Effect of inhaled carbon ultrafine particles on reactive hyperemia in healthy human subjects

BACKGROUND: Ultrafine particles (UFP) may contribute to the cardiovascular effects of exposure to particulate air pollution, partly because of their relatively efficient alveolar deposition and potential to enter the pulmonary vascular space. OBJECTIVES: This study tested the hypothesis that inhalation of elemental carbon UFP alters systemic vascular function. METHODS: Sixteen healthy subjects (mean age, 26.9 +/- 6.5 years) inhaled air or 50 microg/m3 elemental carbon UFP by mouthpiece for 2 hr, while exercising intermittently. Measurements at preexposure baseline, 0 hr (immediately after exposure), 3.5 hr, 21 hr, and 45 hr included vital signs, venous occlusion plethysmography and reactive hyperemia of the forearm, and venous plasma nitrate and nitrite levels. RESULTS: Peak forearm blood flow after ischemia increased 3.5 hr after exposure to air but not UFP (change from preexposure baseline, air: 9.31 +/- 3.41; UFP: 1.09 +/- 2.55 mL/min/100 mL; t-test, p = 0.03). Blood pressure did not change, so minimal resistance after ischemia (mean blood pressure divided by forearm blood flow) decreased with air, but not UFP [change from preexposure baseline, air: -0.48 +/- 0.21; UFP: 0.07 +/- 0.19 mmHg/mL/min; analysis of variance (ANOVA), p = 0.024]. There was no UFP effect on pre-ischemia forearm blood flow or resistance, or on total forearm blood flow after ischemia. Venous nitrate levels were significantly lower after exposure to carbon UFP compared with air (ANOVA, p = 0.038). There were no differences in venous nitrite levels. CONCLUSIONS: Inhalation of 50 microg/m3 carbon UFP during intermittent exercise impairs peak forearm blood flow during reactive hyperemia in healthy human subjects.     

Immune markers and ornithine decarboxylase activity among electric utility workers

The effects of a 60-Hz magnetic field (MF) exposure on white blood cell ornithine decarboxylase (ODC) activity, natural killer (NK) cell activity, lymphocyte phenotypes, and differential cell counts were studied among 60 electric utility workers. Personal MF exposure monitoring over 3 consecutive workdays was followed by collection of a peripheral blood sample. There were no MF-related changes in NK activity or the number of circulating neutrophils, eosinophils, basophils, or T-lymphocytes (CD4, CD8, CD4:CD8 ratio). MF exposure intensity was associated with decreased ODC activity (P<0.01) and lower NK cell counts (P=0.04). Melatonin production, which stimulates the immune system, was quantified on the night preceding immune marker determinations. Exposure-related reductions in ODC activity, NK and B cells, and monocytes were strongest among workers with reduced melatonin production. The biological significance or long-term health consequences associated with these changes are not known.     

Personal exposure to ultrafine particles and oxidative DNA damage

Exposure to ultrafine particles (UFPs) from vehicle exhaust has been related to risk of cardiovascular and pulmonary disease and cancer, even though exposure assessment is difficult. We studied personal exposure in terms of number concentrations of UFPs in the breathing zone, using portable instruments in six 18-hr periods in 15 healthy nonsmoking subjects. Exposure contrasts of outdoor pollution were achieved by bicycling in traffic for 5 days and in the laboratory for 1 day. Oxidative DNA damage was assessed as strand breaks and oxidized purines in mononuclear cells isolated from venous blood the morning after exposure measurement. Cumulated outdoor and cumulated indoor exposures to UFPs each were independent significant predictors of the level of purine oxidation in DNA but not of strand breaks. Ambient air concentrations of particulate matter with an aerodynamic diameter of < or = 10 microm (PM10), nitrous oxide, nitrogen dioxide, carbon monoxide, and/or number concentration of UFPs at urban background or busy street monitoring stations was not a significant predictor of DNA damage, although personal UFP exposure was correlated with urban background concentrations of CO and NO2, particularly during bicycling in traffic. The results indicate that biologic effects of UFPs occur at modest exposure, such as that occurring in traffic, which supports the relationship of UFPs and the adverse health effects of air pollution.     

