深圳市龙岗区大气污染物与医院呼吸系统疾病门诊量的广义相加模型分析

目的 探讨深圳市龙岗区主要大气污染物(SO₂、NO₂、PM₁₀与PM_2.5)与医院呼吸系统疾病门诊量的关系。 方法 收集2013年1月1日－2015年12月31日深圳市龙岗区2家公立医院呼吸系统疾病逐日门诊量资料,深圳市龙岗区逐日大气污染物浓度及逐日气象资料分别来自深圳市环境监测站及气象局,运用时间序列分析广义相加模型对大气污染物日均浓度与呼吸系统疾病门诊量的关系及滞后效应进行分析。 结果 深圳市龙岗区2013－2015年SO₂ 、NO₂ 、PM₁₀ 与PM_2.5浓度中位数分别为8.08、38.08、46.05 μg/m³及31.04 μg/m³。2家医院三年呼吸系统门诊总量为549 169人次,日门诊量中位数为499人次/d。广义相加模型分析结果表明,除NO₂对呼吸系统疾病门诊量影响差异无统计学意义外,其余三种污染物对呼吸系统疾病门诊量影响均存在滞后效应,污染物每升高10 μg/m³,滞后2 d时SO₂对门诊量影响最强(相对危险度RR为1.030 7,95%CI:1.015 7~1.045 9),滞后3 d时PM₁₀与PM_2.5浓度对呼吸系统疾病门诊量影响最强(PM₁₀:RR=1.005 4,95%CI:1.002 8~1.008 0,PM_2.5:RR=1.006 0, 95%CI:1.002 7~1.009 4)。 结论 深圳市龙岗区大气SO₂、PM₁₀与PM_2.5浓度对医院呼吸系统疾病门诊量影响存在滞后效应。     

Tuberculosis and other chronic morbidity profile of sewage workers of Delhi

Background

Sewage management is hazardous due to chronic exposure to chemical gases, bioaerosols and micro-organisms through inhalation; accidental oral intake and penetration through skin or mucous membranes through injuries or breech in personal protective equipment. While there has been some research on isolated infections and multisystem symptom profiling of sewage workers, there is little research on the burden of chronic illnesses like Tuberculosis and Non Communicable Diseases (NCDs).

The Relationship Between Air Pollution and Lung Cancer in Nonsmokers in Taiwan

Introduction

For never-smokers (smoked <100 lifetime cigarettes), lung cancer (LC) has emerged as an important issue. We aimed to investigate the effects of prevalence changes in tobacco smoking and particulate matter (PM) 2.5 (PM_2.5) levels on LC in Taiwan, in relation to contrasting PM_2.5 levels, between Northern Taiwan (NT) and Southern Taiwan (ST).

Peat smoke inhalation alters blood pressure,baroreflex sensitivity,and cardiac arrhythmia risk in rats

ABSTRACT

Wildland fires (WF) are linked to adverse health impacts related to poor air quality. The cardiovascular impacts of emissions from specific biomass sources are however unknown. The purpose of this study was to assess the cardiovascular impacts of a single exposure to peat smoke, a key regional WF air pollution source, and relate these to baroreceptor sensitivity and inflammation. Three-month-old male Wistar-Kyoto rats, implanted with radiotelemeters for continuous monitoring of heart rate (HR), blood pressure (BP), and spontaneous baroreflex sensitivity (BRS), were exposed once, for 1-hr, to filtered air or low (0.38 mg/m³ PM) or high (4.04 mg/m³) concentrations of peat smoke. Systemic markers of inflammation and sensitivity to aconitine-induced cardiac arrhythmias, a measure of latent myocardial vulnerability, were assessed in separate cohorts of rats 24 hr after exposure. PM size (low peat = 0.4–0.5 microns vs. high peat = 0.8–1.2 microns) and proportion of organic carbon (low peat = 77% vs. high peat = 65%) varied with exposure level. Exposure to high peat and to a lesser extent low peat increased systolic and diastolic BP relative to filtered air. In contrast, only exposure to low peat elevated BRS and aconitine-induced arrhythmogenesis relative to filtered air and increased circulating levels of low-density lipoprotein cholesterol, complement components C3 and C4, angiotensin-converting enzyme (ACE), and white blood cells. Taken together, exposure to peat smoke produced overt and latent cardiovascular consequences that were likely influenced by physicochemical characteristics of the smoke and associated adaptive homeostatic mechanisms.