older Americans. We also examined the impact of PM2.5 and NO2 on prevalent diabetes mellitus (DM) in this cohort. METHODS:We used multilevel logistic and linear regression models to evaluate the association between long-term average air pollutant levels and prevalence of DM and HbA1c levels, respectively, among 4121 older (57+ years) Americans enrolled in the National Social Life, Health, and Aging Project between 2005 and 2011. All models adjusted for age, sex, body mass index, smoking status, race, household income, education level, neighborhood socioeconomic status, geographic region, urbanicity and diabetic medication use. We estimated participant-specific exposures to PM2.5 on a six-kilometer grid covering the conterminous U.S. using spatio-temporal models, and to NO2 using nearest measurements from the Environmental Protection Agency's Air Quality System. HbA1c levels were measured for participants in each of two data collection waves from dried blood spots and log-transformed prior to analysis. Participants were considered diabetic if they had HbA1c values?6.5% or reported taking diabetic medication. RESULTS:The prevalence of diabetes at study entry was 22.2% (n=916) and the mean HbA1c was 6.0±1.1%. Mean one-year moving average PM2.5 and NO2 exposures were 10.4±3.0?g/m3 and 13.1±7.0 ppb, respectively. An inter-quartile range (IQR, 3.9?g/m3) increase in one-year moving average PM2.5 was positively associated with increased diabetes prevalence (prevalence odds ratio, POR 1.35, 95% CI: 1.19, 1.53). Similarly, an IQR (8.6 ppb) increase in NO2 was also significantly associated with diabetes prevalence (POR 1.27, 95% CI: 1.10, 1.48). PM2.5 (1.8%±0.6%, p<0.01) and NO2 (2.0%±0.7%, p<0.01) exposures were associated with higher HbA1c levels in diabetic participants, while only NO2 was significantly associated with HbA1c in non-diabetic participants (0.8%±0.2%, p<0.01). Significant dose response relationships were identified for both pollutants in diabetic participants and for NO2 in non-diabetic participants. CONCLUSIONS/INTERPRETATIONS:In a cohort of older men and women in the United States, PM2.5 and NO2 exposures were significantly associated with prevalence of DM and increased HbA1c levels among both non-diabetic and diabetic participants. These associations suggest that air pollution could be a key risk factor for abnormal glucose metabolism and diabetes in the elderly.
| S-EPMC5580354 | biostudies-literature
Project description:BACKGROUND:Ambient air pollution and maternal diabetes may affect common biological pathways underlying adverse neurodevelopmental effects. However, joint effects of maternal diabetes and air pollution on autism spectrum disorder (ASD) have not been studied. OBJECTIVE:We evaluated whether prenatal and early-life air pollution exposure interacts with maternal diabetes status to affect ASD risk. METHODS:This retrospective cohort study included 246,420 singleton children born in Kaiser Permanente Southern California hospitals in 1999-2009. Children were followed from birth until age 5, during which 2471 ASD cases were diagnosed. Ozone (O3), particulate matter?<?2.5??m (PM2.5) and <10??m in aerodynamic diameter, and nitrogen dioxide measured at regulatory air monitoring stations were interpolated to estimate exposures during preconception and each pregnancy trimester, and first year of life at each child's birth address. Hazard ratios (HRs) for ASD were estimated adjusting for birth year, KPSC service areas, and relevant maternal and child characteristics. For each exposure window, interactions were tested between pollutants and a 4-category maternal diabetes variable (none, GDM???24 and <24?weeks' gestation, and pre-existing type 2 diabetes). For an exposure window with statistically significant global interaction between pollutant and diabetes (p?<?0.05), pollutant-associated HRs were estimated separately for each category of maternal diabetes. RESULTS:There were associations of ASD with preconception, first and third trimesters, and first year of life PM2.5, but not with other pollutants. There were, however, interactions of maternal diabetes with first trimester and first year of life O3. Increased ASD risk was associated with first trimester O3 among mothers with GDM?<?24?weeks' gestation [adjusted HR 1.50 per 15.7?ppb O3 (95% CI: 1.08-2.09)]. No O3 associations with ASD were observed in other categories of maternal diabetes. CONCLUSIONS:GDM onset early in pregnancy may increase children's susceptibility to prenatal O3-associated ASD risk. These novel findings merit further investigation.
