Research Article Impact of Atmospheric Microparticles on ...

Research ArticleImpact of Atmospheric Microparticles on the Development ofOxidative Stress in Healthy CityIndustrial Seaport Residents

Kirill Golokhvast12 Tatyana Vitkina1 Tatyana Gvozdenko1 Victor Kolosov3

Vera Yankova1 Elena Kondratieva1 Anna Gorkavaya1 Anna Nazarenko1

Vladimir Chaika2 Tatyana Romanova4 Alexander Karabtsov4 Juliy Perelman3

Pavel Kiku2 and Aristidis Tsatsakis5

1Vladivostok Branch of the Far Eastern Center of Physiology and Pathology of Respiration Institute of Medical Climatology andRehabilitative Treatment 73g Russkaya Street Vladivostok 690105 Russia2Far Eastern Federal University 8 Sukhanova Street Vladivostok 690950 Russia3Far Eastern Center of Physiology and Pathology of Respiration 22 Kalinina Street Blagoveshchensk 675000 Russia4Far Eastern Geological Institute FEB RAS 159 Prospekt 100-letiya Vladivostok 690022 Russia5Department of Toxicology and Forensics Medical School University of Crete Heraklion 71300 Crete Greece

Correspondence should be addressed to Kirill Golokhvast droopymailru

Received 4 November 2014 Revised 7 April 2015 Accepted 8 April 2015

Academic Editor Vladimir Jakovljevic

Copyright copy 2015 Kirill Golokhvast et al This is an open access article distributed under the Creative Commons AttributionLicense which permits unrestricted use distribution and reproduction in any medium provided the original work is properlycited

Atmospheric microsized particles producing reactive oxygen species can pose a serious health risk for city residents We studiedthe responses of organisms to microparticles in 255 healthy volunteers living in areas with different levels of microparticle airpollution We analyzed the distribution of microparticles in snow samples by size and content ELISA and flow cytometry methodswere employed to determine the parameters of the thiol-disulfide metabolism peroxidation and antioxidant genotoxicity andenergy state of the leukocytes We found that in the park areas microparticles with a size of 800 120583m or more were predominant(96) while in the industrial areas they tended to be less than 50 120583m (93) including size 200ndash300 nm (7) In the industrialareas we determined the oxidative modification of proteins (21 compared to the park areas 119901 le 005) and DNA (12 119901 le 005)as well as changes in leukocytesrsquo energy potential (53 119901 le 005) An increase in total antioxidant activity (82 119901 le 001) andthiol-disulfide system response (thioredoxin increasing by 33 119901 le 001 glutathione 30 119901 le 001 with stable reductases levels)maintains a balance of peroxidation-antioxidant processes protecting cellular and subcellular structures from significant oxidativedamage

1 Introduction

The development of the research direction of city ecologywas caused by the global challenges which humanity is facingdue to the increasing industrial activity Furthermore theworld urban population continues to grow and so doesthe prevalence of environmental diseases City air is thefirst marker of total environmental pollution Atmosphericpollution in general is one of the leading factors relatedto health risks in cities [1ndash3] Of all atmospheric particlesmicrosized particles are the most dangerous [4] especiallythose smaller than 10 120583m Such particles slowly disappear

from the atmosphere and have a relatively long life in asuspended state They significantly accumulate in the envi-ronment even at a considerable distance from the sourcesof pollution Unlike gases microparticles are heterogeneouscomplex mixtures consisting of numerous components andtheir properties vary widely in terms of time and space [5]

It has been shown that long-term exposure to highlevels of particulate matter lt25 120583m in aerodynamic diameter(PM25) in the atmosphere reduces life expectancy among

the population from several months to a few years [6] Inaddition suspended particles absorb a large amount of toxicsubstances that can enter an organism [7]

Hindawi Publishing CorporationOxidative Medicine and Cellular LongevityVolume 2015 Article ID 412173 10 pageshttpdxdoiorg1011552015412173

2 Oxidative Medicine and Cellular Longevity

The impact of microsized particles on a living organismis fundamentally different from that of large-scale pollutants[4] One of themainmechanisms of toxic action bymicropar-ticles is linked with their ability to induce the productionof reactive oxygen species (ROS) Moderate levels of ROSmodulate cell signaling proliferation and gene expressionThe increase in ROS levels reduce the cellular antioxidantcapacity destroy the cell antioxidant defense system andlead to oxidative stress development [8] Oxidative stresscauses direct or indirect damage to key cell componentssuch as lipids proteins and nucleic acids and also inhibitsDNA repair [9] Cell competency in resisting pathogenicmicrosized xenobiotics mainly depends on the efficiency ofthe individual repair mechanisms

Redox systems are one of universal intracellular unitsmediating ROS regulatory functions They are presentedmainly by glutathione (GSH) and thioredoxin (TRX) [10]the most sensitive to oxidative stress systemsThey effectivelyrestore disulfide bonds in proteins through the activationof specific enzymatic systems For the glutathione systemthis is NADPH-dependent glutathione reductase and for theTRX system NADPH-dependent TRX-reductase (TrxR) Bymodulating the transcription factorsrsquo activity particularly inthe case of NF-120581B the TRX system plays a key role in the pro-tection of the cell components from the destructive effect ofvarious manifestations of oxidative stress [11] Different TRXsystem agents affect the activity of DNA repair endonucleaseaccording to shifts in the cell redox balance [12]

