Long-Term Continuous Exposure to Sulfur Dioxide and Fly Ash Mixtures

Three groups of cynomolgus monkeys and three groups of guinea pigs were exposed to mixtures of sulfur dioxide (SO₂) and fly ash while one group of each species was used as a control group. The exposure concentrations for SO₂ were 0.1, 1.0, and 5 ppm, and 0.5 mg/cu m of fly ash was combined with each of the SO₂ concentrations. The duration of exposure was 52 weeks in guinea pigs and 78 weeks in monkeys. Pulmonary function tests and serum biochemical and hematological analyses were conducted prior to and during the exposure period. At termination of exposure, microscopic examination of the lung was performed. Analysis of the data revealed that no adverse effects in guinea pigs or monkeys could he attributed to exposure to the mixtures of SO₂ and fly ash.     

Thyroid Function of Newborns and Exposure to Chlorine Dioxide By-products

In this study, the authors compared thyroid function of newborns from 11 municipalities where drinking water was disinfected by chlorine dioxide (ClO₂) with that of newborns from 15 municipalities using chlorine disinfection. They estimated the mean neonatal blood thyroid stimulating hormone (TSH) levels and proportion of congenital hypothyroidism cases using the results of the Québec neonatal screening for congenital hypothyroidism for 32,978 newborns over the period 1993–1999. There was no significant increase in the TSH level and no excess of congenital hypothyroidism when all newborns exposed to ClO₂ were considered. However, for newborns with low birth weight, mean TSH level was significantly higher among those exposed to ClO₂ than for those in the reference group.     

Low Level Exposure to Carbon Monoxide and Driving Performance

Subjects were exposed to low levels (700 ppm) of carbon monoxide (CO) until carboxyhemoglobin (COHb) levels of 6%, 11%, and 17% were reached, and they were then tested as to their ability to perform both selected driving-related laboratory tests of visual response and control reactions and over-the-road vehicle driving. These test results were then compared with those on the same subjects taken under control conditions without exposure to CO.

The overall pattern of results indicates that a 6% COHb level had no effect on driving ability, and that COHb levels of 11 % and 17% did not appear to seriously affect the ability to drive motor vehicles, as measured by the tests administered in this study. However, certain statistically significant differences were found in some of the tests that suggest some decrement in performance as a result of CO exposure.     

接触黄麻粉尘工人累计接尘量与肺功能损害的研究

本文测定了某麻纺织厂488名接触黄麻粉尘工人和332名对照工人的肺功能。并进行了累计接尘量与肺功能损害关系的分析。结果表明,随着累计接尘量的增加,接触黄麻粉尘工人的肺功能损害程度有加重趋势。其中接尘组吸烟男工的FVC、FEV_1、MMF、V_(50)、V_(25)及女工的V_(50)、V_(25)呈显著下降(P<0.05或P<0.01)。随着累计接尘量的增加,肺功能异常率增大(P<0.05或P<0.01)。接触黄麻粉尘工人的累计接尘量与肺功都损害呈现接触水平-反应关系。双因素方差分析表明,接尘对肺功能各指标均有明显影响,吸烟影响不显著,接尘和吸烟对FVC及FEV_1有交互影响(P<0.05或P<0.01)。     

Long-Term Exposure to Sulfur Dioxide,Sulfuric Acid Mist,Fly Ash,and Their Mixtures

Groups of cynomolgus monkeys and guinea pigs were exposed to mixtures of sulfur dioxide, fly ash, and sulfuric acid mist. The exposure concentrations varied between 0.1 and 5.0 ppm for sulfur dioxide, 0.1 and 1 mg/cu m for sulfuric acid mist, while a concentration of approximately 0.5 mg/cu m was used for fly ash. The duration of exposure was 52 weeks for guinea-pigs and 78 weeks for monkeys.

Pulmonary function tests and serum biochemical and hematological analyses were conducted prior to and periodically during the exposure period. At the termination of exposure, the lungs were examined microscopically. Analysis of the data revealed that in groups exposed to the mixtures of pollutants, sulfuric acid mist was responsible for the effects observed. No synergistic action between the pollutants was detected.     