Brief exposures to NO2 augment the allergic inflammation in asthmatics

Exposure to high ambient levels of nitrogen dioxide (NO2) enhances the airway reaction in humans to allergen, measured as decreased pulmonary function. We tested whether this NO2 effect is associated with an increased inflammatory response to allergen in the airways. To mimic real-life conditions, in which exposure to high ambient levels of NO2 occurs only during short periods of time but often several times a day, we used a repeated-exposure model. On day 1, 18 subjects with allergic asthma were exposed, in randomized order, to purified air or to 500 microg/m3 NO2 for 15 min, and on day 2 for 2 x 15 min. Allergen was inhaled 3-4h after the NO2 exposures on both days. Symptoms, pulmonary function, and inflammatory response in sputum and blood were measured daily. Eosinophil cationic protein in both sputum and blood increased more from day 1 to day 3 after NO2+allergen than after air+allergen, whereas eosinophil counts did not differ. The change in myeloperoxidase was significantly greater after NO2+allergen than after air+allergen in blood but not in sputum. This finding was not accompanied by raised levels of neutrophils in sputum and blood. Symptoms and pulmonary function were equally affected by NO2+allergen and air+allergen. We conclude that two to three brief exposures to ambient levels of NO2 can prime circulating eosinophils and enhance the eosinophilic activity in sputum in response to inhaled allergen. This might be an important mechanism by which air pollutants amplify the inflammatory reactions in the airways.     

Vascular Effects of Ultrafine Particles in Persons with Type 2 Diabetes

Background

Diabetes confers an increased risk for cardiovascular effects of airborne particles.

Objective

We hypothesized that inhalation of elemental carbon ultrafine particles (UFP) would activate blood platelets and vascular endothelium in people with type 2 diabetes.

Methods

In a randomized, double-blind, crossover trial, 19 subjects with type 2 diabetes inhaled filtered air or 50 μg/m³ elemental carbon UFP (count median diameter, 32 nm) by mouthpiece for 2 hr at rest. We repeatedly measured markers of vascular activation, coagulation, and systemic inflammation before and after exposure.

Results

Compared with air, particle exposure increased platelet expression of CD40 ligand (CD40L) and the number of platelet-leukocyte conjugates 3.5 hr after exposure. Soluble CD40L decreased with UFP exposure. Plasma von Willebrand factor increased immediately after exposure. There were no effects of particles on plasma tissue factor, coagulation factors VII or IX, or D-dimer.

Conclusions

Inhalation of elemental carbon UFP for 2-hr transiently activated platelets, and possibly the vascular endothelium, in people with type 2 diabetes.     

Associations between Leukocyte Counts and Cardiovascular Disease Risk Factors in Apparently Healthy Japanese Men

Increased leukocyte counts, particularly white blood cell and neutrophil counts, are reportedly associated with increased incidence of cardiovascular diseases (CVD) and mortality in subjects with acute and moderate coronary diseases. However, few reports have determined the associations between leukocyte subset (i.e., white blood cells, neutrophils, monocytes, lymphocytes, basophils and eosinophils) counts and CVD risk factors. In this study, we examined the associations between leukocyte subset counts and CVD risk factors in apparently healthy Japanese men. We conducted a cross-sectional study of men who participated in health checkups, and selected those who were not being treated for metabolic diseases. We determined associations between leukocyte subset counts and CVD risk factors by multivariate linear regression (MLR) analysis and analysis of covariance (ANCOVA). Overall, 3,576 subjects aged 49.3±5.75 (range, 40-59) y were recruited. MLR and ANCOVA showed that white blood cell, neutrophil, monocyte counts are associated with decreased high-density lipoprotein cholesterol (HDL-C) and increased C-reactive protein levels, the lymphocyte count is positively associated with lipid abnormalities (i.e., decreased HDL-C, increased low-density lipoprotein cholesterol and increased triacylglycerol (TG)), and the basophil count is associated with increased TG and liver injury marker levels (i.e., alanine aminotransferase). Our results in this study demonstrated that leukocyte subset counts showed differential associations with CVD risk factors in apparently healthy Japanese men.     

