Dataset Information

Chronic exposure to air pollution particles increases the risk of obesity and metabolic syndrome: findings from a natural experiment in Beijing.

ABSTRACT: Epidemiologic evidence suggests that air pollution is a risk factor for childhood obesity. Limited experimental data have shown that early-life exposure to ambient particles either increases susceptibility to diet-induced weight gain in adulthood or increases insulin resistance, adiposity, and inflammation. However, no data have directly supported a link between air pollution and non-diet-induced weight increases. In a rodent model, we found that breathing Beijing's highly polluted air resulted in weight gain and cardiorespiratory and metabolic dysfunction. Compared to those exposed to filtered air, pregnant rats exposed to unfiltered Beijing air were significantly heavier at the end of pregnancy. At 8 wk old, the offspring prenatally and postnatally exposed to unfiltered air were significantly heavier than those exposed to filtered air. In both rat dams and their offspring, after continuous exposure to unfiltered air we observed pronounced histologic evidence for both perivascular and peribronchial inflammation in the lungs, increased tissue and systemic oxidative stress, dyslipidemia, and an enhanced proinflammatory status of epididymal fat. Results suggest that TLR2/4-dependent inflammatory activation and lipid oxidation in the lung can spill over systemically, leading to metabolic dysfunction and weight gain.-Wei, Y., Zhang, J., Li, Z., Gow, A., Chung, K. F., Hu, M., Sun, Z., Zeng, L., Zhu, T., Jia, G., Li, X., Duarte, M., Tang, X. Chronic exposure to air pollution particles increases the risk of obesity and metabolic syndrome: findings from a natural experiment in Beijing.

SUBMITTER: Wei Y

PROVIDER: S-EPMC6137545 | biostudies-literature | 2016 Jun

REPOSITORIES: biostudies-literature

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Chronic exposure to air pollution particles increases the risk of obesity and metabolic syndrome: findings from a natural experiment in Beijing.

Wei Yongjie Y Zhang Junfeng Jim JJ Li Zhigang Z Gow Andrew A Chung Kian Fan KF Hu Min M Sun Zhongsheng Z Zeng Limin L Zhu Tong T Jia Guang G Li Xiaoqian X Duarte Marlyn M Tang Xiaoyan X

FASEB journal : official publication of the Federation of American Societies for Experimental Biology 20160218 6

Epidemiologic evidence suggests that air pollution is a risk factor for childhood obesity. Limited experimental data have shown that early-life exposure to ambient particles either increases susceptibility to diet-induced weight gain in adulthood or increases insulin resistance, adiposity, and inflammation. However, no data have directly supported a link between air pollution and non-diet-induced weight increases. In a rodent model, we found that breathing Beijing's highly polluted air resulted ...[more]

PMID: 26891735

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Project description:BackgroundPrevious studies have reported decreased birth weight associated with increased air pollutant concentrations during pregnancy. However, it is not clear when during pregnancy increases in air pollution are associated with the largest differences in birth weight.ObjectivesUsing the natural experiment of air pollution declines during the 2008 Beijing Olympics, we evaluated whether having specific months of pregnancy (i.e., 1st…8th) during the 2008 Olympics period was associated with larger birth weights, compared with pregnancies during the same dates in 2007 or 2009.MethodsUsing n = 83,672 term births to mothers residing in four urban districts of Beijing, we estimated the difference in birth weight associated with having individual months of pregnancy during the 2008 Olympics (8 August-24 September 2008) compared with the same dates in 2007 and 2009. We also estimated the difference in birth weight associated with interquartile range (IQR) increases in mean ambient particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5), sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO) concentrations during each pregnancy month.ResultsBabies whose 8th month of gestation occurred during the 2008 Olympics were, on average, 23 g larger (95% CI: 5 g, 40 g) than babies whose 8th month occurred during the same calendar dates in 2007 or 2009. IQR increases in PM2.5 (19.8 μg/m3), CO (0.3 ppm), SO2 (1.8 ppb), and NO2 (13.6 ppb) concentrations during the 8th month of pregnancy were associated with 18 g (95% CI: -32 g, -3 g), 17 g (95% CI: -28 g, -6 g), 23 g (95% CI: -36 g, -10 g), and 34 g (95% CI: -70 g, 3 g) decreases in birth weight, respectively. We did not see significant associations for months 1-7.ConclusionsShort-term decreases in air pollution late in pregnancy in Beijing during the 2008 Summer Olympics, a normally heavily polluted city, were associated with higher birth weight.CitationRich DQ, Liu K, Zhang J, Thurston SW, Stevens TP, Pan Y, Kane C, Weinberger B, Ohman-Strickland P, Woodruff TJ, Duan X, Assibey-Mensah V, Zhang J. 2015. Differences in birth weight associated with the 2008 Beijing Olympics air pollution reduction: results from a natural experiment. Environ Health Perspect 123:880-887; http://dx.doi.org/10.1289/ehp.1408795.