[... formula ...] and Lung Function: An in Vivo Exploration of Potential Climate Change Implications

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Atmospheric carbon dioxide (CO2) hit a milestone in 2015, when global average concentrations reached 400ppm for the first time in recorded history.1 By 2100, the global average could more than double if emissions remain unabated, according to the RCP8.5 (“business as usual”) scenario used by the Intergovernmental Panel on Climate Change in its assessments.2 Although much attention has been paid to the effect of CO2 as a climate forcing agent, multiple reports suggest this greenhouse gas also may have direct health effects.3 A recent report in Environmental Health Perspectives used a mouse model to assess the pulmonary effects of chronic exposure to ambient CO2 at concentrations comparable to those projected by climate modeling.4Open in a separate windowHumans have been exposed to atmospheric CO2 concentrations averaging roughly 230ppm since the time of our earliest ancestor.9^,10 However, intensified human activity and associated CO2 emissions have led to increases of 2–3ppm per year for the past 50 years. In its most recent update as of this writing, Hawaii’s Mauna Loa Observatory reported a seasonally adjusted CO2 concentration of 414.88ppm for the month of December 2020.11 Image: National Aeronautics and Space Administration. Based on data from Lüthi et al. (2008).12A 2019 review in Nature Sustainability summarized evidence on the effects on lung function of very high (>1,000ppm), acute CO2 exposures.3 In contrast, current report is the first known study to directly assess the physiological impact of long-term exposure to CO2 concentrations that are realistically possible in the near future, says first author Alexander Larcombe, an associate professor at the Telethon Kids Institute and Wal-yan Respiratory Research Center in Nedlands, Australia.In the new study, investigators exposed adult female mice and their offspring to either control (approximately465ppm) or elevated (approximately890ppm) concentrations of CO2. Dams began exposure with a 1-week acclimation period before mating, and offspring were exposed from preconception to adulthood. At postnatal week 12, the investigators assessed the offspring’s respiratory function and lung structure. To compare the effects of exposure during lung development versus exposure during adulthood, they also examined the dams’ lung function.Their results indicate that, among female offspring, exposures to high ambient CO2 caused modest measurable changes in lung function and structure compared with exposure to control CO2 levels. The fact that deficits were seen only in offspring suggests the differences were developmental rather than adaptational.Lung development impairment is well documented to occur in a low-oxygen environment (hypoxia);5 however, the exposure model used in this study did not mimic hypoxic conditions, where oxygen levels are significantly lower while CO2 levels remain unchanged. In the lung, gas exchange occurs in tiny air sacs called alveoli, and perturbations in ambient CO2 levels would be expected to result in increased lung area through alveolarization,6 which in the mouse develops almost exclusively after birth.7 Consistent with this notion, male mice exhibited higher numbers of alveoli; conversely, females showed decreased alveolarization. Other markers of lung function suggested that high CO2 exposure affected female mice exclusively.The authors proposed respiratory acidosis, a change in blood chemistry that results from CO2 exposure, as a possible basis for impaired lung function in female mice. However, they explored no foundation for the sex-specific effects.The findings reported by the authors might not rule out an effect on male mice given the relatively small sample size and inherent animal-to-animal variability, cautions Darryl Zeldin, head of the Environmental Cardiopulmonary Disease Group and scientific director of the National Institute of Environmental Health Sciences. Zeldin was not involved in the study.An additional caveat to the study is the choice of animal model. As burrowing animals, mice are more tolerant to elevated CO2 than animals that stay aboveground.8 Larcombe suggests that future studies should address whether similar outcomes occur in larger, nonburrowing mammals, which would help to give further insight into potential implications for human health.     

Impacts of Climate Change on Indirect Human Exposure to Pathogens and Chemicals from Agriculture

Objective

Climate change is likely to affect the nature of pathogens and chemicals in the environment and their fate and transport. Future risks of pathogens and chemicals could therefore be very different from those of today. In this review, we assess the implications of climate change for changes in human exposures to pathogens and chemicals in agricultural systems in the United Kingdom and discuss the subsequent effects on health impacts.