超细颗粒物对上海市某区65岁以上老年人群外周血 白细胞计数影响的定群研究

目的 研究超细颗粒物（ultrafine particles, UFPs）对65岁以上老年人群外周血白细胞计数（white blood cell count, WBC）的影响。方法 招募上海市某区65岁以上老年居民，采用定群研究方法，于2014年1月1日至2018年12月29日进行至少2次健康体检，采集外周静脉血测定WBC水平；收集区域同期大气UFPs每小时粒数浓度（particle number concentration, PNC）、常规大气污染物逐日浓度和气象资料，利用线性混合效应模型分析UFPs对WBC短期变化的影响，同时对人员特征、温度、相对湿度、星期几效应及时间趋势等协变量进行控制。结果 共纳入研究对象108 006名，WBC为（6.2±1.4）×109/L。UFPs中以粒径0.05~0.10 μm颗粒物的PNC值最高，粒径0.03~0.05 μm的颗粒物次之，粒径0.01~0.03 μm颗粒物的PNC值则相对较低。Lag 01 d时，粒径范围0.01~0.03 μm、0.03~0.05 μm、0.05~0.10 μm的UFPs 和总颗粒物（0.01~0.10 μm）PNC值每增加1个IQR，WBC分别升高9.98（95% CI : 1.12~18.84）×106/L、11.88（95% CI : 2.99~20.76）×106/L、28.78（95% CI : 18.07~39.49）×106/L和20.66（95% CI : 11.09~30.23）×106/L。结论 UFPs短期暴露可导致上海市某区65岁以上老年人群炎症水平升高。     

迈瑞BC-5500全自动血细胞分析仪性能的初步评价

目的：评价BC-5500全自动血细胞分析仪全血细胞计数（CBC）和白细胞分类（DC）的性能。方法：按照有关文件规定对该仪器CBC的性能指标进行评价，并与人工分类进行比较。结果：该仪器CBC的精密度、携带污染率和总重复性均符合要求；在正常及常见的病理范围线性良好；与XE一2100的结果进行比较．其相关性好（r〉0．99）。DC：中性粒细胞（Neut）、淋巴细胞（Lym）、单核细胞（MON）、嗜酸性粒细胞（Eos）和嗜碱性中粒细胞（Baso）的重复性好；WBC形态正常的样本，仪器与人工DC的结果进行比较，Neut、Lym和Eos相关性较好（r值为0．968～0．983）；Mon次之（r=0．917），Baso的相关性欠佳（r=0．659）。较高比例的杆状核粒细胞、异常／异形Lvm和幼稚细胞可出现WBC散点图变化或报警。结论：该仪器检测的结果准确、可靠，主要性能指标符合实验要求；对怀疑WBC分类异常的标本，仪器DC结果必须经显微镜复核后才能报告。     

Exposure to work-related levels of swine dust up-regulates CD106 on human alveolar macrophages

BACKGROUND: Exposure to dust from swine confinement buildings, causes an inflammatory response. Monocyte recruitment to the murine lung after instillation of lipopolysaccharide (LPS) has been shown to partially depend on CD106/VCAM1. We wanted to determine whether this can be confirmed in man. METHODS: Non-na?ve persons bearing personal air samples were exposed for 3 hr in a swine confinement building, and were bronchoscopied before and after exposure. Blood samples were taken at the time of bronchoscopy. Expression of adhesion molecules on leukocytes was investigated by flow cytometry in bronchoaveloar lavage (BAL) and blood. RESULTS: Expression of CD106 on alveolar macrophages, but not on neutrophils or T cells in BAL or blood, was up-regulated in proportion to the amount of LPS that individuals were exposed. CONCLUSIONS: This argues for requirement of CD106 during inflammatory recruitment of monocytes to the human lung.     

Biomarkers of Mn exposure in humans

BACKGROUND: Studies have reported associations between manganese (Mn) exposures and Mn levels in blood and urine, though the suitability of these biological measures as biomarkers of exposure is not well known. METHODS: We evaluated whether whole blood, plasma, and urine Mn levels reflect exposures in occupationally exposed humans. RESULTS: In active ferroalloy workers, blood Mn was associated with total air Mn levels in subjects currently exposed to low (median = 0.42 microg/m(3), P = 0.009) and moderate (median = 4.2 microg/m(3), P = 0.007) air Mn levels, but not in workers exposed to the highest Mn levels (median = 292 microg/m(3), P = 0.31). In bridge welders blood Mn (P < 0.01), but not plasma or urine Mn was significantly associated with their cumulative respiratory exposure index. In welders, approximately 6% (range approximately 3-9%) of whole blood Mn was contained in the plasma fraction, though there was no association between whole blood and plasma Mn levels (Pearson's R = 0.258, P = 0.12). In contrast, in fresh whole blood samples spiked with Mn ex vivo approximately 80% or more of added Mn partitioned in the plasma, while only approximately 20% or less partitioned in the cellular fraction. CONCLUSIONS: These data suggest a complex and limited relationship between exposure and blood Mn levels that may depend upon exposure attributes and the latency of blood sampling relative to exposure; plasma and urine Mn appear to be of little utility as exposure biomarkers. This underscores the need to fully characterize and validate these or other biomarkers for use in constructing appropriate exposure metrics and determining exposure-effect relationships.     

