蚊香烟尘和焦油的测定及对小鼠的影响

目的测定蚊香燃烧时产生的烟尘和焦油量,并研究其产生的毒性.方法采用物理方法测定三种类型蚊香的烟尘和焦油量,并用小鼠做经口和吸入毒性实验.结果不同类型的蚊香产生的烟尘和焦油量不同,微烟蚊香焦油含量是无烟蚊香的3倍,绿蚊香的焦油量比微烟蚊香高1倍.微香蚊香的烟尘量是无烟蚊香的4倍,绿/黄蚊香的烟尘量比微烟蚊香高1～3倍,小鼠经吸入3种蚊香不同浓度的烟尘后,出现不同程度的中毒症状,并导致体重降低,摄食量减少,高剂量时还可造成肺和气管充血或水肿等症状.结论不同类型的蚊香产生的烟尘和焦油量有很大差异,过多的烟尘和焦油量对小鼠健康会造成不同程度的影响,因此选择使用烟尘和焦油量适中的蚊香灭蚊有利于提高人们生活质量,减少对环境的污染.     

Maternal allergy acts synergistically with cigarette smoke exposure during pregnancy to induce hepatic fibrosis in adult male offspring

Maternal environmental exposures during pregnancy are known to affect disease onset in adult offspring. For example, maternal asthma exacerbations during pregnancy can worsen adult asthma in the offspring. Cigarette smoking during pregnancy is associated with future onset of cardiovascular disease, obesity and diabetes. However, little is known about the effect of maternal environmental exposures on offspring susceptibility to liver disease. This pilot study examined the long-term effect of maternal allergen challenge and/or cigarette smoking during pregnancy on hepatic inflammation and fibrosis in adult mouse offspring. Ovalbumin (OVA) or phosphate-buffered saline (PBS)-sensitized/challenged CD-1 dams were exposed to mainstream cigarette smoke (MCS) or filtered air from gestational day 4 until parturition. Eight weeks postnatally, offspring were sacrificed for comparison of hepatic histology and mRNA expression. Adult male offspring of OVA-sensitized/challenged dams exposed to MCS (OSM) displayed significantly increased liver fibrosis (9.2% collagen content vs. <4% for all other treatment groups). These mice also had 1.8-fold greater collagen 1A1 mRNA levels. From the results here, we concluded that maternal allergen challenge in combination with cigarette smoke exposure during pregnancy may be an important risk factor for liver disease in adult male offspring.     

Temporal structure/function variation in cultured differentiated human nasal epithelium associated with acute single exposure to tobacco smoke or E-cigarette vapor

Objective: Mucociliary clearance sustains a baseline functionality and an “on demand” capability to upregulate clearance upon irritant exposure involving mucus hypersecretion and accelerated ciliary beat frequency (CBF) modulated by nitric oxide (NO). This study characterized these elements as well as cellular and exogenous NO concentrations subsequent to a single exposure to tobacco smoke (TS) or e-cigarette vapor (EV) on cultured human airway epithelium.

Materials and methods: Air–liquid interface (ALI) airway epithelial cultures per nonsmoking human subjects were subjected to single TS or EV exposures. Measures of ciliary function and secretion were performed and cellular and exogenous NO concentrations under control and experimental conditions were assessed.

Results: Both TS and EV exposures resulted similar patterns of decline in CBF within 1?min of the completion of exposure followed by a gradual return often exceeding baseline within 1?h. Post-exposure examination of exposed cultures suggested morphologic differences in secretory function relative to controls. The relative NO concentrations of TS and EV chamber air were sharply different with EV NO being only slightly elevated relative to cellular NO production.

Discussion and conclusions: Epithelial remodeling and mucociliary dysfunction have been clearly associated with TS exposure. However, information contrasting epithelial structure/function following a single acute TS or EV exposure is limited. This study demonstrates a similar pattern of epithelial response to acute TS or EV exposure. Inasmuch as NO may contribute to an inflammatory milieu and generation of toxic metabolites, it is plausible that recurrent exposures over time may be contributory to chronic pathologies.     

The protective effect of melatonin on smoke‐induced vascular injury in rats and humans: a randomized controlled trial

Smoking is one of the most harmful lifestyles in the world. Very few studies have investigated the effects of melatonin in smoke‐induced vascular injury. This study was designed to investigate whether melatonin could protect rats and humans from smoke‐induced vascular injury. 32 male rats and a double‐blind randomized controlled trial (RCT) containing 63 participants formed the subjects of this study. In rats, 10 mg/kg of melatonin was intraperitoneally injected. Blood samples and abdominal artery were harvested two weeks later. Melatonin decreased the expression of platelet endothelial cell adhesion molecule‐1 (CD31), intercellular adhesion molecule‐1 (ICAM‐1), vascular cell adhesion molecule‐1 (VCAM‐1) and endothelin‐1 (ET‐1) compared with the smoke exposed group (P < 0.05), whereas endothelial nitric oxide synthase (eNOS), nuclear erythroid 2‐related factor 2 (Nrf2), NAD(P)H quinone oxidoreductase 1 (NQO‐1), catalytic glutamate cysteine ligase (GCLC) and heme oxygenase‐1 (HO‐1) recovered markedly (P < 0.05). In humans, 3 mg/day of melatonin was taken orally by the participants. Blood samples were drawn at baseline and after two weeks of treatment. Compared with the oral placebo group, melatonin decreased the concentration of fibrinogen (Fbg) (P = 0.04) and free fatty acids (FFA) (P = 0.04) in smokers, along with the decreased expression of ICAM‐1, VCAM‐1 and ET‐1 (P = 0.004, P = 0.001, P < 0.0001, respectively). In contrast, Nrf2 and HO‐1 expression were markedly increased (P = 0.0001, P = 0.0049, respectively) after smokers took melatonin orally. In summary, our present data suggest that melatonin could ameliorate smoke‐induced vascular injury.     