Data sources

In this review, we used expert input and considered literature on climate change; health effects resulting from exposure to pathogens and chemicals arising from agriculture; inputs of chemicals and pathogens to agricultural systems; and human exposure pathways for pathogens and chemicals in agricultural systems.

Data synthesis

We established the current evidence base for health effects of chemicals and pathogens in the agricultural environment; determined the potential implications of climate change on chemical and pathogen inputs in agricultural systems; and explored the effects of climate change on environmental transport and fate of different contaminant types. We combined these data to assess the implications of climate change in terms of indirect human exposure to pathogens and chemicals in agricultural systems. We then developed recommendations on future research and policy changes to manage any adverse increases in risks.

Conclusions

Overall, climate change is likely to increase human exposures to agricultural contaminants. The magnitude of the increases will be highly dependent on the contaminant type. Risks from many pathogens and particulate and particle-associated contaminants could increase significantly. These increases in exposure can, however, be managed for the most part through targeted research and policy changes.     

二硫化碳接触水平与神经行为功能的剂量效应分析

目的运用多媒体神经行为测试评价系统中文版第三版(NES-C3),探讨二硫化碳(CS2)作业工人神经行为功能与CS2接触水平之间的关系。方法使用NES-C3对81名接触CS2工人的神经行为功能进行测试,并与其接触水平进行相关分析。结果接触二硫化碳水平与负性情绪(困惑—迷惘)呈正相关;与“瞬时记忆能力(记忆扫描准确数)”、“感知—注意力调转”能力等判断能力呈负相关。结论表明接触二硫化碳浓度越高,相应神经行为功能的影响越严重。     

Air Pollution and Lung Function in Dutch Children: A Comparison of Exposure Estimates and Associations Based on Land Use Regression and Dispersion Exposure Modeling Approaches

Background

There is limited knowledge about the extent to which estimates of air pollution effects on health are affected by the choice for a specific exposure model.

Objectives

We aimed to evaluate the correlation between long-term air pollution exposure estimates using two commonly used exposure modeling techniques [dispersion and land use regression (LUR) models] and, in addition, to compare the estimates of the association between long-term exposure to air pollution and lung function in children using these exposure modeling techniques.

Methods

We used data of 1,058 participants of a Dutch birth cohort study with measured forced expiratory volume in 1 sec (FEV₁), forced vital capacity (FVC), and peak expiratory flow (PEF) measurements at 8 years of age. For each child, annual average outdoor air pollution exposure [nitrogen dioxide (NO₂), mass concentration of particulate matter with diameters ≤ 2.5 and ≤ 10 μm (PM_2.5, PM₁₀), and PM_2.5 soot] was estimated for the current addresses of the participants by a dispersion and a LUR model. Associations between exposures to air pollution and lung function parameters were estimated using linear regression analysis with confounder adjustment.

Results

Correlations between LUR- and dispersion-modeled pollution concentrations were high for NO₂, PM_2.5, and PM_2.5 soot (R = 0.86–0.90) but low for PM₁₀ (R = 0.57). Associations with lung function were similar for air pollutant exposures estimated using LUR and dispersion modeling, except for associations of PM_2.5 with FEV₁ and FVC, which were stronger but less precise for exposures based on LUR compared with dispersion model.

Conclusions

Predictions from LUR and dispersion models correlated very well for PM_2.5, NO₂, and PM_2.5 soot but not for PM₁₀. Health effect estimates did not depend on the type of model used to estimate exposure in a population of Dutch children.

