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).

Biological monitoring of occupational exposure to low levels of benzene.

To obtain reference values for the biological monitoring of benzene, the kinetics of benzene were studied in volunteers. Benzene in blood and expired air could easily be followed until the next morning after a 4-h exposure to a benzene concentration of 10 cm3.m-3. Even after exposure to 1.7 cm3.m-3 the benzene levels in the morning blood and expired air samples differed from those in unexposed subjects. One hour after exposure to 10 and 1.7 cm3.m-3 the mean levels of benzene were 238 and 25 nmol.l-1 in blood and 13.2 and 2.5 mumol.m-3 in exhaled air, respectively. It was concluded that, at high benzene levels (approximately 10 cm3.m-3), samples collected 16 h after exposure reflect the body burden of benzene, while at low exposure (< 1 cm3.m-3) samples collected 1 h after exposure may be used to estimate the exposure over the preceding few hours. Exposure to benzene from smoking is a potential confounder in estimating occupational exposure to low levels of benzene.     

Effects of commercial chlorophenolate, 2,3,7,8-TCDD,and pure phenoxyacetic acids on hepatic peroxisome proliferation,xenobiotic metabolism and sister chromatid exchange in the rat

The induction of hepatic peroxisome proliferation and drug metabolizing enzymes and of sister chromatid exchange (SCE) in lymphocytes was studied in male Han/Wistar rats after exposing them for 2 weeks to a commercial chlorophenolate formulation (Ky-5) (100mg/kg/ day), to 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD; 0.05–5 g/kg/wk) and to the pure phenoxyacetic acids, 2,4-dichlorophenoxyacetic acid (2,4-D; 100 mg/kg/day) and 2-chloro-4-methylphenoxyacetic acid (MCPA; 100 mg/kg/day). The chlorophenolate formulation and pure 2,4-D and MCPA caused significant increases in the number of peroxisomes in liver cells, although the average size of peroxisomes was not affected, whereas the effect of even the highest dose of 2,3,7,8-TCDD remained small. This finding indicates that dioxin impurities do not account for the peroxisome proliferation induced by chlorophenolate. The relative weight of the liver increased significantly in rats treated with the chlorophenolate formulation and with 2,3,7,8-TCDD (5.0 and 0.5 g/kg). The pattern of induction of xenobiotic metabolizing enzymes showed some differences between chlorophenolate treatment and 2,3,7,8-TCDD treatment. Furthermore, the effects of pure phenoxyacetic acids were different from that seen with chlorophenolate and 2,3,7,8-TCDD. The highest dose of 2,3,7,8-TCDD increased the frequency of SCE in circulating lymphocytes slightly, but significantly.     

Immunochemical characterization of cytochrome P-450 isozymes responsible for benzene oxidation in the rat liver

The contribution of cytochrome P-450 isozymes to benzene metabolismin liver microsomes from fed, fasted, pyrazole-, pbenobarbital(PB)- and ethanol-treated rats and in respective isocaloriccontrols was investigated using monoclonal antibodies (mAbs).Clone 1-7-1 mAb did not inhibit benzene metabolism, whereasclone 2-66-3 inhibited only in PB-induced microsomes at a highconcentration of benzene (6.26 mM), and clone 1-91-3 mAb inhibitedbenzene metabolism in all cases. The degree of inhibition wasas follows: fed isocaloric control PB < fasted < pyrazole ethanol. The pattern of inhibition was similar with clone 1-91-3for low (0.23 mM) and high concentrations of benzene, exceptin PB-induced mkrosomes. Western blot analysis showed that clone1-7-1 mAb did not bind any liver mkrosomal protein in the regionof cytochrome P-450s, whereas with clone 2-66-3 a clear-cutband was seen only in liver microsomes from PB-treated rats,with clone 1-98-1, a band was detected in mkrosomes from alltreated groups, in the following order: PB = isocaloric control< fed < fasted < pyrazole < ethanol. These resultsindicate that (i) cytochromes P-450b,e and P-450J contributeto benzene metabolism in rat liver; (ii) the former has a lowaffinity to benzene and is induced by PB; and (iii) P-450J hasa high affinity to benzene and is induced by 1-day fasting,pyrazole and ethanol, but decreased by PB treatment.     

Micronuclei induced by alachlor, mitomycin-C and vinblastine in human lymphocytes: presence of centromeres and kinetochores and influence of staining technique

