Dataset Information

Ambient Fine Particulate Matter Exposure and Risk of Cardiovascular Mortality: Adjustment of the Meteorological Factors.

ABSTRACT: Few studies have explicitly explored the impacts of the extensive adjustment (with a lag period of more than one week) of temperature and humidity on the association between ambient fine particulate matter (PM2.5) and cardiovascular mortality. In a time stratified case-crossover study, we used a distributed lag nonlinear model to assess the impacts of extensive adjustments of temperature and humidity for longer lag periods (for 7, 14, 21, 28 and 40 days) on effects of PM2.5 on total cardiovascular mortality and mortality of cerebrovascular and ischemic heart disease and corresponding exposure-response relationships in Beijing, China, between 2008 and 2011. Compared with results only controlled for temperature and humidity for 2 days, the estimated effects of PM2.5 were smaller and magnitudes of exposure-response curves were decreased when longer lag periods of temperature and relative humidity were included for adjustments, but these changes varied across subpopulation, with marked decreases occurring in males and the elderly who are more susceptible to PM2.5-related mortalities. Our findings suggest that the adjustment of meteorological factors using lag periods shorter than one week may lead to overestimated effects of PM2.5. The associations of PM2.5 with cardiovascular mortality in susceptible populations were more sensitive to further adjustments for temperature and relative humidity.

SUBMITTER: Luo K

PROVIDER: S-EPMC5129292 | biostudies-literature | 2016 Nov

REPOSITORIES: biostudies-literature

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Ambient Fine Particulate Matter Exposure and Risk of Cardiovascular Mortality: Adjustment of the Meteorological Factors.

Luo Kai K Li Wenjing W Zhang Ruiming R Li Runkui R Xu Qun Q Cao Yang Y

International journal of environmental research and public health 20161104 11

Few studies have explicitly explored the impacts of the extensive adjustment (with a lag period of more than one week) of temperature and humidity on the association between ambient fine particulate matter (PM<sub>2.5</sub>) and cardiovascular mortality. In a time stratified case-crossover study, we used a distributed lag nonlinear model to assess the impacts of extensive adjustments of temperature and humidity for longer lag periods (for 7, 14, 21, 28 and 40 days) on effects of PM<sub>2.5</sub> ...[more]

PMID: 27827945

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Project description:BackgroundFetal growth restriction (FGR) is not only a major determinant of perinatal morbidity and mortality but also leads to adverse health effects in later life. Over the past decade, numerous studies have indicated that maternal exposure to ambient air pollution has been a risk factor for abnormal fetal growth in developed countries where PM2.5 levels are relatively low. However, studies in highly polluted regions, such as China, and studies that rely on assessments in utero are scarce.MethodsA total of 7965 women were selected from 11,441 women from the Shanghai Maternity and Infant Living Environment (SMILE) cohort who were pregnant between January 1, 2014, and April 30, 2015. From January 1, 2014, to April 30, 2015, weekly average PM2.5 values from 53 monitors were calculated and the inverse distance weighted (IDW) method was used to create a Shanghai pollution surface map according to the participants residential addresses. Individual exposure was the average PM2.5 value of every gestational week between the first gestational week and one week before the ultrasound measurement date (the range of measurements per participant was 1 to 10). Repeated fetal ultrasound measurements during gestational weeks 14~40 were selected. The estimated fetal weight (EFW) was calculated by biparietal diameter (BPD), abdominal circumference (AC), and femur length (FL) formulas. In total, 29,926 ultrasound measurements were analysed. Demographic variables, other pollutants (SO2, NO2, PM10 and O3) and relative humidity and temperature were controlled for potential confounding through generalized estimating equations (GEE).ResultsThe full model showed that with each 10 μg/m3 increase in PM2.5 exposure, the means (mm) of AC, BPD, FL decreased by 5.48 (- 9.06, - 1.91), 5.57 (- 6.66, - 4.47), and 5.47 (- 6.39, - 4.55), respectively; the mean EFW decreased by 14.49 (- 16.05, - 13.49) grams by Hadlock's third formula and 13.56 (- 14.71, - 12.50) grams by Shepard's formula with each 10 μg/m3 increase in PM2.5 exposure.ConclusionsA negative correlation existed between maternal PM2.5 exposure during pregnancy and fetal growth indicators, which may increase the risk of fetal growth restriction.