Citation

Wang M, Gehring U, Hoek G, Keuken M, Jonkers S, Beelen R, Eeftens M, Postma DS, Brunekreef B. 2015. Air pollution and lung function in Dutch children: a comparison of exposure estimates and associations based on land use regression and dispersion exposure modeling approaches. Environ Health Perspect 123:847–851; http://dx.doi.org/10.1289/ehp.1408541     

不同浓度SO_2吸入染毒诱导运动大鼠心肺组织的氧化损伤效应

目的 研究不同浓度SO_2吸入染毒对运动大鼠心肺组织超氧化物歧化酶(SOD)活力、还原型谷胱甘肽(GSH)及丙二醛(MDA)含量的影响,探讨SO_2污染对运动者心肺组织损伤的机制.方法 48只SD雄性大鼠随机分为8组:空白对照组、单纯运动组、低污染运动组、低污染安静组、中污染运动组、中污染安静组、高污染运动组和高污染安静组.除了空白对照组和单纯运动组,其余各组均置于不同浓度SO_2污染环境中(低、中、高污染组SO_2浓度分别为5、10、15mg/m~3),运动组大鼠进行跑轮运动(8 m/min,2 h/d,共10 d).24 h后处死大鼠,取心肺组织匀浆后立即进行抗氧化酶和脂质过氧化水平测定.结果 肺组织SOD活力在高污染运动组、高污染安静组、中污染运动组、中污染安静组、低污染运动组较空白对照组显著降低(P＜0.05);心组织SOD活力却出现单纯运动组、中污染安静组升高而高污染安静组、高污染运动组下降的变化趋势(P＜0.05).心肺组织的GSH含量中污染安静组升高而高污染运动组、高污染安静组、中污染运动组下降(P＜0.05).MDA水平各实验组较安静对照组显著升高(P＜0.05).同一浓度污染环境中运动组与安静组相比,SOD活力、GSH含量显著降低,MDA水平显著升高(P＜0.05),且存在剂量-效应关系.结论 SO_2污染可引起大鼠心肺组织的氧化损伤,而SO_2污染对运动大鼠心肺组织的氧化损伤效应比安静组更明显.

Abstract：

Objective To investigate the effects of sulfur dioxide(SO_2)pollution in difierent concentrations on activity of SOD,levels of GSH and MDA in heart and lung tissue of exercised rats,in order to elucidate the toxicological mechanism of SO_2 pollution.Methods Forty-eight SD rats were randomly divided into eight groups:a rest group(RG),an exercise group(EG),a low pollution exercise group (LEG),a low pollution rest group(LRG),a moderate pollution exercise group(MEG),a moderate pollution rest group(MRG),a high pollution exercise group(HEG)and a high pollution rest group(HRG).All groups,except RG and EG,were exposed to SO_2 with difierent concentrations(5 mg/m~3,10 mg/m~3,15 mg/m~3),meanwhile exercised rats run in a motor-driven wheel at a speed of 8 m/min,2 h/d for 10 days.Rats were sacrificed at 24 h after treatment and the anti-oxidative enzymes activity and lipid peroxidation(LPO)levels were measured.Results Compared with RG,SOD activity of lung tissue significantly decreased in HEG,MEG,LEG(P＜0.05),whereas the change of SOD activity of heart showed a tendency that EG,MRG raised and HRG,HEG declined(P＜0.05).GSH levels of heart and lung tissue appeared a conspicuous increase in MRG and a noticeable decrease in HEG,HRG,MEG(P＜0.05).MDA levels of heart and lung tissue in each group had a significant increase in comparison with RG(P＜0.05).Compared with the rest group in the same polluted environment,SOD activity and GSH levels of heart and lung tissue in exercise groups had a markedly decrease while MDA levels significantly increased(P＜0.05),with a dose-dependent manner.Conclusion SO_2 exposure can induce oxidative damage in exercised rats' heart and lung tissue,which is more significant than rest rats.     