TRX and GSH systems participate in the regulation ofproinflammatory cytokines expression and apoptosis [1314] In addition to its function as a key regulator of theoxidative stress-associated redox processes thioredoxin playsan important role in protein folding the regulation ofnitrosative stress [15] cell growth and differentiation [1315 16] Interaction between glutathione and thioredoxinredox cell systems proceeds in particular through thioredoxinglutathionylation [17 18]

At the end of the last century (1979) suspended particleswere included within a number of polluting substances con-sideredwithin the ldquoConvention on long-range transboundaryair pollutionrdquo by the Economic Commission for Europe of theUnited Nations (UNECE) whose tasks include the qualitymanagement of atmospheric air as well as the regulationand control of emissions of polluting substances in theatmosphere in Europe

The impact of atmospheric microsized particles on theurban population under different environmental loads andthe assessment of the organismsrsquo response are importantresearch problems in this new century

Based on all the mentioned above the aim of the presentresearchwas to assess the contents and qualitative structure ofatmosphericmicroparticles and their role in the developmentof oxidative stress in healthy residents of the industrial city

2 Methods and Materials

21 Area and Particles Sample Collection Vladivostok thelargest city in the Far Eastern Federal District of Russia

and the largest Russian seaport on the Pacific Ocean islocated in the southern extremity of a peninsula that jutsfar out into the sea In Vladivostok there are relatively fewindustrial enterprises but the road traffic is quite intensiveThis determined our choice of it as an object for studyinga background of natural and anthropogenic atmosphericsuspensions in the city and its suburban area

Snow samples were collected during snowfall periodsfrom2010 to 2014 in 13 districts ofVladivostok [19]Theupperlayer (5ndash10 cm) of fresh snow from a 1m2 area was collectedinto 3 L sterile containers that had been prewashed withdouble-distilled water This collection method was chosen toavoid secondary contamination by anthropogenic aerosols

22 Particles Sample Analysis From each sample we took60mL of melted snow and analyzed it using a laser particlesizer analyzer Analysette 22 NanoTec (Fritsch Germany)During a single measurement set we determined the sizedistribution and shape of the particles

To obtain dry samples directly from the air we usedan LSV 31 sampler (Derenda Germany) with MGG filter(microglass fibre paper) with a diameter of 47mm (MunktellGermany) In work we used a reference device to collectparticulates from outdoor air in compliance with the CEN12341 (PM

10) standard We dried the filters prior to the

measurement in the thermostat at 40∘C and thenweighed thefilters on scales (Shimadzu AW-220 Japan) 10 times beforeand after the measurements

Substantial analysis was performed using a NikonSMZ1000 light microscope and a Hitachi S-3400N scanningelectron microscope with an Ultra Dry (Thermo ScientificUSA) energy-dispersive spectrometerThe sample depositionfor the electron microscopy was made with platinum

A high resolution inductively coupled plasma mass spec-troscopy (HR-ICP-MS) employing Element XR (ThermoFisher Scientific USA) was used to assess the Me in the col-lected snow PM samples The liquid part of the samples wasstored at 40∘C before evaporation and analyzed according totechnique CV 31805-2005 [20]

Our long-term observations (2010ndash2014) and laser parti-cle size electronmicroscopy andmass spectrometry analyses[19] allowed us to select 2 model points for this work from13 studied points the park area (the coast of Russky IslandVladivostok suburb) and the industrial area (the largesttransport hub in the city the continental part of Vladivostok)

Studies were conducted with use of the equipment of theInterdepartmental Center of Analytical Control of a State ofEnvironment of Far Eastern Federal University

23 Biomedical Study Subjects and Sample Collection Thestudy was approved by the Committee on Biomedical Ethicsand performed in 2012-2013 in Primorsky Krai (RussianFederation)

The study involved healthy residents of Vladivostok andRussky Island who had lived and worked for at least 5 yearswithin 1 km from model areas We surveyed 121 men and 134women with an age range from 28 to 54 years (mean age37 plusmn 6) All volunteers were fully informed about the goals

Oxidative Medicine and Cellular Longevity 3

Table 1 Characteristics of the population studied subjects

Subjects Group 1 Group 2119873 125 130Men 58 63Women 64 70Age (years) mean plusmn SD 35 plusmn 56 38 plusmn 61Smoking Never NeverProfessional hazard No No

Alcohol consumption frequency Rarelydrinking

Rarelydrinking

objectives and procedures of the study all of them signed aninformed consent form and passed the clinical and laboratoryexaminations The criteria for exclusion from the studywere occupational hazards smoking alcohol dependencepregnancy chronic disease (as stated in medical recordsor reported personally) acute illness andor current drugtreatment (Table 1)

The participants were divided into two groups compa-rable by age and sex and selected according to the place ofresidence Group 1 includes the inhabitants of the park areaRussky Island (one of the administrative districts of Vladivos-tok) and Group 2 the industrial area the inhabitants of thecontinental area of the cityindustrial seaport (Vladivostok)[19]

Venous blood samples (9mL) were collected in theearly morning following overnight fasting in vacuum EDTAtubes (Vacutainer) For enzyme-linked immunosorbent assay(ELISA) analyses we centrifuged the tubes for 10 minutes on1200 g and collected plasma Plasma samples were stored atminus80∘C until analysis Flow cytometry analysis was performedimmediately

