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11.
The rapid growth in the number of older adults has many implications for public health, including the need to better understand the risks posed by environmental exposures. Aging leads to a decline and deterioration of functional properties at the cellular, tissue and organ level. This loss of functional properties yields to a loss of homeostasis and decreased adaptability to internal and external stress. Frailty is a geriatric syndrome characterized by weakness, weight loss, and low activity that is associated with adverse health outcomes. Frailty manifests as an age-related, biological vulnerability to stressors and decreased physiological reserves. Ambient air pollution exposure affects human health, and elderly people appear to be particularly susceptible to its adverse effects.The aim of this paper is to discuss the role of air pollution in the modulation of several biological mechanisms involved in aging. Evidence is presented on how air pollution can modify the bidirectional association between successful and pathological aging throughout the frailty conditions. 相似文献
12.
《Experimental and toxicologic pathology》2014,66(8):383-389
Coal dust is a pollutant found in coal mines that are capable of inducing oxidative stress and inflammation, but the effects on lung metaplasia as an early step of carcinogenesis remain unknown. The purpose of the present study was to evaluate the effects of PM10 coal dust on lung histology, MUC5AC expression, epidermal growth factor (EGF) expression, and epidermal growth factor receptor (EGFR) expression. An experimental study was done on male Wistar rats, which were divided into the following groups: control groups exposed to coal dust for 14 days (at doses of 6.25 mg/m3, 12.5 mg/m3, and 25 mg/m3), and the groups exposed to coal dust for 28 days (at doses of 6.25 mg/m3, 12.5 mg/m3, and 25 mg/m3). EGF expressions in rat lungs were measured by ELISA. EGFR and MUC5AC were measured by a confocal laser scanning microscope. The bronchoalveolar epithelial image of the group exposed to coal dust for 14 and 28 days showed a epithelial rearrangement, hyperplastic (metaplastic) goblet cells, and scattered massive inflammatory cells. The pulmonary parenchymal image of the group of exposed to coal dust for 14 and 28 days showed scattered inflammatory cells filling up the pulmonary alveolar networks, leading to an appearance of thickened parenchymal alveoli until emphysema-like structure. There was no significant difference in MUC5AC, EGF, and EGFR expressions for 14-d exposure (p > 0.05). There was no significant difference in EGF and EGFR expressions for 28-d exposure (p > 0.05), but there was a significant difference in MUC5AC expression (p < 0.05). We concluded that subchronic inhalation of coal dust particulate matter 10 induces bronchoalveolar reactive hyperplasia and rearrangement of epithelial cells which accompanied by decrease expression MUC5AC in male rats. 相似文献
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室外大气颗粒物严重影响人体健康,而儿童由于生长发育的特点对颗粒物较为敏感.大气颗粒物按空气动力学粒径可分为总悬浮颗粒物、可吸入颗粒物、细颗粒物和超细颗粒物等.为探讨颗粒物对儿童哮喘急性发作的影响,该文对不同粒径颗粒物的来源、组成、理化性质、作用机制及其与儿童哮喘相关性的流行病学研究进行综述,为深入研究不同粒径颗粒物对儿童哮喘的影响提供依据. 相似文献
16.