Project description:It is well known that exceeded levels of particulate matter in the air and other air pollutants harmfully affect the cardiovascular system. Empirical analyses of the effects of these factors on stroke incidence and mortality are still limited. The main objective of our analyses was to determine the association between short-term exposure to air pollutants and stroke incidence in non-industrial areas, more specifically in north-eastern Poland. To achieve this aim, we used data from the National Health Fund on patients hospitalized for stroke between 2011 and 2020 in the largest city of the region described as the Green Lungs of Poland. The pollution levels and atmospheric conditions data were obtained from the Provincial Inspectorate for Environmental Protection and the Institute of Meteorology and Water Management. Using daily data on hospitalizations, atmospheric conditions, and pollution, as well as ordered logistic regression models the hypotheses on the impact of weather and air pollution conditions on ischemic strokes were tested. The study group included 4838 patients, 45.6% of whom were male; the average patient age was approximately 74 years. The average concentrations of PM2.5 were 19.09 µg/m3, PM10 26.66 µg/m3 and CO 0.35 µg/m3. Analyses showed that an increase in PM2.5 and PM10 concentrations by 10 µg/m3 was associated with an increase in the incidence of stroke on the day of exposure (OR = 1.075, 95% CI 0.999-1.157, P = 0.053; OR = 1.056, 95% CI 1.004-1.110, P = 0.035) and the effect was even several times greater on the occurrence of a stroke event in general (PM2.5: OR = 1.120, 95% CI 1.013-1.237, P = 0.026; PM10: OR = 1.103, 95% CI 1.028-1.182, P = 0.006). Furthermore, a short-term (up to 3 days) effect of CO on stroke incidence was observed in the study area. An increase of 1 μg/m3 CO was associated with a lower incidence of stroke 2 days after the exposure (OR = 0.976, 95% CI 0.953-0.998, P = 0.037) and a higher incidence 3 days after the exposure (OR = 1.026, 95% CI 1.004-1.049, P = 0.022).

Project description:BackgroundAir pollution has emerged as an unexpected risk factor for diabetes. However, the mechanism behind remains ill-defined. So far, the lung has been considered as the main target organ of air pollution. In contrast, the gut has received little scientific attention. Since air pollution particles can reach the gut after mucociliary clearance from the lungs and through contaminated food, our aim was to assess whether exposure deposition of air pollution particles in the lung or the gut drive metabolic dysfunction in mice.MethodsTo study the effects of gut versus lung exposure, we exposed mice on standard diet to diesel exhaust particles (DEP; NIST 1650b), particulate matter (PM; NIST 1649b) or phosphate-buffered saline by either intratracheal instillation (30 µg 2 days/week) or gavage (12 µg 5 days/week) over at least 3 months (total dose of 60 µg/week for both administration routes, equivalent to a daily inhalation exposure in humans of 160 µg/m3 PM2.5) and monitored metabolic parameters and tissue changes. Additionally, we tested the impact of the exposure route in a "prestressed" condition (high-fat diet (HFD) and streptozotocin (STZ)).ResultsMice on standard diet exposed to particulate air pollutants by intratracheal instillation developed lung inflammation. While both lung and gut exposure resulted in increased liver lipids, glucose intolerance and impaired insulin secretion was only observed in mice exposed to particles by gavage. Gavage with DEP created an inflammatory milieu in the gut as shown by up-regulated gene expression of pro-inflammatory cytokines and monocyte/macrophage markers. In contrast, liver and adipose inflammation markers were not increased. Beta-cell secretory capacity was impaired on a functional level, most likely induced by the inflammatory milieu in the gut, and not due to beta-cell loss. The differential metabolic effects of lung and gut exposures were confirmed in a "prestressed" HFD/STZ model.ConclusionsWe conclude that separate lung and gut exposures to air pollution particles lead to distinct metabolic outcomes in mice. Both exposure routes elevate liver lipids, while gut exposure to particulate air pollutants specifically impairs beta-cell secretory capacity, potentially instigated by an inflammatory milieu in the gut.

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Chronic exposure to air pollution particles increases the risk of obesity and metabolic syndrome: findings from a natural experiment in Beijing.

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Chronic exposure to air pollution particles increases the risk of obesity and metabolic syndrome: findings from a natural experiment in Beijing.

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