| S-EPMC7250244 | biostudies-literature
Project description:RationaleSeveral studies have linked long-term exposure to particulate air pollution with increased cardiopulmonary mortality; only two have also examined incident circulatory disease.ObjectivesTo examine associations of individualized long-term exposures to particulate and gaseous air pollution with incident myocardial infarction and stroke, as well as all-cause and cause specific mortality.MethodsWe estimated long-term residential air pollution exposure for more than 100,000 participants in the California Teachers Study, a prospective cohort of female public school professionals.We linked geocoded residential addresses with inverse distance-weighted monthly pollutant surfaces for two measures of particulate matter and for several gaseous pollutants. We examined associations between exposure to these pollutants and risks of incident myocardial infarction and stroke, and of all-cause and cause-specific mortality, using Cox proportional hazards models.Measurements and main resultsWe found elevated hazard ratios linking long-term exposure to particulate matter less than 2.5 ?m in aerodynamic diameter (PM2.5), scaled to an increment of 10 ?g/m3 with mortality from ischemic heart disease (IHD) (1.20; 95% confidence interval [CI], 1.02-1.41) and, particularly among postmenopausal women, incident stroke (1.19; 95% CI, 1.02-1.38). Long-term exposure to particulate matter less than 10 ?m in aerodynamic diameter (PM10) was associated with elevated risks for IHD mortality (1.06; 95% CI, 0.99-1.14) and incident stroke (1.06; 95% CI, 1.00-1.13), while exposure to nitrogen oxides was associated with elevated risks for IHD and all cardiovascular mortality.ConclusionsThis study provides evidence linking long-term exposure to PM2.5 and PM10 with increased risks of incident stroke as well as IHD mortality; exposure to nitrogen oxides was also related to death from cardiovascular diseases.
| S-EPMC3208653 | biostudies-literature
Project description:Cirrhosis is an advanced liver disease affecting millions of people worldwide, involving high healthcare costs. Despite experimental evidence suggesting a possible role of airborne pollutants in liver diseases, epidemiological studies are lacking. We aimed at investigating the association between exposure to air pollutants and incidence of cirrhosis in a large population-based cohort in Rome.MethodsWe used an administrative cohort established from the 2001 census. We included all adults of 30 years of age or older who were free of cirrhosis, resulting in a study population of over 1.2 million subjects. Follow-up of the subjects ended on 31 December 2015. We ascertained incident cases of cirrhosis from regional mortality and hospital discharge registries using a validated algorithm. We assessed exposure of the subjects to PM10, PM coarse, PM2.5, PM2.5 absorbance, NO2, NOx, and PM metal components at their residential address using Land Use Regression models. We used Cox regression models, adjusted for relevant covariates, to estimate the association between air pollution exposure and cirrhosis incidence.ResultsWe observed 10,111 incident cases of cirrhosis, with a crude incidence rate of 67 × 100,000 person-years. Long-term exposure to all pollutants tested was significantly associated with cirrhosis, e.g., PM10 (hazard ratios [HR], 1.05; 95% confidence interval [CI], 1.01-1.09, per 10 µg/m3 increments), PM coarse (HR, 1.11; 95% CI, 1.05-1.17, per 10 µg/m3 increments), PM2.5 (HR, 1.08; 95% CI, 1.03-1.13, per 5 µg/m3 increments), and NO2 (HR, 1.03; 95% CI, 1.02-1.05, per 10 µg/m3 increments). The associations were robust in secondary analyses.ConclusionsOur findings suggest a possible contribution of air pollution to the development of cirrhosis.
| S-EPMC7941789 | biostudies-literature
Project description:BackgroundStudies of effects of air pollution on gestational diabetes mellitus (GDM) have not been consistent, and there has been little investigation of effects of exposure preceding pregnancy. In previous studies, the temporal relationship between exposure and GDM onset has been difficult to establish.MethodsData were obtained for 239,574 pregnancies between 1999 and 2009 in a population-based health care system with comprehensive electronic medical records. Concentrations of ambient nitrogen dioxide (NO2), particulate matter (PM) ≤2.5 μm in aerodynamic diameter (PM2.5) and ≤10 μm (PM10), and ozone (O3) during preconception and the first trimester of pregnancy at the residential birth address were estimated from regulatory air monitoring stations. Odds ratios (ORs) of GDM diagnosed in the second and third trimesters in association with pollutant exposure were estimated using generalized estimating equation models adjusted for birth year, medical center service areas, maternal age, race/ethnicity, education, census-tract household income, and parity.ResultsIn single-pollutant models, preconception NO2 was associated with increased risk of GDM (OR = 1.10 per 10.4 ppb, 95% confidence interval [CI]: 1.07, 1.13). First trimester NO2 was weakly associated with GDM, and this was not statistically significant (OR = 1.02 per 10.4 ppb, 95% CI: 0.99, 1.05). Preconception NO2 associations were robust in multi-pollutant models adjusted for first trimester NO2 with another co-pollutant from both exposure windows. In single-pollutant models, preconception PM2.5 and PM10 associations were associated with increased risk of GDM (OR = 1.04 per 6.5 μg/m3, 95% CI: 1.01, 1.06; OR = 1.03 per 16.1 μg/m3, 95% CI: 1.00, 1.06, respectively), but these effect estimates were not robust to adjustment for other pollutants. In single-pollutant models, preconception and first trimester O3 were associated with reduced risk of GDM (OR = 0.94 per 15.7 ppb, 95% CI: 0.92, 0.95; OR = 0.95 per 15.7 ppb, 95% CI: 0.94, 0.97), associations that were robust to adjustment for co-pollutants.ConclusionsMaternal exposure to NO2 during the preconception trimester may increase risk of GDM.
