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Estimating the Causal Effect of Low Levels of Fine Particulate Matter on Hospitalization.

ABSTRACT: BACKGROUND:In 2012, the EPA enacted more stringent National Ambient Air Quality Standards (NAAQS) for fine particulate matter (PM2.5). Few studies have characterized the health effects of air pollution levels lower than the most recent NAAQS for long-term exposure to PM2.5 (now 12 ?g/m). METHODS:We constructed a cohort of 32,119 Medicare beneficiaries residing in 5138 US ZIP codes who were interviewed as part of the Medicare Current Beneficiary Survey (MCBS) between 2002 and 2010 and had 1 year of follow-up. We considered four outcomes: all-cause hospitalizations, hospitalizations for circulatory diseases and respiratory diseases, and death. RESULTS:We found that increasing exposure to PM2.5 from levels lower than 12 ?g/m to levels higher than 12 ?g/m is associated with increases in all-cause admission rates of 7% (95% CI = 3%, 10%) and in circulatory admission hazard rates of 6% (95% CI = 2%, 9%). When we restricted analysis to enrollees with exposure always lower than 12 ?g/m, we found that increasing exposure from levels lower than 8 ?g/m to levels higher than 8 ?g/m increased all-cause admission hazard rates by 15% (95% CI = 8%, 23%), circulatory by 18% (95% CI = 10%, 27%), and respiratory by 21% (95% CI = 9%, 34%). CONCLUSIONS:In a nationally representative sample of Medicare enrollees, changes in exposure to PM2.5, even at levels consistently below standards, are associated with increases in hospital admissions for all causes and cardiovascular and respiratory diseases. The robustness of our results to inclusion of many additional individual level potential confounders adds validity to studies of air pollution that rely entirely on administrative data.

SUBMITTER: Makar M

PROVIDER: S-EPMC5624531 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature

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Estimating the Causal Effect of Low Levels of Fine Particulate Matter on Hospitalization.

Makar Maggie M Antonelli Joseph J Di Qian Q Cutler David D Schwartz Joel J Dominici Francesca F

Epidemiology (Cambridge, Mass.) 20170901 5

<h4>Background</h4>In 2012, the EPA enacted more stringent National Ambient Air Quality Standards (NAAQS) for fine particulate matter (PM2.5). Few studies have characterized the health effects of air pollution levels lower than the most recent NAAQS for long-term exposure to PM2.5 (now 12 μg/m).<h4>Methods</h4>We constructed a cohort of 32,119 Medicare beneficiaries residing in 5138 US ZIP codes who were interviewed as part of the Medicare Current Beneficiary Survey (MCBS) between 2002 and 2010 ...[more]

PMID: 28768298

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Project description:BackgroundFine particulate matter (PM2.5) related mild inflammation, altered autonomic control of cardiovascular function, and changes to cell function have been observed in controlled human exposure studies.MethodsTo measure the systemic and cardiopulmonary impacts of low-level PM exposure, we exposed 20 healthy, young volunteers to PM2.5, in the form of concentrated ambient particles (mean: 37.8 μg/m3, SD 6.5), and filtered air (mean: 2.1 μg/m3, SD 2.6). In this double-blind, crossover study the exposure order was randomized. During the 4 h exposure, volunteers (7 females and 13 males) underwent light intensity exercise to regulate ventilation rate. We measured pulmonary, cardiac, and hematologic end points before exposure, 1 h after exposure, and again 20 h after exposure.ResultsLow-level PM2.5 resulted in both pulmonary and extra-pulmonary changes characterized by alterations in systematic inflammation markers, cardiac repolarization, and decreased pulmonary function. A mean increase in PM2.5 concentration (37.8 μg/m3) significantly increased serum amyloid A (SAA), C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1), and soluble vascular cell adhesion molecule-1 (sVCAM-1), 1 h after exposure by 8.7, 9.1, 10.7, and 6.6%, respectively, relative to the filtered air control. SAA remained significantly elevated (34.6%) 20 h after PM2.5 exposure which was accompanied by a 5.7% decrease in percent neutrophils. Decreased pulmonary function was observed 1 h after exposure through a 0.8 and 1.2% decrease in forced expiratory volume in 1 s (FEV1) and FEV1/ forced vital capacity (FEV1/FVC) respectively. Additionally, sex specific changes were observed in repolarization outcomes following PM2.5 exposure. In males, P-wave and QRS complex were increased by 15.4 and 5.4% 1 h after exposure.ConclusionsThis study is the first controlled human exposure study to demonstrate biological effects in response to exposure to concentrated ambient air PM2.5 particles at levels near the PM2.5 US NAAQS standard.Clinical trial registration informationclinicaltrials.gov ; Identifier: NCT03232086 . The study was registered retrospectively on July 25, 2017, prior to final data collection on October 25, 2017 and data analysis.

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.

Dataset Information

Estimating the Causal Effect of Low Levels of Fine Particulate Matter on Hospitalization.

Publications

Estimating the Causal Effect of Low Levels of Fine Particulate Matter on Hospitalization.

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