Influence of measurement uncertainty on the world health organization recommended regulation for mainstream cigarette smoke constituents

The World Health Organization Study Group on Tobacco Product Regulation (WHO TobReg) proposed mandated ceilings on 9 prioritized mainstream cigarette smoke constituents determined from the market-specific median of nicotine-normalized yield distributions. Considering the requirements for assessing and reporting of compliance with ceilings, it is of great importance to estimate the measurement uncertainty. To have a better understanding of influence of measurement uncertainty on the WHO recommended regulation for cigarette smoke constituents, in the present study, the measurement uncertainties were evaluated systematically based on series of collaborative studies reported by three different authorities over the years from 2012 to 2016, according to the approaches guided in ISO/TS 21748. Furthermore, the compliance assessment of 20 representative cigarette samples with proposed ceilings was conducted by taking measurement uncertainty into account. This work demonstrated that measurement uncertainty had great influence on the implementation of the regulated mandated lowering of toxic smoke constituents, both on the setting of ceilings and the compliance assessment as well.     

Cadmium Levels in the Lung,Liver, Kidney Cortex,and Urine Samples from Australians without Occupational Exposure to Metals

The authors undertook this study to assess levels of cadmium exposure in the general population. Samples of lung, liver, and kidney were obtained from 61 cadavers (43 males, 18 females; 2–89 yr of age, mean age = 38.5 yr) who died from accidental causes and who were subject to postmortem examinations at the John Tonge Centre for Forensic Sciences, Queensland Health Scientific Services, Brisbane, Australia, in 1997 and 1998. Samples of bladder urine were also obtained from 22 cadavers. Tissue and urine samples were analyzed for cadmium, zinc, and copper with inductively coupled plasm (ICP) mass spectrometry. The overall mean values for cadmium in the lung, liver, and kidney cortex samples were 0.13, 0.95, and 15.45 μg/gm wet tissue weight. The average renal cadmium level in subjects with high lung-cadmium levels (n = 13) was 6 μg/gm wet tissue weight higher than that of similarly aged subjects who had medium lung-cadmium levels (n = 30). In females, the average level of cadmium in the liver was 74% greater than in males, and the average liver cadmium in females with high lung-cadmium levels was 100% higher than in males in the same age range who had the same high lung-cadmium levels. Renal cadmium accumulation tended to be greater in females than in males who were in the same age range and who had similar lung-cadmium levels, a result that suggested that there was a higher absorption rate of cadmium in females. The mean value for a urinary cadmium excretion of 2.30 μg/gm creatinine was found in a subset of samples that had a mean age of 39 yr and a renal cortex cadmium concentration of 18.6 μg/gm wet tissue weight. Urinary cadmium excretion rates were correlated more strongly with lung and kidney cadmium content than with age or liver cadmium levels. The results suggest that urinary cadmium excretion may be increased in smokers and could provide some estimate of body cadmium burdens in future Australian epidemiological studies.     

不同焦油释放量卷烟全烟气气-液界面暴露致细胞毒性、炎症因子释放和细胞凋亡的研究

目的:探讨两种不同焦油释放量卷烟对人支气管上皮细胞的细胞毒性、炎症因子释放水平和细胞凋亡的影响。方法:选取国际标准化组织(ISO)规定抽吸参数下焦油释放量分别为每支9.4 mg的卷烟样品1和每支14.0 mg的卷烟样品2作为研究对象。实验分为洁净空气对照组和烟气染毒组。利用VITROCELL系统产生的洁净空气或稀释的主流烟气以气-液界面方式暴露染毒Beas-2b细胞,经计算洁净空气对照组剂量为0支卷烟产生的主流烟气,烟气染毒组剂量分别为0.12%支、0.27%支、0.57%支、1%支卷烟产生的主流烟气;利用中性红细胞毒性试验检测细胞存活率;ELISA法检测细胞培养液中的IL-6、IL-8释放水平;Annexin V-FITC/PI流式细胞分析法检测细胞凋亡水平。结果:样品1和样品2产生的主流烟气均可引起Beas-2b细胞存活率降低,炎症因子IL-6、IL-8的释放水平和细胞凋亡率显著增加。在0.12%支的烟气剂量下,样品1与样品2烟气引起的细胞毒性、炎症因子释放水平和细胞凋亡率的差异无统计学意义;在0.57%和1%支的烟气剂量下,样品2的细胞毒性高于样品1。结论:两种不同焦油释放量卷烟样品均可引起细胞毒性、促炎症因子释放和细胞凋亡。在0.57%支~1%支烟气剂量范围内,具有高焦油释放量的卷烟烟气引起的细胞毒性强于低焦油释放量的卷烟烟气。