采暖期大气超细颗粒物污染浓度特征研究

目的调查我国大气污染典型地区采暖期超细颗粒物(UFPs)的污染特征,为今后开展UFPs的健康效应研究提供实验依据。方法于2017年1月2-15日在天津市中心某交通路口采用WPS-1000XP型宽范围颗粒粒度仪监测UFPs的粒数浓度、表面积浓度和质量浓度;使用DUSTMATE型手持式环境粉尘检测仪同步监测PM_(2.5)和PM_1的质量浓度。结果监测点采暖期PM_(0.5)和UFPs粒数浓度最高可达33 484粒/cm~3和22 461粒/cm~3,平均水平分别为19 185粒/cm~3和13 184粒/cm~3;UFPs表面积浓度最高可达264.2μm~2/cm~3,平均水平为126.69μm~2/cm~3;UFPs质量浓度最高观测到3.2μg/m~3,平均水平为1.6μg/m~3;PM_(2.5)和PM_1最高质量浓度分别可达600.0μg/m~3和201.6μg/m~3,平均水平分别为96.94μg/m~3和45.33μg/m~3;相关性分析显示,在8:30这一时刻UFPs粒数浓度与PM_(2.5)质量浓度呈负相关。结论监测点采暖期UFPs污染水平较高,有必要针对UFPs开展长期监测及健康危害研究。     

Different recovery responses from dietary zinc-deficiency in the distribution of rat granulocytes

The purpose of this study was to elucidate the effects of the recovery from dietary zinc-deficiency on the number of total white blood cells (WBCs), neutrophils, eosinophils and basophils, and plasma zinc and corticosterone concentrations in weanling male Sprague Dawley rats. Rats (n=34) of the zinc-deficient diet (0.6 mg zinc/kg diet) and control diet (35.2 mg zinc/kg diet) groups were fed for 4 wk, and then rats of both groups were fed with the control diet for 3 wk. Zinc-deficiency increased duration-dependently and clearly the number of total WBCs, neutrophils and eosinophils, and the increased numbers of these cells recovered to the control levels in week 2 of the recovery. On the other hand, the number of basophils increased by the zinc-deficiency recovered to the control levels in week 1 of the recovery. Zinc-deficiency significantly decreased plasma zinc concentrations by 85%, and markedly increased plasma corticosterone concentrations by 317%, as compared with the control group. In the recovery period, plasma zinc and corticosterone concentrations recovered to the control levels in week 2 of the recovery. These results suggest that zinc-deficiency and its recovery responses in the number of granulocytes and total WBCs are reversible, and their recovery rates depend on the subsets of granulocytes in rats.     

Up-regulation of tissue factor in human pulmonary artery endothelial cells after ultrafine particle exposure

BACKGROUND: Epidemiology studies have linked exposure to pollutant particles to increased cardiovascular mortality and morbidity, but the mechanisms remain unknown. OBJECTIVES: We tested the hypothesis that the ultrafine fraction of ambient pollutant particles would cause endothelial cell dysfunction. METHODS: We profiled gene expression of human pulmonary artery endothelial cells (HPAEC) exposed to ultrafine particles (UFPs; 100 microg/mL) from Chapel Hill, North Carolina, or vehicle for 4 hr with Affymetrix HG U133 Plus 2.0 chips (n = 4 each). RESULTS: We found 320 up-regulated genes and 106 down-regulated genes (p < 0.01, 5% false discovery rate). We noted up-regulation of genes related to coagulation [tissue factor (F3) and coagulation factor II receptor-like 2 (F2RL2)] and differential regulation of genes related to F3 signaling (FOS, JUN, and NFKBIA). Results of quantitative polymerase chain reaction show a significant up-regulation of F3 after 10 and 100 microg/mLUFP exposures. Additionally, the water-soluble fractions of UFPs were sufficient to induce the expression of F3, F2RL2, and heme oxygenase 1 (HMOX1). Treatment of HPAEC with UFPs for 16 hr increased the release of interleukin (IL)-6 and IL-8. Pretreatment of HPAEC with a blocking antibody against F3 attenuated IL-6 and IL-8 release by 30 and 70%, respectively. CONCLUSIONS: Using gene profiling, we discovered that UFPs may induce vascular endothelial cells to express genes related to clotting. These results indicate that PM may cause adverse cardiovascular health effects by activating coagulation-inflammation circuitry.     