| S-EPMC6684238 | biostudies-literature
Project description:BackgroundAir pollution exposure has been linked to coronary heart disease, although evidence on PM2.5 and myocardial infarction (MI) incidence is mixed.ObjectivesThis prospective cohort study aimed to investigate associations between long-term exposure to air pollution and MI incidence, adjusting for road traffic noise.MethodsWe used data from the nationwide Danish Nurse Cohort on 22,882 female nurses (>44?years of age) who, at recruitment in 1993 or 1999, reported information on cardiovascular disease risk factors. Data on MI incidence was collected from the Danish National Patient Register until the end of 2014. Annual mean concentrations of particulate matter (PM) with a diameter <2.5??g/m3 (PM2.5), PM10, nitrogen dioxide (NO2), and nitrogen oxides (NOx) at the nurses' residences since 1990 (PM10 and PM2.5) or 1970 (NO2 and NOx) were estimated using the Danish Eulerian Hemispheric Model/Urban Background Model/AirGIS (DEHM/UBM/AirGIS) dispersion model. We used time-varying Cox regression models to examine the association between 1- and 3-y running means of these pollutants, as well as 23-y running means of NO2 and NOx, with both overall and fatal incident MI. Associations were explored in three progressively adjusted models: Model 1, adjusted for age and baseline year; Model 2, with further adjustment for potential confounding by lifestyle and cardiovascular disease risk factors; and Model 3, with further adjustment for road traffic noise, modeled as the annual mean of a weighted 24-h average (Lden).ResultsOf the 22,882 women, 641 developed MI during a mean follow-up of 18.6 y, 121 (18.9%) of which were fatal. Reported hazard ratios (HRs) were based on interquartile range increases of 5.3, 5.5, 8.1, and 11.5??g/m3 for PM2.5, PM10, NO2, and NOx, respectively. In Model 1, we observed a positive association between a 3-y running mean of PM2.5 and an overall incident MI with an HR=?1.20 (95% CI: 1.07, 1.35), which attenuated to HR=?1.06 (95% CI: 0.92, 1.23) in Model 2. In Model 1 for incident fatal MI, we observed a strong association with a 3-y running mean of PM2.5, with an HR=?1.69 (95% CI: 1.33, 2.13), which attenuated to HR=?1.35 (95% CI: 1.01, 1.81) in Model 2. Similar associations were seen for PM10, with 3-y, Model 2 estimates for overall and fatal incident MI of HR=?1.06 (95% CI: 0.91, 1.23) and HR=?1.35 (95% CI: 1.01, 1.81), respectively. No evidence of an association was observed for NO2 or NOx. For all pollutants, associations in Model 2 were robust to further adjustment for road traffic noise in Model 3 and were similar for a 1-y running mean exposure.ConclusionsWe found no association between long-term exposure to PM2.5, PM10, NO2, or NOx and overall MI incidence, but we observed positive associations for PM2.5 and PM10 with fatal MI. We present novel findings that the association between PM and MI incidence is robust to adjustment for road traffic noise. https://doi.org/10.1289/EHP5818.