Project description:BackgroundAir pollution, especially fine particulate matter (PM), can cause brain damage, cognitive decline, and an increased risk of neurodegenerative disease, especially alzheimer's disease (AD). Typical pathological findings of amyloid and tau protein accumulation have been detected in the brain after exposure in animal studies. However, these observations were based on high levels of PM exposure, which were far from the WHO guidelines and those present in our environment. In addition, white matter involvement by air pollution has been less reported. Thus, this experiment was designed to simulate the true human world and to discuss the possible white matter pathology caused by air pollution.Results6 month-old female 3xTg-AD mice were divided into exposure and control groups and housed in the Taipei Air Pollutant Exposure System (TAPES) for 5 months. The mice were subjected to the Morris water maze test after exposure and were then sacrificed with brain dissection for further analyses. The mean mass concentration of PM2.5 during the exposure period was 13.85 μg/m3. After exposure, there was no difference in spatial learning function between the two groups, but there was significant decay of memory in the exposure group. Significantly decreased total brain volume and more neuronal death in the cerebral and entorhinal cortex and demyelination of the corpus callosum were noted by histopathological staining after exposure. However, there was no difference in the accumulation of amyloid or tau on immunohistochemistry staining. For the protein analysis, amyloid was detected at significantly higher levels in the cerebral cortex, with lower expression of myelin basic protein in the white matter. A diffuse tensor image study also revealed insults in multiple white matter tracts, including the optic tract.ConclusionsIn conclusion, this pilot study showed that even chronic exposure to low PM2.5 concentrations still caused brain damage, such as gross brain atrophy, cortical neuron damage, and multiple white matter tract damage. Typical amyloid cascade pathology did not appear prominently in the vulnerable brain region after exposure. These findings imply that multiple pathogenic pathways induce brain injury by air pollution, and the optic nerve may be another direct invasion route in addition to olfactory nerve.

Project description:BackgroundExposure to fine particulate matter (PM2.5), an ambient air pollutant with mass-based standards promulgated under the Clean Air Act, and black carbon (BC), a common component of PM2.5, are both associated with cardiovascular health effects.ObjectivesTo elucidate whether BC is associated with distinct, or stronger, cardiovascular responses compared to PM2.5, we conducted a systematic review. We evaluated the associations of short- and long-term BC, or the related component elemental carbon (EC), with cardiovascular endpoints including heart rate variability, heart rhythm, blood pressure and vascular function, ST segment depression, repolarization abnormalities, atherosclerosis and heart function, in the context of what is already known about PM2.5.Data sourcesWe conducted a stepwise systematic literature search of the PubMed, Web of Science and TOXLINE databases and applied Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) guidelines for reporting our results.Study eligibility criteriaStudies reporting effect estimates for the association of quantitative measurements of ambient BC (or EC) and PM2.5, with relevant cardiovascular endpoints (i.e. meeting inclusion criteria) were included in the review. Included studies were evaluated for risk of bias in study design and results.Study appraisal and synthesis methodsRisk of bias evaluations assessed aspects of internal validity of study findings based on study design, conduct, and reporting to identify potential issues related to confounding or other biases. Study results are presented to facilitate comparison of the consistency of associations with PM2.5 and BC within and across studies.ResultsOur results demonstrate similar associations for BC (or EC) and PM2.5 with the cardiovascular endpoints examined. Across studies, associations for BC and PM2.5 varied in their magnitude and precision, and confidence intervals were generally overlapping within studies. Where differences in the magnitude of the association between BC or EC and PM2.5 within a study could be discerned, no consistent pattern across the studies examined was apparent.LimitationsWe were unable to assess the independence of the effect of BC, relative the effect of PM2.5, on the cardiovascular system, nor was information available to understand the impact of differential exposure misclassification.ConclusionsOverall, the evidence indicates that both BC (or EC) and PM2.5 are associated with cardiovascular effects but the available evidence is not sufficient to distinguish the effect of BC (or EC) from that of PM2.5 mass.

Project description:BackgroundThe association between daily changes in ambient fine particulate matter (PM2.5) and cardiovascular diseases have been well established in mechanistic, epidemiologic and exposure studies. Only a few studies examined the effect of hourly variations in air pollution on triggering cardiovascular events. Whether the current PM2.5 standards can protect vulnerable individuals with chronic cardiovascular diseases remain uncertain.Methodswe conducted a time-stratified, case-crossover study to assess the associations between hourly changes in PM2.5 levels and the vascular disease onset in residents of Tainan City, Taiwan, visiting Emergency Room of Chi Mei Medical Center between January 2006 and December 2016. There were 26,749 cases including 10,310 females (38.5%) and 16,439 males (61.5%) identified. The time of emergency visit was identified as the onset for each case and control cases were selected as the same times on other days, on the same day of the week in the same month and year respectively. Residential address was used to identify the ambient air pollution exposure concentrations from the closest station. Conditional logistic regression with the stepwise selection method was used to estimate adjusted odds ratios (ORs) for the association.ResultsWhen we only included cases occurring at PM2.5>10 μg/m3 and PM2.5>25 μg/m3, very significant ORs could be observed for 10 μg/m3 increases in PM2.5 at 0 and 1 hour, implying fine particulate exposure could promptly trigger vascular disease events. Moreover, a very clear increase in risk could be observed with cumulative exposure from 0 to 48 hours, especially in those cases where PM2.5>25 μg/m3.ConclusionsOur study demonstrated that transient and low concentrations of ambient PM2.5 trigger adult vascular disease events, especially cerebrovascular disease, regardless of age, sex, and exposure timing. Warning and delivery systems should be setup to protect people from these prompt adverse health impacts.

Dataset Information

Ambient Fine Particulate Matter Exposure and Risk of Cardiovascular Mortality: Adjustment of the Meteorological Factors.

Publications

Ambient Fine Particulate Matter Exposure and Risk of Cardiovascular Mortality: Adjustment of the Meteorological Factors.

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