Veronika Pilz Kathrin Wolf Susanne Breitner Regina Rückerl Wolfgang Koenig Wolfgang Rathmann Josef Cyrys Annette Peters Alexandra Schneider 《International journal of hygiene and environmental health》2018,221(3):510-518
Background
Long-term exposure to ambient air pollution contributes to the global burden of disease by particularly affecting cardiovascular (CV) causes of death. We investigated the association between particle number concentration (PNC), a marker for ultrafine particles, and other air pollutants and high sensitivity C-reactive protein (hs-CRP) as a potential link between air pollution and CV disease.Methods
We cross-sectionally analysed data from the second follow up (2013 and 2014) of the German KORA baseline survey which was conducted in 1999–2001. Residential long-term exposure to PNC and various other size fractions of particulate matter (PM10 with size of <10?μm in aerodynamic diameter, PMcoarse 2.5–10?μm or PM2.5?<?2.5?μm, respectively), soot (PM2.5abs: absorbance of PM2.5), nitrogen oxides (nitrogen dioxide NO2 or oxides NOx, respectively) and ozone (O3) were estimated by land-use regression models. Associations between annual air pollution concentrations and hs-CRP were modeled in 2252 participants using linear regression models adjusted for several confounders. Potential effect-modifiers were examined by interaction terms and two-pollutant models were calculated for pollutants with Spearman inter-correlation <0.70.Results
Single pollutant models for PNC, PM10, PMcoarse, PM2.5abs, NO2 and NOx showed positive but non-significant associations with hs-CRP. For PNC, an interquartile range (2000 particles/cm3) increase was associated with a 3.6% (95% CI: ?0.9%, 8.3%) increase in hs-CRP. A null association was found for PM2.5. Effect estimates were higher for women, non‐obese participants, for participants without diabetes and without a history of cardiovascular disease whereas ex-smokers showed lower estimates compared to smokers or non-smokers. For O3, the dose-response function suggested a non-linear relationship. In two-pollutant models, adjustment for PM2.5 strengthened the effect estimates for PNC and PM10 (6.3% increase per 2000 particles/cm3 [95% CI: 0.4%; 12.5%] and 7.3% per 16.5?μg/m3 [95% CI: 0.4%; 14.8%], respectively).Conclusion
This study adds to a scarce but growing body of literature showing associations between long-term exposure to ultrafine particles and hs-CRP, one of the most intensely studied blood biomarkers for cardiovascular health. Our results highlight the role of ultrafine particles within the complex mixture of ambient air pollution and their inflammatory potential. 相似文献17.
目的颗粒酶B促进组织炎症的作用日益引起重视,但其在PM2.5导致的肺部炎症中是否发挥作用还不清楚,本文对在PM2.5导致的肺部炎症中颗粒酶B的作用进行了研究。 方法第一步构建经气管滴注PM2.5混悬液诱导大鼠肺部炎症的动物模型,实验分组为PBS组、PM2.5(2 mg/kg)组、PM2.5(6 mg/kg)组、PM2.5(18 mg/kg)组。通过设置PM2.5滴注剂量梯度,检测不同PM2.5暴露剂量下大鼠肺组织颗粒酶B表达、病理和炎症评分,以探讨颗粒酶B表达水平与肺部炎症严重程度间有无相关性。第二步通过阻断颗粒酶B,探究在PM2.5导致的肺部炎症中颗粒酶B是否发挥促进作用。第三步通过阻断IL-18,探究在PM2.5导致的肺部炎症中颗粒酶B是否通过IL-18发挥作用。 结果随着PM2.5滴注剂量升高,肺组织颗粒酶B表达增加,肺组织病理切片炎症细胞浸润和肺水肿程度加重,炎症评分增加,PM2.5促进了肺组织颗粒酶B表达和肺部炎症;阻断颗粒酶B抑制了IL-18表达和NF-κB磷酸化,改善了PM2.5导致的肺部炎症;阻断IL-18抑制了NF-κB磷酸化,改善了PM2.5导致的肺部炎症。 结论PM2.5通过上调颗粒酶B促进IL-18表达加重肺部炎症,其机制可能与激活NF-κB信号通路有关。 相似文献
18.