| S-EPMC7263451 | biostudies-literature
Project description:Background and Purpose- China bears a heavy burden of stroke because of its large population of elderly people and the propensity for stroke. Previous studies have examined the association between air pollution and stroke mortality or hospital admission. However, the global evidence for adverse effects of air pollution on survival after stroke is scarce. Methods- We used the first national hospital-based prospective registry cohort of stroke in China, which included 12?291 ischemic stroke patients who visited hospitals during 2007 to 2008. All patients were followed for 1-year poststroke. Deaths during the follow-up period were recorded. Participants' 3-year prestroke exposures to ambient PM1, PM2.5, PM10 (particulate matter with aerodynamic diameters ?1, ?2.5, and ?10 ?m, respectively) and NO2 (nitrogen dioxide) were estimated by machine learning algorithms with satellite remote sensing, land use information, and meteorological data. Cox proportional hazards models were used to examine the association between air pollution and survival after ischemic stroke. Results- In total, 1649 deaths were identified during the 1-year follow-up period. After controlling for potential confounders, significant associations were observed between exposure to PM1 and PM2.5 and incident fatal ischemic stroke. The corresponding hazard ratios and 95% CIs associated with 10 µg/m3 increase in PM1 and PM2.5 were 1.05 (1.02-1.09) and 1.03 (1.00-1.06), respectively. No significant association was observed for PM10 or NO2 (hazard ratios and 95% CIs, 1.01 [1.00-1.03] and 1.03 [0.99-1.06], respectively). Higher hazard ratios (and 95% CIs) were observed for male, elderly and obese individuals. Conclusions- Prestroke exposure to PM1 and PM2.5 was associated with increased incident fatal ischemic stroke in the year following an ischemic stroke in China. Improved air quality may be beneficial for people to recover from stroke.
| S-EPMC6389419 | biostudies-literature
Project description:Long-term exposure to air pollution is associated with age-related diseases. We explored the association between accelerated biological aging and air pollution, a potential mechanism linking air pollution and health. We estimated long-term exposure to PM10, PM2.5, PM2.5 absorbance/black carbon (BC), and NOx via land-use regression models in individuals from the KORA F4 cohort. Accelerated biological aging was assessed using telomere length (TeloAA) and three epigenetic measures: DNA methylation age acceleration (DNAmAA), extrinsic epigenetic age acceleration (correlated with immune cell counts, EEAA), and intrinsic epigenetic age acceleration (independent of immune cell counts, IEAA). We also investigated sex-specific associations between air pollution and biological aging, given the published association between sex and aging measures. In KORA an interquartile range (0.97 µg/m3) increase in PM2.5 was associated with a 0.33 y increase in EEAA (CI = 0.01, 0.64; P = 0.04). BC and NOx (indicators or traffic exposure) were associated with DNAmAA and IEAA in women, while TeloAA was inversely associated with BC in men. We replicated this inverse BC-TeloAA association in the Normative Aging Study, a male cohort based in the USA. A multiple phenotype analysis in KORA F4 combining all aging measures showed that BC and PM10 were broadly associated with biological aging in men. Thus, we conclude that long-term exposure to air pollution is associated with biological aging measures, potentially in a sex-specific manner. However, many of the associations were relatively weak and further replication of overall and sex-specific associations is warranted.
| S-EPMC5342683 | biostudies-literature
Project description:The evidence for an association between particulate air pollution and type 2 diabetes mellitus (T2DM) in developing countries was very scarce.To investigate the associations of long-term exposure to fine particulate matter (PM2.5) with T2DM prevalence and with fasting glucose and glycosylated hemoglobin (HbA1c) levels in China.This is a cross-sectional study based on a nation-wide baseline survey of 11,847 adults who participated in the China Health and Retirement Longitudinal Study from June 2011 to March 2012. The average residential exposure to PM2.5 for each participant in the same period was estimated using a satellite-based spatial statistical model. We determined the association between PM2.5 and T2DM prevalence by multivariable logistic regression models. We also evaluated the association between PM2.5 and fasting glucose and HbA1c levels using multivariable linear regression models. Stratification analyses were conducted to explore potential effect modification.We identified 1760 cases of T2DM, corresponding to 14.9% of the study population. The average PM2.5 exposure for all participants was 72.6?g/m(3) during the study period. An interquartile range increase in PM2.5 (41.1?g/m(3)) was significantly associated with increased T2DM prevalence (prevalence ratio, PR=1.14), and elevated levels of fasting glucose (0.26mmol/L) and HbA1c (0.08%). The associations of PM2.5 with T2DM prevalence and with fasting glucose and HbA1c were stronger in several subgroups.This nationwide cross-sectional study suggested that long-term exposure to PM2.5 might increase the risk of T2DM in China.
| S-EPMC4902714 | biostudies-other