24 Biomedical Sample Analysis Plasma samples were ana-lyzed using ELISA and the colorimetric method For themeasurement we used the reagents in Table 2

Measurement of MMPL was done via the BD FAC-SCANTO II (BD Biosciences USA) flow cytometer

25 Statistical Analysis Statistica 100 (Statsoft) software wasused for the statistical analysis All data were presented as themean plusmn standard error of the mean The differences betweenthe groups were analyzed using the Mann-Whitney testThe correlation was analyzed using the Pearson correlationmethod

3 Results

31 Atmospheric Suspensions in Different Areas of VladivostokOur long-term observations [19] made it possible to select abackground for the conversion of certain city areas to the parkor industrial area in relation to microparticles air pollution(Table 3)

We measured a mass fraction of suspensions (PM10)

using sampler (Comde-Derenda Germany) which equaledon average 006ndash009mgm3 for park area and 012ndash023mgm3 for industrial area

Figure 1 Soot and ashes particles from the industrial area of Vlad-ivostok Measure line 40120583m

311 Atmospheric Suspensions in the Park Area We consid-ered Russky Island as a model park point Russky Islandan administrative district of Vladivostok is environmentallya park area there are no large enterprises or heavy roadtrafficThemain influence on the composition of atmosphericsuspension is caused by the sea coast (halite silicates) andforest (organic detritus pollen)

Natural coarsely dispersed dust prevails in samples fromRussky Island with a particle size of hundreds 120583m whichcannot be inhalated Such large natural particles do notpenetrate into the lungs but are deposited in the upperrespiratory tract and nasal cavity due to natural protectiveprocesses and thereby do not have significant negative effectson the functional state of organisms [4]

Scanning electron microscopy detected that in the sam-ples from Russky Island the atmospheric particles containedmainly halite and aluminosilicates Mass spectrometry ofsnow samples showed normal heavy metal levels

312 Atmospheric Suspensions in the Industrial Area Weconsidered the area of the largest transport hub as themodel industrial area in the continental part of VladivostokEmissions of most of the industrial enterprises are producedat a height of up to 50m Besides industrial emissionsVladivostokrsquos air is polluted by smoke ash frommedium andlarge boilers and combustion plants Dust pollution exceedsthe maximum permissible concentration on average in a fewcases for example the maximum values of the air pollutionvary from 15mgm3 in summer up to 34mgm3 in spring[21] Dust prevailing in samples from industrial area has aparticle size from 01 to tens 120583mMotor vehicle exhaust fumescontribute up to 51 of the air pollution in Vladivostok [21]

Data from the electron microscopic analysis show thatin the samples from the industrial area technogenic parti-cles originating from vehicles prevail soot ashes (Figure 1)metal-containing particles (Fe Cr Ni Pb and Zn) rubberand asphalt

In addition to large particles (Figure 1) we observed alarge amount of microparticles with potentially hazardoussize 200ndash300 nm (7) that were not identified in samplesfrom the park area These particles are mainly composed ofmetal and soot


Table 2 Analyzed blood parameters and used reagents

Parameter Functions Reagent

Thioredoxin 1 (TRX 1)

Thioredoxin acts as antioxidant by facilitating the reduction ofother proteins by cysteine thiol-disulfide exchange and alsoserves as electron donor for enzymes such as ribonucleotidereductases thioredoxin peroxidases (peroxiredoxins) andmethionine sulfoxide reductases It is critical for redoxregulation of protein function and signaling via thiol redoxcontrol

Thioredoxin-1 ELISA (NorthwestLife Science Specialties LLCUSA)

Thioredoxin reductase 1 (TrxR1)

Thioredoxin reductases are the only enzymes known to catalyzethe reduction of thioredoxin

Thioredoxin Reductase 1 ELISA(Northwest Life ScienceSpecialties LLC USA)

Malondialdehyde (MDA)Malondialdehyde is a product of lipid peroxidation andprostaglandin biosynthesis It reacts with DNA to form adductsto deoxyguanosine and deoxyadenosine

Malondialdehyde Assay(Northwest Life ScienceSpecialties LLC USA)

8-Hydroxy-21015840-deoxyguanosine(8-OHdG)

8-OHdG is one of the most sensitive biomarkers for oxidativestress It is formed when DNA is oxidatively damaged by ROS

8-OHdG ELISA (Northwest LifeScience Specialties LLC USA)

Protein carbonyl (PC)Protein CO groups are biomarkers of oxidative stress They areforming relatively early and have relative stability in comparisonwith other oxidation products

Protein Carbonyl ELISA (BioCellCorporation Ltd New Zealand)

Antioxidant activity (AOA)Antioxidant activity or total antioxidant status is an assessmentof the integrated antioxidant system which encompasses allbiological components with antioxidant activity

Total antioxidant assay TotalAntioxidant Status Control(Randox Laboratories Ltd UK)

Glutathione (GSH)

Glutathione is the major endogenous antioxidant participatingdirectly in the neutralization of free radicals and reactive oxygencompounds as well as maintaining exogenous antioxidants suchas vitamins C and E

Glutathione ELISA Kit(MyBioSource Inc USA)

Glutathione reductase (GR)

Glutathione reductase catalyzes the reduction of glutathionedisulfide to the sulfhydryl form glutathione Their ration is a keyfactor in properly maintaining the oxidative balance of the cellReduced glutathione reduces the oxidized form of the enzymeglutathione peroxidase