低浓度O3和NO2对小鼠气道炎症单独及联合作用

目的 探讨O3和NO2单独和混合暴露对小鼠气道的损伤和炎症水平影响.方法 将80只清洁级BALB/C小鼠随机分为8组:其中4组为致敏模型组(根据暴露不同分为空气对照组、O2组、NO2组及混合暴露组),另外4组为非致敏组(分组同前).O3暴露浓度采用0.16 mg/m3,NO2为0.30 mg/m3,每天暴露2 h,连续7 d.暴露完成后处死动物进行气管灌洗,取支气管肺泡灌洗液(BALF)进行细胞计数和细胞因子含量检测.结果 致敏组中,NO2和O3单独和混合暴露后均可导致BALF中性粒细胞比例、IL-6水平明显升高(均为P＜0.05),,其中O3单独暴露和混合暴露还导致IL-2和MDA的明显升高(均为P＜0.05);非致敏组中,只有O3暴露和混合暴露可引起BALF细胞总数、中性粒细胞比例增高和IL-2、IL-6、MDA水平明显升高(均为P＜0.05),且致敏组IL-2和IL-6水平高于相同暴露条件非致敏组(P＜0.05);混合暴露时致敏小鼠气道内细胞总数和MDA明显高于O3或NO2单独暴露(P＜0.05).结论 O3和NO2暴露均会加重致敏小鼠气道炎症,其中O3暴露还会引起非致敏小鼠气道炎症发生,引起炎症反应均是以中性粒细胞增高为主要特征;混合暴露对小鼠气道炎症存在联合作用;相对于非致敏小鼠,致敏小鼠对O3和NO2暴露更敏感.     

In Utero Exposure to Arsenic Alters Lung Development and Genes Related to Immune and Mucociliary Function in Mice

Background: Exposure to arsenic via drinking water is a global environmental health problem. In utero exposure to arsenic via drinking water increases the risk of lower respiratory tract infections during infancy and mortality from bronchiectasis in early adulthood.Objectives: We aimed to investigate how arsenic exposure in early life alters lung development and pathways involved in innate immunity.Methods: Pregnant BALB/c, C57BL/6, and C3H/HeARC mice were exposed to 0 (control) or 100 μg/L arsenic via drinking water from gestation day 8 until the birth of their offspring. We measured somatic growth, lung volume, and lung mechanics of mice at 2 weeks of age. We used fixed lungs for structural analysis and collected lung tissue for gene expression analysis by microarray.Results: The response to arsenic was genetically determined, and C57BL/6 mice were the most susceptible. Arsenic-exposed C57BL/6 mice were smaller in size, had smaller lungs, and had impaired lung mechanics compared with controls. Exposure to arsenic in utero up-regulated the expression of genes in the lung involved in mucus production (Clca3, Muc5b, Scgb3a1), innate immunity (Reg3γ, Tff2, Dynlrb2, Lplunc1), and lung morphogenesis (Sox2). Arsenic exposure also induced mucous cell metaplasia and increased expression of CLCA3 protein in the large airways.Conclusions: Alterations in somatic growth, lung development, and the expression of genes involved in mucociliary clearance and innate immunity in the lung are potential mechanisms through which early life arsenic exposure impacts respiratory health.     

Impact of Geocoding Methods on Associations between Long-term Exposure to Urban Air Pollution and Lung Function

Background: Errors in address geocodes may affect estimates of the effects of air pollution on health.Objective: We investigated the impact of four geocoding techniques on the association between urban air pollution estimated with a fine-scale (10 m × 10 m) dispersion model and lung function in adults.Methods: We measured forced expiratory volume in 1 sec (FEV₁) and forced vital capacity (FVC) in 354 adult residents of Grenoble, France, who were participants in two well-characterized studies, the Epidemiological Study on the Genetics and Environment on Asthma (EGEA) and the European Community Respiratory Health Survey (ECRHS). Home addresses were geocoded using individual building matching as the reference approach and three spatial interpolation approaches. We used a dispersion model to estimate mean PM₁₀ and nitrogen dioxide concentrations at each participant’s address during the 12 months preceding their lung function measurements. Associations between exposures and lung function parameters were adjusted for individual confounders and same-day exposure to air pollutants. The geocoding techniques were compared with regard to geographical distances between coordinates, exposure estimates, and associations between the estimated exposures and health effects.Results: Median distances between coordinates estimated using the building matching and the three interpolation techniques were 26.4, 27.9, and 35.6 m. Compared with exposure estimates based on building matching, PM₁₀ concentrations based on the three interpolation techniques tended to be overestimated. When building matching was used to estimate exposures, a one-interquartile range increase in PM₁₀ (3.0 μg/m³) was associated with a 3.72-point decrease in FVC% predicted (95% CI: –0.56, –6.88) and a 3.86-point decrease in FEV₁% predicted (95% CI: –0.14, –3.24). The magnitude of associations decreased when other geocoding approaches were used [e.g., for FVC% predicted –2.81 (95% CI: –0.26, –5.35) using NavTEQ, or 2.08 (95% CI –4.63, 0.47, p = 0.11) using Google Maps].Conclusions: Our findings suggest that the choice of geocoding technique may influence estimated health effects when air pollution exposures are estimated using a fine-scale exposure model.Citation: Jacquemin B, Lepeule J, Boudier A, Arnould C, Benmerad M, Chappaz C, Ferran J, Kauffmann F, Morelli X, Pin I, Pison C, Rios I, Temam S, Künzli N, Slama R, Siroux V. 2013. Impact of geocoding methods on associations between long-term exposure to urban air pollution and lung function. Environ Health Perspect 121:1054–1060; http://dx.doi.org/10.1289/ehp.1206016     