《International journal of hygiene and environmental health》2014,217(2-3):133-144
Cardiovascular diseases (CVD) are major contributors to mortality and morbidity in South Asia. Chronic exposure to air pollution is an important risk factor for cardiovascular diseases, although the majority of studies to date have been conducted in developed countries. Both indoor and outdoor air pollution are growing problems in developing countries in South Asia yet the impact on rising rates of CVD in these regions has largely been ignored. We aimed to assess the evidence available regarding air pollution effects on CVD and CVD risk factors in lower income countries in South Asia. A literature search was conducted in PubMed and Web of Science. Our inclusion criteria included peer-reviewed, original, empirical articles published in English between the years 1990 and 2012, conducted in the World Bank South Asia region (Afghanistan, Bangladesh, Bhutan, India, Maldives, Nepal, Pakistan and Sri Lanka). This resulted in 30 articles. Nine articles met our inclusion criteria and were assessed for this systematic review. Most of the studies were cross-sectional and examined measured particulate matter effects on CVD outcomes and indicators. We observed a bias as nearly all of the studies were from India. Hypertension and CVD deaths were positively associated with higher particulate matter levels. Biomarkers of oxidative stress such as increased levels of P-selection expressing platelets, depleted superoxide dismutase and reactive oxygen species generation as well as elevated levels of inflammatory-related C-reactive protein, interleukin-6 and interleukin-8 were also positively associated with biomass use or elevated particulate matter levels. An important outcome of this investigation was the evidence suggesting important air pollution effects regarding CVD risk in South Asia. However, too few studies have been conducted. There is as an urgent need for longer term investigations using robust measures of air pollution with different population groups that include a wider range of air pollutants and outcomes, including early indicators of CVD. These regions are facing burdens from increasing urbanization, air pollution and populations, generally weaker health infrastructure, aging populations and increased incidence of non-communicable diseases, included CVD. The extent to which the problem of air pollution and CVD will impact these countries will depend largely on the information available to inform policy and programs, which are still lacking, political will as well as social and economic development. 相似文献
19.
Udomratana Vattanasit Panida Navasumrit Man Bahadur Khadka Jantamas Kanitwithayanun Jeerawan Promvijit Herman Autrup Mathuros Ruchirawat 《International journal of hygiene and environmental health》2014,217(1):23-33
Particulate pollution is a major public health concern because epidemiological studies have demonstrated that exposure to particles is associated with respiratory diseases and lung cancer. Diesel exhaust particles (DEP), which is classified as a human carcinogen (IARC, 2012), are considered a major contributor to traffic-related particulate matter (PM) in urban areas. DEP consists of various compounds, including PAHs and metals which are the principal components that contribute to the toxicity of PM. The present study aimed to investigate effects of PM on induction of oxidative DNA damage and inflammation by using lymphocytes in vitro and in human exposed to PM in the environment. Human lymphoblasts (RPMI 1788) were treated with DEP (SRM 2975) at various concentrations (25–100 μg/ml) to compare the extent of responses with alveolar epithelial cells (A549). ROS generation was determined in each cell cycle phase of DEP-treated cells in order to investigate the influence of the cell cycle stage on induction of oxidative stress. The oxidative DNA damage was determined by measurement of 8-hydroxy-deoxyguanosine (8-OHdG) whereas the inflammatory responses were determined by mRNA expression of interleukin-6 and -8 (IL-6 and IL-8), Clara cell protein (CC16), and lung surfactant protein-A (SP-A). The results showed that RPMI 1788 and A549 cells had a similar pattern of dose-dependent responses to DEP in terms of particle uptake, ROS generation with highest level found in G2/M phase, 8-OHdG formation, and induction of IL-6 and IL-8 expression. The human study was conducted in 51 healthy subjects residing in traffic-congested areas. The effects of exposure to PM2.5 and particle-bound PAHs and toxic metals on the levels of 8-OHdG in lymphocyte DNA, IL-8 expression in lymphocytes, and serum CC16 were evaluated. 8-OHdG levels correlated with the exposure levels of PM2.5 (P < 0.01) and PAHs (P < 0.05), but this was not the case with IL-8. Serum CC16 showed significantly negative correlations with B[a]P equivalent (P < 0.05) levels, but positive correlation with Pb (P < 0.05). In conclusion, a similar pattern of the dose-dependent responses to DEP in the lymphoblasts and lung cells suggests that circulating lymphocytes could be used as a surrogate for assessing PM-induced oxidative DNA damage and inflammatory responses in the lung. Human exposure to PM leads to oxidative DNA damage whereas PM-induced inflammation was not conclusive and should be further investigated. 相似文献
20.
Samya de Lara Lins de Araujo Pinheiro Paulo Hilário Nascimento Saldiva Joel Schwartz Antonella Zanobetti 《Revista de saúde pública》2014,48(6):881-888