Glutathione Reductase ELISAKit (MyBioSource Inc USA)

Glutathione peroxidase (GPx) Glutathione peroxidase reduces lipid hydroperoxides to theircorresponding alcohols and free hydrogen peroxide to water

Glutathione Peroxidase 1 ELISAKit (MyBioSource Inc USA)

Superoxide dismutase(CuZn-SOD)

Superoxide dismutase converts naturally occurring superoxideradicals to molecular oxygen and hydrogen peroxide

Human CuZnSOD ELISA(eBioscience USA)

Mitochondrial membranepotential in leukocytes (MMPL)

The evaluation of MMPL allows us to estimate cellular energystate

MitoProbe JC-1 Assay Kit (LifeTechnologies USA)

Table 3 Characteristics of areas by objects presented in their territory and their influence on atmospheric suspension composition

Typical park area Typical industrial area

Objects Influence on atmosphericsuspensions Objects Influence on atmospheric

suspensionsNo large industrial enterpriseswith large-tonnage wasteemissions into atmosphere

mdashLarge industrial enterprises withlarge-tonnage waste emissionsinto atmosphere

Sinters slags polymetallic particlesglass synthetic fibers soot andblack carbon

No heat-electric generatingstations mdash Heat-electric generating stations Coal sinters slags soot and black

carbon

No large road interchanges andhighways mdash Large road interchanges and

highways

Finely dispersed black carbon andsoot rubber and metal-containingparticles (Fe Cr Pb Zn Au Pt andIr)

No metalworking and galvaniccompanies mdash Metalworking and galvanic

companiesMetal-containing particles (Fe Crand Zn)

Large forest park zones Organic detritus mdash mdash

Riverside or sea coastHalite sylvinite silicatesaluminosilicates marineorganic detritus

mdash mdash

Coarsely dispersed particles are mostly presented Finely dispersed particles are mostly presented


(a)

2 4 6 8

(keV)

0

500

1000

1500

2000CO

Fe

Fe

FeMg

Na Al

Si

Cl K CaCr

Cr

klm-1-H

(b)

Figure 2 (a) Microphotograph of particles from the industrial area on sampler filter in reflected electronsThe light-colored threads are filterfibers Measure line 20120583m (b) Spectre of metal-containing particle (a large light particle on the left)

(a)

2 4 6 8

(keV)

0

0

500

1000

1500

2000

C

O

Na Al

Si

klm-1-H

(b)

Figure 3 (a) Microphotograph of particles from the park area on the sampler filter in the reflected electrons The light-colored threads arefilter fibers Measure line 20 120583m (b) Spectre of a metal-containing particle (a the large grey particle in the left)

Table 4 Parameters of prooxidant system and energy state of cells in healthy residents of the park and industrial areas in cityindustrialseaport

Parametersgroup MDA 120583molL MDAAOA PC nmolmg 8-OHdG ngmL MMPL Group 1(park area)119873 = 125 22 plusmn 003 081 plusmn 004 042 plusmn 003 712 plusmn 007 067 plusmn 003

Group 2(industrial area)119873 = 130 31 plusmn 022 105 plusmn 015 051 plusmn 002 798 plusmn 023 103 plusmn 005

Note statistically significant differences between groups at p le 005 MDA malondialdehyde AOA antioxidant activity PC protein carbonyl 8-OHdG 8-hydroxy-21015840-deoxyguanosine MMPL mitochondrial membrane potential in leukocytes

Table 5 Parameters of antioxidant system in healthy residents of the park and industrial areas in cityindustrial seaport

Parametersgroup TRX 1 ngmL TrxR 1 ngmL GSH 120583gmL GPx ngmL GR ngmL 00 mmolL CuZn-SOD ngmLGroup 1(park area)119873 = 125 687 plusmn 008 209 plusmn 001 4159 plusmn 176 082 plusmn 001 133 plusmn 013 21 plusmn 022 1327 plusmn 020

Group 2(industrial area)119873 = 130 912 plusmn 028 227 plusmn 002 5406 plusmn 281 054 plusmn 005 138 plusmn 031 382 plusmn 006 1533 plusmn 018

Note statistically significant differences between groups at p le 005 p le 001 TRX 1 thioredoxin 1 TrxR 1 thioredoxin reductase 1 GSH glutathione GPxglutathione peroxidase GR glutathione reductase AOA antioxidant activity CuZn-SOD superoxide dismutase (CuZn)

As can be seen in Figure 2(b) a typical polymetallicparticle is composed of Fe and Cr The particle is aggregatedand contains smaller needle-like components

As can be seen in Figure 3(b) a typical mineral particleis composed of Si and Al The particle is aggregated andcontains smaller ball-like components

The chemical composition of snow in Vladivostok ana-lyzed by mass spectrometry shows that the Cr content

increased in the industrial area (5826 plusmn 17 versus 035 plusmn 02in the park area 119901 le 0001)

32 Blood Parameters inHealthyResidents inDifferentAreas ofVladivostok The measured blood parameters are presentedin Tables 4 and 5

We found increased protein (21 compared to thepark area) and DNA (12) oxidative damage level and