环境空气PM_(2.5)短期暴露与未确诊COPD人群肺功能的关联性

目的分析环境空气中PM_(2.5)短期暴露与未确诊COPD人群肺功能的关联,为该类人群的空气污染防护提供科学依据。方法以肺功能检测筛查的未确诊COPD人群作为受试者;于2018年1、3、8和10月4个时间段,对28名受试者进行了重复测量,包括肺功能检测,及每次测量前5 d的环境PM_(2.5)质量浓度监测、问卷调查;用混合效应模型,分析PM_(2.5)与肺功能的关联性。PM_(2.5)质量浓度对肺功能的影响考虑了滞后效应,按照lag0～lag4滞后日期的浓度代入模型。结果 PM_(2.5)日均质量浓度最高为250.46μg/m~3。单日滞后效应结果显示,FEV_1、MEF_(25)、MEF_(50)和一秒率与PM_(2.5)的质量浓度在lag1有显著的关联性;PM_(2.5)质量浓度每升高10μg/m~3,FEV_1下降0.05 L,MEF_(25)下降0.03 L/s,MEF_(50)下降0.10 L/s,一秒率下降1.09%;FVC、MEF_(75)和PEF与PM_(2.5)质量浓度无关联。滑动平均滞后效应结果中,仅MEF_(50)与PM_(2.5)质量浓度在lag01有一定显著关联性(P<0.1);PM_(2.5)质量浓度每升高10μg/m~3,MEF_(50)下降0.07 L/s。结论环境空气PM_(2.5)可以导致未确诊COPD人群肺功能通气功能指标的下降,应注重此类人群重污染天气的防护。空气污染对小气道的影响更值得关注。     

Effect of Exposure to Atmospheric Ultrafine Particles on Production of Free Fatty Acids and Lipid Metabolites in the Mouse Small Intestine

Background: Exposure to ambient ultrafine particulate matter (UFP) is a well-recognized risk factor for cardiovascular and respiratory diseases. However, little is known about the effects of air pollution on gastrointestinal disorders.Objective: We sought to assess whether exposure to ambient UFP (diameter < 180 nm) increased free fatty acids and lipid metabolites in the mouse small intestine.Methods: Ldlr-null mice were exposed to filtered air (FA) or UFP collected at an urban Los Angeles, California, site that was heavily affected by vehicular emissions; the exposure was carried out for 10 weeks in the presence or absence of D-4F, an apolipoprotein A-I mimetic peptide with antioxidant and anti-inflammation properties on a high-fat or normal chow diet.Results: Compared with FA, exposure to UFP significantly increased intestinal hydroxyeicosatetraenoic acids (HETEs), including 15-HETE, 12-HETE, 5-HETE, as well as hydroxyoctadecadienoic acids (HODEs), including 13-HODE and 9-HODE. Arachidonic acid (AA) and prostaglandin D₂ (PGD₂) as well as some of the lysophosphatidic acids (LPA) in the small intestine were also increased in response to UFP exposure. Administration of D-4F significantly reduced UFP-mediated increase in HETEs, HODEs, AA, PGD₂, and LPA. Although exposure to UFP further led to shortened villus length accompanied by prominent macrophage and neutrophil infiltration into the intestinal villi, administration of D-4F mitigated macrophage infiltration.Conclusions: Exposure to UFP promotes lipid metabolism, villus shortening, and inflammatory responses in mouse small intestine, whereas administration of D-4F attenuated these effects. Our findings provide a basis to further assess the mechanisms underlying UFP-mediated lipid metabolism in the digestive system with clinical relevance to gut homeostasis and diseases.Citation: Li R, Navab K, Hough G, Daher N, Zhang M, Mittelstein D, Lee K, Pakbin P, Saffari A, Bhetraratana M, Sulaiman D, Beebe T, Wu L, Jen N, Wine E, Tseng CH, Araujo JA, Fogelman A, Sioutas C, Navab M, Hsiai TK. 2015. Effect of exposure to atmospheric ultrafine particles on production of free fatty acids and lipid metabolites in the mouse small intestine. Environ Health Perspect 123:34–41; http://dx.doi.org/10.1289/ehp.1307036     