Pulmonary epithelial integrity in children: relationship to ambient ozone exposure and swimming pool attendance

Airway irritants such as ozone are known to impair lung function and induce airway inflammation. Clara cell protein (CC16) is a small anti-inflammatory protein secreted by the nonciliated bronchiolar Clara cells. CC16 in serum has been proposed as a noninvasive and sensitive marker of lung epithelial injury. In this study, we used lung function and serum CC16 concentration to examine the pulmonary responses to ambient O3 exposure and swimming pool attendance. The measurements were made on 57 children 10-11 years of age before and after outdoor exercise for 2 hr. Individual O3 exposure was estimated as the total exposure dose between 0700 hr until the second blood sample was obtained (mean O3 concentration/m3 times symbol hours). The maximal 1-hr value was 118 microg/m3 (59 ppb), and the individual exposure dose ranged between 352 and 914 microg/m3hr. These O3 levels did not cause any significant changes in mean serum CC16 concentrations before or after outdoor exercise, nor was any decrease in lung function detected. However, children who regularly visited chlorinated indoor swimming pools had significantly lower CC16 levels in serum than did nonswimming children both before and after exercise (respectively, 57 +/- 2.4 and 53 +/- 1.7 microg/L vs. 8.2 +/- 2.8 and 8.0 +/- 2.6 microg/L; p < 0.002). These results indicate that repeated exposure to chlorination by-products in the air of indoor swimming pools has adverse effects on the Clara cell function in children. A possible relation between such damage to Clara cells and pulmonary morbidity (e.g., asthma) should be further investigated.     

Effect of formaldehyde on asthmatic response to inhaled allergen challenge

BACKGROUND: Exposure to formaldehyde may lead to exacerbation of asthma. OBJECTIVES: Our aim in this study was to investigate whether exposure to a low level (500 microg/m(3)) of formaldehyde enhances inhaled allergen responses. METHODS: Twelve subjects with intermittent asthma and allergy to pollen were exposed, at rest, in a double-blind crossover study to either formaldehyde or purified air for 60 min. The order of exposure to formaldehyde and air-only was randomized, and exposures were separated by 2 weeks. We also performed an allergen inhalation challenge after each exposure. Airway responsiveness to methacholine and lower airway inflammation (induced sputum) were assessed 8 hr after allergen challenge. RESULTS: The median dose of allergen producing a 15% decrease in forced expiratory volume in 1 sec (PD(15)FEV(1)) was 0.80 IR (index of reactivity) after formaldehyde exposure compared with 0.25 IR after air-only exposure (p = 0.06). Formaldehyde exposure did not affect allergen-induced increase in responsiveness to methacholine (p = 0.42). We found no formaldehyde-associated effect on the airway inflammatory response, in particular the eosinophilic inflammatory response, induced by the allergen challenge 8 hr before. CONCLUSION: In this study, exposure to 500 microg/m(3) formaldehyde had no significant deleterious effect on airway allergen responsiveness of patients with intermittent asthma; we found a trend toward a protective effect.     