Table 6 The interrelations of analyzed blood parameters

Parameters 8-OHdg TRX 1 PC TrxR 1 CuZn-SOD MDA AOA MDAAOA MMPL GPx

TRX 1 063p = 0004

PC 052p = 0027

TrxR 1 053p = 0022

minus058p = 0011

CuZn-SOD 072p = 0001

066p = 0002

AOA minus084p = 00001

MMPL minus055p = 002

GR 071p = 0001

minus062p = 0005

071p = 00001

GPx 054p = 0021

055p = 0017

051p = 0035

minus057p = 0002

GSH 053p = 0022

minus054p = 0022

minus054p = 0023

051p = 0006

minus055p = 0002

Note TRX 1 thioredoxin 1 TrxR 1 thioredoxin reductase 1 MDA malondialdehyde 8-OHdG 8-hydroxy-21015840-deoxyguanosine PC protein carbonylAOA antioxidant activity GSH glutathione GR glutathione reductase GPx glutathione peroxidase CuZn-SOD superoxide dismutase (CuZn) MMPLmitochondrial membrane potential in leukocytes

significantly increased (53) levels of leukocytes withreduced mitochondrial membrane potential in healthy res-idents of the industrial area of the cityindustrial seaportThe increasing MDA level (41) andMDAAOA ratio (29)indicate the activation of free radical peroxidation andshifting balance in the lipid peroxidation-antioxidant defense(LPO-AOD) system towards peroxidation

Theone of themainmechanisms of negative health effectscaused by atmospheric microparticles is linked with theirability to induce the production of ROS and the oxidativestress [22 23] Microparticles can penetrate more deeply intothe respiratory tract than larger particles [4 24] In additionmicroparticles can adsorb toxic substances including metals[7] The increase in the levels of prooxidant markers (MDA8-OHdG PC) in residents of an industrial area comparing topark areas (Table 4) is possibly linked to differences in thecontent of transition metals in particles (Figures 2 and 3)These metals enhance the generation of ROS promoting viaFenton or Haber-Weiss reaction [25] the formation of highlyreactive hydroxyl radicals that can react with almost all cellmolecules [26ndash28]

The intensification of peroxidation in healthy residentsof industrial area causes the reaction from AOD system Theincreasing total antioxidant activity (AOA on 82) makes itpossible to some extent restrain the oxidative modification ofmacromolecules and maintain the redox potential on a levelcorresponding to the intense organism response to industrialenvironment exposure CuZn-SOD synthesis is increasing(15) to maintain antioxidant defense inactivating freeradicals and reducing hydroperoxides formation whichleads to decreased GPx (20) The reduction potential of

the thiol-disulfide unit is due to the increasing Trx (33) andGSH (30) together with stable reductases levels (GR andTrxR 1)

The results of the correlation analysis between the ana-lyzed processes in healthy residents of the industrial area areshown in Table 6

The highest level of correlation (minus084 119901 = 00001Table 6) was found for AOA and MDA Negative directionof link reflects the restraining effect of AOD systems on theaccumulation of lipid peroxidation products at this stage ofinteraction Both MDA (minus054 119901 = 0022 071 119901 = 0001)and MDAAOA (minus054 119901 = 0023 071 119901 = 00001)have shown correlation with glutathione system parametersGSH provides the reduction of hydroperoxides in membranephospholipids via glutathione-S-transferases and GPx andthereby the activation of glutathione antioxidant systeminterrupts lipid peroxidation chain reaction [29 30]

The intensity of protein oxidative modifications is highlyaffected by the thioredoxine system (minus058 119901 = 0011) Thethioredoxin system prevents the formation of lipid perox-ides conjugating with amino acids in proteins In additionTRX restores the disulfide bonds in oxidized proteins Themajor role in maintaining the level of MMPL in exposureto microparticles belong to glutathione unit glutathioneperoxidase and glutathione (minus057 119901 = 0002 051 119901 =0006)

Oxidative DNA damage in healthy residents of industrialarea causes an active response from the thioredoxine system(063 119901 = 0004 053 119901 = 0022) and SOD (072 119901 = 0001)The thioredoxine unit provides DNA integrity protection bymaintaining the cell redox potential signaling to the other


AOD units and participating in DNA damage repair SODprovides the first line of defense against free radical damage tomacromolecules due to the inactivation of superoxide anionradicals

4 Discussion

Currently air pollution is one of the most dangerous envi-ronmental risks to public health According to World HealthOrganization air pollution causes 37 million deaths per yearinworld [31]Themicrosized particles are themost dangerousto health in industrial air pollution It has been shownthat the microparticles have proinflammatory carcinogenicteratogenic cytotoxic effects and cause allergy [19 21 32]

Atmospheric suspension in the park area consists ofnatural ingredients with which people and animals havecome into contact throughout their evolution particlesof minerals and rocks and organic components (pollendetritus insect fragments and aeroplankton) Technogenicsuspensions in the industrial area contain toxic componentsThemost dangerous technogenic particles are soot andmetalmicroparticles Particularly noteworthy are the solid particlesfromdiesel exhaust Soot from transport exhaust is a complexmulticomponent system containing not only soot but also alarge number ofmetals including toxicmetalsThe capabilityof soot particles to increase the risk of cancer and causepremature mortality due to respiratory complications andcardiovascular disease was shown previously [33] especiallyfor nanoscale particles [34 35] Recent researches on tox-icology show that the importance of indicating metals inatmospheric particles suspensions is due to fact that nano-and microparticles of metals and metal oxides have the mostevident toxicity [36] and can cause metal allergies [37 38]