低浓度酸气(雾)对鼻粘膜和肺功能的慢性职业损害

目的探索低浓度下单一和混合性酸气（雾）对鼻粘膜和肺功能慢性损害的特点及剂量效应关系。方法以车间作业工人呼吸带酸气（雾）平均浓度低于国家最高容许浓度（ＭＡＣ）的上海市１８家工厂７６６名接触氢氟酸（ＨＦ）、铬酸（ＣｒＯ３）、三酸（Ｈ２ＳＯ４,ＨＮＯ３,ＨＣｌ）及ＨＦ混合三酸和ＣｒＯ３混合三酸作业工人为接触组,１７４名不接触酸气的健康人员为对照组,统一行系统体检和肺功能测定。结果接触组３０１６％（２３１／７６６）作业工人有不同程度鼻粘膜糜烂（２２５例）、溃疡（３例）和中隔穿孔（３例）,２９５１％（１８５／６２７）出现小气道阻塞（１６７例）及不同程度肺功能减退（１８例）。５组酸气接触组鼻粘膜、肺功能损害检出率均显著高于对照组（Ｐ＜００５～００１）。铬酸与三酸的低浓度酸气（雾）混合接触,对鼻粘膜损害有明显协同作用（Ｐ＜０００１）,损害发生与工龄呈正相关关系（ｒｓ＝０８９２）。结论长期接触现行卫生标准下的５种酸气（雾）有明显鼻粘膜和肺小气道功能损害作用,对安全限值尚须进一步研究,鼻粘膜和肺小气道功能损害是检测低浓度酸气（雾）职业危害的客观指标。     

环境性吸烟导致的肺癌生物标记物水平变化及口岸控烟现状

环境性吸烟可导致肺癌生物标记物水平的变化,通过监测检测NNK、可替宁、CYP1A1基因等的变化,可早期识别肺癌。烟草导致的环境性吸烟和直接吸烟危害,使人罹患癌症、肺部疾病、心血管疾病的几率大增。越来越多国家加入《烟草控制框架公约》,推进了包括口岸公共场所在内的公共场所控烟工作的开展。     

原子力显微镜观察抗生素后效应期间大肠埃希菌形态学变化

目的通过对加替沙星体外抗生素后效应(PAE)期间E.coli ATCC25922的形态学观察以及菌体大小、DNA含量变化的研究,探讨PAE形成机制.方法于加替沙星体外PAE期间不同时间点吸取培养物,应用原子力光显微镜观察E.coli ATCC25922的形态学变化,采用流式细胞仪技术与荧光探针碘化丙啶结合,检测其菌体大小、DNA含量变化.结果原子力显微镜结果表明E.coliATCC25922在菌落计数法所测定的PAE之后仍有丝状体存在,流式细胞仪分析结果表明:与空白对照组比较,其体外PAE期间E.coliATCC25922菌体显著延长、DNA含量变化显著升高.结论加替沙星体外PAE期间E.coliATCC25922呈特征性的丝状体变化,而其菌体大小、DNA含量变化随之相应变化,提示丝状体形成与DNA含量变化相关.