Antikinetochore antibodies and fluorescence in situ hybridizationwith an alphoid centromeric probe were applied to the cytokinesis-blockmicronucleus (MN) assay to study the suitability of these methodologiesto detect clastogenic/aneugenic activity in isolated human lymphocytes.The chemicals selected for this study were the herbicide alachlor,the clastogen mitomycin-C (MMC), and the aneugen vinblastinesulphate (VBL). Futhermore, MN frequencies obtained from slidesstained with May–Grünwald–Giemsa (MGG) andwith the DNA fluorochrome 4', 6'diamidino-2-phenylindole (DAPI)were compared to check if the DNA-specific DAPI facilitateda more accurate recording of MN than the unspecific MGG. Theresults showed that the detection of kinetochores (KC) or centromeres(CM) within MN are equally reliable and sensitive techniquesto study the mode of action of clastogenic and aneugenic agents.The comparison of CM and KC detection in control cultures suggestedthat up to 17% of spontaneous chromosomecontaining MN may bedue to KC disruption, whereas the majority are caused by dysfunctionin other components of the mitotic apparatus. Alachlor (7.5–20µg/ml) and MMC (0.6 µM) acted as pure clastogenswithout aneugenic activity, inducing exclusively KC- and CM-negativeMN. VBL produced primarily KC- and CM-positive MN, in accordancewith its known mechanism of action. A comparison between CMand KC data in the VBL treatment suggested that some 7% of KC-containingMN may not be detected by the probe. The frequencies of MN weregenerally higher in slides stained with DAPI than in those stainedwith MGG, especially in controls and clastogen-treated cultures.This finding probably reflects an underestimation with MGG ofsmall, light MN indistinguishable from the cytoplasmic background. ⁴To whom correspondence should be addressed     

Analysis of the renal tissue of a woman chronically exposed to cadmium

Summary In a 61-year-old woman, who had been exposed for 20 years to cadmium in the production of Ni-Cd batteries, nephrectomy of the contracted kidney was performed. The removed kidney was examined histologically and the cadmium concentration was determined in the cortex (44.97 g g^–1) and in the medulla (7.71 g g^–1). The homogenates of the renal cortex and medulla were subjected to gel filtration on Sephadex G-75. In the cortex, as well as the medulla, cadmium was predominantly found in the low-molecular (metallothionein) fraction, but in the cortex, Cd content in this fraction was six times higher than in the medulla. The determination of SH groups and proteins in high- and low-molecular fractions indicates an induction of the metallothionein formation primarily in the renal cortex.     

Ultrastructure of carbon disulphide neuropathy

Summary Adult Wistar rats were exposed to carbon disulphide (CS₂) vapour at a concentration of 2.4 mg/l of air for 5 days a week (6h a day), and the ultrastructure of peripheral nerves, neuromuscular junctions and muscles was investigated after 6 months of exposure to CS₂. Numerous giant axons, i.e. paranodal or internodal swellings, were seen in the peripheral nerves. At the swollen paranodes, the myelin sheath was thinned, in other regions large intramyelinic vacuoles indicative of more dramatic demyelination were observed at axonal enlargements. Axonal enlargements consisted essentially of whorls of tightly packed neurofilaments. A number of nerve fibres underwent complete degeneration, but at the same time there was evidence of nerve regeneration. Nerve terminals were affected in a similar way following CS₂ exposure. At neuromuscular junctions, filamentous swellings of nerve terminals preceded their degeneration and eventual denudation of synaptic gutters. As a rule, the postsynaptic part of neuromuscular junctions remained unimpaired by CS₂ treatment. Muscles were affected by both atrophy and degeneration. Clusters of dense and lamellar bodies and numerous autophagosomes indicative of direct myotoxic effect of CS₂ were frequently encountered in the investigated muscles. Some muscle fibres apparently underwent necrosis judging from the occurrence of myotubes characteristic of muscle degeneration and regeneration.The pathomorphology of CS₂ neuropathy resembles that of other toxic neuropathies which presumably have a common origin in impaired energy metabolism.     

中国八城市老年人能量及蛋白质摄入与肌肉衰减症的关系

目的探究中国八城市老年人能量、蛋白质摄入水平与肌肉衰减症的关系。方法数据来源于2016年的"中国城市成年人群膳食与健康关系研究"。采用立意抽样和多阶段整群抽样相结合的方法,抽取65岁及以上研究对象427人,采用问卷调查的方法获得社会人口学特征和生活习惯,采用24小时膳食回顾调查法获得调查对象膳食摄入情况并根据《中国食物成分表》计算能量、蛋白质摄入。使用四分位数将研究对象按照能量摄入水平分为4组:Q1(<1197.6 kcal/d)、Q2(1197.6~1531.4 kacl/d)、Q3(1531.4~1984.1 kcal/d)、Q4(≥1984.1 kacl/d);使用四分位数将研究对象按照蛋白质摄入水平分为4组:Q1(<36.8 g/d)、Q2(36.8~50.4 g/d)、Q3(50.4~68.6 g/d)、Q4(≥68.6 g/d)。生物电阻抗法测量四肢骨骼肌质量,使用手持握力计测量骨骼肌力量,四米步速测试测量骨骼肌功能。根据亚洲肌肉衰减症工作组的标准评价调查人群的骨骼肌健康现状。结果与Q1组相比,能量摄入水平较高的Q2~Q4组的四肢骨骼肌质量、握力、步速以及肌肉衰减症检出率差异无统计学意义。与Q1组相比,蛋白质摄入Q2组具有较大的握力(β=0.12,95%CI 0.03~0.21,P=0.009)和较快的步速(β=0.20,95%CI 0.07~0.34,P=0.003)。结论膳食蛋白质摄入水平与中国老年人握力及步速存在关联,但与肌肉衰减症检出率无显著关联。