In our study we determined that the chrome content washigher in snow samples from the industrial area than in thepark area Chrome is capable of causing significant changesin chromatids due to chronic exposure which indicates itsmutagenic and carcinogenic properties The mechanism ofchrome genotoxicity is linked with the inhibition of DNAsynthesis and the activation of DNA oxidative damage andapoptosis [39ndash41] Recent data indicate the involvement ofmismatch repair in DNA double-strand breaks Mutagenicadducts of ascorbate-chromium-DNA cause double-strandbreaks repair errors through nonhomologous end joining[42]

In addition to the direct effects microparticles cause theinduction of oxidative stress which activates various sig-naling pathways Oxidative stress may trigger inflammatoryresponses in the lungs circulatory system or even remotetissues [43] ROS as the inducers of oxidative stress disruptthe functioning of cells and damage their genome [44]The genotoxic changes affect the genetic expression and theregulation of the inflammation [45] The thioredoxin systemprotects cells from apoptosis and maintains the immune cellshomeostasis [46]

The parameters of the antioxidant defense system ana-lyzed in our study indicate the negative impact of microparti-cles on human health The observed dynamics of the studiedprocesses specify an early stage of ROS damage responseAt this stage oxidative damage affects the most sensitive

parameters the structural and functional state of proteinsand leukocyte predisposition to apoptotic changes ROSexcess and the increasing concentration of lipid peroxidationproducts in the blood contribute to the induction of proteinoxidative modification including irreversible carbonylation[30 47] DNA oxidative damage causes the disruption oftranscription and the possible synthesis of proteins withaltered physical and chemical properties that can change themetabolism and structuralfunctional cell status Disordersin catalytic capabilities and protein repair can lead to theactivation of apoptosis The further degradation of proteinscan cause necrotic lysis [30 48]

The character of the disorders related to exposure tofinely dispersed atmospheric particles indicates a shift inprooxidant-antioxidant balance A healthy organism undertolerable oxidative stress conditions can partially restrainits damage level [49] Specifically an organism through theactivation of natural adaptive reactions can increase the pro-duction of antioxidantmolecules thus blocking peroxidationand repairing oxidative stress-induced damage [49 50] Forexample in our previous studies we have also reportedthat although different kind of xenobiotics (eg anabolicsinsecticides and pesticides) induced oxidative stress theyalso increased antioxidant molecules (eg GSH and catalase)as a compensatory mechanism [51ndash53] The thioredoxinand glutathione systems selectively control the activity ofcertain proteins and signal transduction pathways and thethioredoxin system regulates a wider range of targets [54]However some proteins are double-regulated by thioredoxinand glutathione both by reduction of a disulfide bond viathioredoxinglutaredoxins and by glutathionylation of a cys-teine [55] The high activity of antioxidant systems in healthyresidents of the industrial area indicates the presence ofadaptive reserves ensuring to some extent the compensationof oxidative modifications

The glutathione unit mainly contributes to protectionGSH works as a hydroperoxides primary utilizer and SODsupports the static concentration of superoxide radicals at acertain level thus protecting the cell structures from damageby superoxide and hydroxyl radicals and creating conditionsfor the normalization of cell energy function and decreasein protein oxidative damage The AOD thioredoxine unit isactivated by increasing oxidative damage as amain reparativeand protective factor for DNA and proteins (thiol-disulfidereducing activity)

The processes of adaptation to oxidative stress are likelyto be associated with an increase in X

22-degrading activity

and its optimal allocation through antiperoxidant enzymesThis is carried out by activating the transcription factor NF-120581B [56] increasing antioxidant enzymes gene expression andlimiting protein and lipid peroxidation

5 Conclusions

The environmental situation in the studied areas of Vladivos-tok is characterized by different levels of coarsely and finelydispersed particles in the air and their varying compositionsthus causing different organism responses


The exposure to finely dispersed particles in atmo-spheric air causes the oxidative modification of proteins andDNA that contribute to changes in the energy potential ofleukocytes in healthy cityindustrial seaport residents Thepronounced response by the AOD thiol-disulfide systemsmaintains the balance of the peroxidation-antioxidation pro-cesses protecting cellular and subcellular structures fromsignificant oxidative damage at this stage on level corre-sponding to the intense organism response to industrialenvironment exposure However long-term stress-inducingexposure to microsized particles can lead to chronic changesin signal transduction and gene expression the depletion ofthe repair and adaptation capabilities of organisms and thedevelopment of pathologies

Conflict of Interests

The authors declare no conflict of interests

Authorsrsquo Contribution

Golokhvast Kirill and Tatyana Vitkina developed themethodological approaches to the research based on theanalysis of literary and experimental data Vera YankovaElena Kondratieva and Anna Nazarenko carried out thelaboratory research Vladimir V Chaika conducted researchon the samples via an electronic microscope Anna Gorkav-aya Pavel Kiku and Victor P Kolosov carried out a set ofclinical groups Golokhvast Kirill Tatyana Vitkina TatyanaGvozdenko Juliy Perelman and Aristidis Tsatsakis analyzedthe obtained data The mass-spectrometry was carried outby Tatyana Romanova and Alexander Karabtsov All authorstook part in the writing of the paper

Acknowledgments

This work was supported by the Scientific Fund of the FarEastern Federal University (no 13-06-0318-m a) Grant ofRussian Scientific Fund (no 14-25-00019) and the Min-istry of Education and Science of the Russian Federation(RFMEFI59414X0006)