职业接触可溶性铬盐个体暴露与尿铬水平的相关性研究

目的通过对职业接触可溶性铬盐个体暴露与尿铬水平的相关性研究,探讨并提出可溶性铬盐职业接触者尿铬生物限值,为铬盐职业接触人群健康监护和危险性评价提供依据。方法通过流行病学横断面调查,以不同剂量铬盐接触的83名劳动者为研究对象,10名非铬盐接触的农民为对照,两组人群在年龄、性别和吸烟状况等方面相匹配,进行了个体铬盐暴露与班末尿铬含量的研究,并对二者之间的关系进行了分析。同时复习了对可溶性铬盐职业接触者尿铬生物限值的相关文献。结果对照组8 h个体空气铬连续监测浓度在0.00~0.08μg/m3之间,尿铬浓度经肌酐校正后在0.40~1.02μg/g肌酐之间。铬盐接触劳动者8 h连续空气个体监测浓度在0.10~287.00μg/m3之间,尿铬浓度范围在1.14~79.07μg/g肌酐。职业接触铬盐工人班末的尿铬浓度随个体铬盐暴露水平的增加而增加,两者具有相关性。其回归方程为尿铬浓度(μg/g肌酐)=4.16+236.86×空气中铬的浓度(mg/m3),尿铬与空气铬的浓度相关系数r=0.976。通过文献复习,美国政府职业卫生工作者协会(ACG IH)推荐的职业接触可溶性铬盐在与我国相同的时间加权平均阈限值0.05mg/m3下,尿铬生物接触限值为65.1μmol/mol肌酐(30μg/g肌酐)。结论职业接触可溶性铬盐工人班末的尿铬含量可以用来评价作业场所铬盐的接触情况。依据美国ACG IH推荐的生物接触限值以及本调查结果,作者提出连续工作5个工作日的工作周末/班末尿铬的推荐值为65.1μmol/mol肌酐(30μg/g肌酐)。     

Changes in cellular immunity among workers occupationally exposed to styrene in a plastics lamination plant

BACKGROUND: Styrene is a widely used industrial chemical. Immune and hematological parameters were examined in 29 hand laminators and sprayers exposed to styrene for an average of 14 years and in 19 in-factory unexposed controls. The workers performed hand lamination procedures in a production area with an average area airborne styrene level of 139.5 mg/m(3). Mean concentration of styrene in the blood of exposed workers was 945.7 microg/L and the mean styrene in exhaled air was 38.8 microg/L. METHODS: Parameters of internal and external exposure, immune function assays, immunoglobulins, acute phase reactants and hematology were evaluated in exposed and non-exposed populations. RESULTS: Using multifactorial analysis of variance we found a significant decrease in proliferation of lymphocytes stimulated by Concanavalin A but not by pokeweed mitogen (PWM) in workers occupationally exposed to styrene. Proliferative response to PWM was significantly correlated with the levels of styrene in blood. Phagocytic activity of monocytes, levels of IgG, IgA, IgM, IgE and alpha-2-macroglobulin in serum were indistinguishable in the two groups. The population exposed to styrene had increased levels of C4-component of complement. Levels of C3-component of complement were positively correlated with duration of exposure. A significant elevation in the percentage and number of monocytes and a significantly decreased number of lymphocytes were seen in exposed workers. Styrene concentrations in both blood and exhaled air were associated with decreased percentage of large granular lymphocytes. CONCLUSIONS: These results suggest immune alterations of cell-mediated immune response of T-lymphocytes and imbalance in leucocyte subsets in peripheral blood of workers exposed to styrene.     

Cariporide counteracts atherosclerosis-related functions in monocytes from obese and normal individuals

OBJECTIVE: This study aimed to show the effect of high glucose concentrations in combination with a pharmaceutical analog of the Na+/H+ antiport inhibitor, cariporide, on scavenger receptor CD36 expression, cell adhesion, and cell migration of human monocytes derived from obese and normal individuals. RESEARCH METHODS AND PROCEDURES: Monocytes were isolated from six healthy obese individuals and six healthy age- and sex-matched controls by use of whole blood Percoll sedimentation and plastic surface monocyte binding. The density of CD36 scavenger receptors on the surface of monocytes was assessed by the use of a fluorescent fluorescein isothiocyanate (FITC)-linked monoclonal antibody. Transmigration of monocytes through laminin-1-coated filters was performed on 5-microm pore Transwell culture inserts. Monocyte attachment to laminin was estimated by a solid phase assay. RESULTS: High glucose concentrations caused an increase in monocytes from normal and obese individuals in the expression of CD36 receptors and positively influenced monocyte migration and adhesion to laminin. Cariporide together with glucose counteracted these effects. The effects of migration and adhesion of monocytes to laminin were specific to glucose, because the effect was significantly higher when monocytes were incubated in the presence of 20 mM of glucose than in the presence of 20 mM of fructose. Monocytes from obese subjects showed greater response than in normal to all of the studied effects, with the highest response in laminin attachment. DISCUSSION: The data of this study suggest that cariporide counteracts atherosclerosis-related functions through Na+/H+ antiport inhibition in monocytes from both normal and obese individuals.