References

[1] D L Crouse P A Peters A van Donkelaar et al ldquoRisk ofnonaccidental and cardiovascular mortality in relation to long-term exposure to low concentrations of fine particulate mattera canadian national-level cohort studyrdquo Environmental HealthPerspectives vol 120 no 5 pp 708ndash714 2012

[2] U Gehring O Gruzieva R M Agius et al ldquoAir pollutionexposure and lung function in children the ESCAPE projectrdquoEnvironmental Health Perspectives vol 121 no 11-12 pp 1357ndash1364 2013

[3] T I Vitkina L V Veremchuk and P F Kiku ldquoThe impact ofenvironmental factors on immunometabolic status of residentsof industrial centers of Primorsky Krairdquo Bjulletenrsquo Vostochno-Sibirskogo nauchnogo centra SO RAMN vol 2-3 no 91 pp 44ndash47 2013

[4] S S Lim T Vos A D Flaxman et al ldquoA comparative riskassessment of burden of disease and injury attributable to 67risk factors and risk factor clusters in 21 regions 1990ndash2010 asystematic analysis for the global burden of disease study 2010rdquoThe Lancet vol 380 no 9859 pp 2224ndash2260 2012

[5] A P Lisitsyn Processes of Oceanic Sedimentation Lithology andGeochemistry Special Publications Series American Geophys-ical Union Washington DC USA 1991

[6] R D Brook S Rajagopalan C A Pope et al ldquoParticulatematter air pollution and cardiovascular disease an update tothe scientific statement from the American Heart AssociationrdquoCirculation vol 121 no 21 pp 2331ndash2378 2010

[7] V P Ivanov S N Truhan D I Kochubei K P Kutsenogiyand V Makarov ldquoAnalysis of nature of adsorbed layers of atmo-spheric aerosolsrdquoHimija v Interesah Ustojchivogo Razvitija vol5 pp 449ndash452 2006

[8] R B Mikkelsen and P Wardman ldquoBiological chemistry ofreactive oxygen and nitrogen and radiation-induced signaltransduction mechanismsrdquo Oncogene vol 22 no 37 pp 5734ndash5754 2003

[9] J L Martindale and N J Holbrook ldquoCellular response tooxidative stress signaling for suicide and survivalrdquo Journal ofCellular Physiology vol 192 no 1 pp 1ndash15 2002

[10] V Y Kulikov ldquoRole of oxidative stress in metabolic regula-tion of activity of extracellular matrix in connective tis-sue (review)rdquo Medicina i Obrazovanie v Sibiri vol 4 2009httpngmurucozomosarticletext fullphpid=363

[11] A Holmgren and J Lu ldquoThioredoxin and thioredoxin reduc-tase current research with special reference to human diseaserdquoBiochemical andBiophysical ResearchCommunications vol 396no 1 pp 120ndash124 2010

[12] D F D Mahmood A Abderrazak K El Hadri T Simmet andM Rouis ldquoThe thioredoxin system as a therapeutic target inhuman health and diseaserdquo Antioxidants and Redox Signalingvol 19 no 11 pp 1266ndash1303 2013

[13] G Powis andW R Montfort ldquoProperties and biological activi-ties of thioredoxinsrdquoAnnual Review of Biophysics and Biomolec-ular Structure vol 30 pp 421ndash455 2001

[14] R B D Carilho Torrao I H K Dias S J Bennett C R Dun-ston andH R Griffiths ldquoHealthy ageing and depletion of intra-cellular glutathione influences T cell membrane thioredoxin-1levels and cytokine secretionrdquo Chemistry Central Journal vol 7no 1 article 150 2013

[15] C H Lillig and A Holmgren ldquoThioredoxin and relatedmoleculesmdashfrom biology to health and diseaserdquo Antioxidantsand Redox Signaling vol 9 no 1 pp 25ndash47 2007

[16] T-C Zschauer K Kunze S Jakob J Haendeler and JAltschmied ldquoOxidative stress-induced degradation of thiore-doxin-1 and apoptosis is inhibited by thioredoxin-1-actin inter-action in endothelial cellsrdquo Arteriosclerosis Thrombosis andVascular Biology vol 31 no 3 pp 650ndash656 2011

[17] I Dalle-Donne R Rossi D Giustarini R Colombo and AMilzani ldquoS-glutathionylation in protein redox regulationrdquo FreeRadical Biology and Medicine vol 43 no 6 pp 883ndash898 2007

[18] P K Mandal A Seiler T Perisic et al ldquoSystem 119909minus119888and thiore-

doxin reductase 1 cooperatively rescue glutathione deficiencyrdquoThe Journal of Biological Chemistry vol 285 no 29 pp 22244ndash22253 2010

[19] K S Golokhvast Atmospheric Suspensions in Cities of Far EastFEFU Publishing Vladivostok Russia 2013

[20] JSC ldquoWater Research and Control Centerrdquo httpaqua-analytcom


[21] K S Golokhvast N K Khristoforova P F Kiku and A NGulkov ldquoGranulometric and mineralogical analysis of particlessuspended in atmospheric airrdquo Bulleten Fiziologii i PatologiiDyhanija vol 2 no 40 pp 94ndash100 2011

[22] K Donaldson ldquoThe biological effects of coarse and fine particu-late matterrdquo Occupational and Environmental Medicine vol 60no 5 pp 313ndash314 2003

[23] V Lushchak and H M Semchyshyn Oxidative StressmdashMolecular Mechanisms and Biological Effects InTech 2012

[24] M J Nieuwenhuijsen Exposure Assessment in Occupationaland Environmental Epidemiology OxfordUniversity Press NewYork NY USA 2003

[25] V I Lushchak ldquoAdaptive response to oxidative stress Bacteriafungi plants and animalsrdquo Comparative Biochemistry and Phys-iology C Toxicology and Pharmacology vol 153 no 2 pp 175ndash190 2011

[26] N Ercal H Gurer-Orhan and N Aykin-Burns ldquoToxic metalsand oxidative stress part I mechanisms involved in metal-induced oxidative damagerdquo Current Topics in Medicinal Chem-istry vol 1 no 6 pp 529ndash539 2001

[27] K Jomova andM Valko ldquoAdvances in metal-induced oxidativestress and human diseaserdquo Toxicology vol 283 no 2-3 pp 65ndash87 2011

[28] M Valko H Morris andM T D Cronin ldquoMetals toxicity andoxidative stressrdquoCurrentMedicinal Chemistry vol 12 no 10 pp1161ndash1208 2005

[29] J D Hayes J U Flanagan and I R Jowsey ldquoGlutathione-transferasesrdquo Annual Review of Pharmacology and Toxicologyvol 45 pp 51ndash88 2005

[30] N K Zenkov E B Menschikova and V O Tkachev ldquoSomeprinciples and mechanisms of redox regulationrdquo Kislorod iantioksidanty vol 1 pp 3ndash64 2009

[31] World Health Organization ldquo7 million premature deaths annu-ally linked to air pollutionrdquo 2014 httpwwwwhointmedia-centrenewsreleases2014air-pollutionen

[32] J Njuguna K Pielichowski and H Zhu Health and Environ-mental Safety of Nanomaterials Elsevier 2014

[33] R Adams H Al-Bulushi K Berube and T Jones ldquoIntratra-cheal instillation of air pollution particles in rats is associatedwith prolonged systemic inflammation increased leukocyteintracellular F-actin and damage to the vascular endotheliumrdquoBiorheology vol 49 pp 14ndash206 2012

[34] F Amato M Pandolfi T Moreno et al ldquoSources and variabilityof inhalable road dust particles in three European citiesrdquoAtmospheric Environment vol 45 no 37 pp 6777ndash6787 2011

[35] A Mastrofrancesco M Alfe E Rosato et al ldquoProinflammatoryeffects of diesel exhaust nanoparticles on scleroderma skincellsrdquo Journal of Immunology Research vol 2014 Article ID138751 9 pages 2014

[36] K L Plathe F von der Kammer M Hassellov et al ldquoThe roleof nanominerals and mineral nanoparticles in the transport oftoxic trace metals field-flow fractionation and analytical TEManalyses after nanoparticle isolation and density separationrdquoGeochimica et Cosmochimica Acta vol 102 pp 213ndash225 2013

[37] M N Tikhonov and V N Tsygan ldquoMetalloallergens generaldescription and assessment of adverse effects on the health ofworkersrdquo Sovremennaja Medicina vol 2 pp 23ndash76 2004

[38] A Faurschou T Menne J D Johansen and J P ThyssenldquoMetal allergen of the 21st centurymdasha review on exposureepidemiology and clinical manifestations of palladium allergyrdquoContact Dermatitis vol 64 no 4 pp 185ndash195 2011

[39] Y P Gichev Human Health and Environment SOS YablokoMoscow Russia 2007

[40] I Dalle-Donne R Rossi R Colombo D Giustarini and AMilzani ldquoBiomarkers of oxidative damage in human diseaserdquoClinical Chemistry vol 52 no 4 pp 601ndash623 2006

[41] K Ogino andD-HWang ldquoBiomarkers of oxidativenitrosativestress an approach to disease preventionrdquo Acta MedicaOkayama vol 61 no 4 pp 181ndash189 2007

[42] IARC Monographs on the Evaluation of Carcinogenic Risksto Humans Overall Evaluations of Carcinogenicity vol 100International Agency for Research on Cancer WHO LyonFrance 2012

[43] HEI Review Panel on Ultrafine Particles Understanding theHealth Effects of Ambient Ultrafine Particles Health EffectsInstitute Boston Mass USA 2013

[44] M Kawanishi S Ogo M Ikemoto et al ldquoGenotoxicity andreactive oxygen species production induced by magnetitenanoparticles in mammalian cellsrdquo Journal of ToxicologicalSciences vol 38 no 3 pp 503ndash511 2013

[45] D Bayarsaihan ldquoEpigenetic mechanisms in inflammationrdquoJournal of Dental Research vol 90 no 1 pp 9ndash17 2011

[46] S-H Kim J Oh J-Y Choi J-Y Jang M-W Kang and C-E Lee ldquoIdentification of human thioredoxin as a novel IFN-gamma-induced factor mechanism of induction and its role incytokine productionrdquoBMC Immunology vol 9 article 64 2008

[47] E E Dubinina Products of Oxygen Metabolism in FunctionalActivity of Cells (Life and Death Creation and Destruction)Physiological and Clinical Biochemical Aspects MedicinskajaPressa Saint Petersburg Russia 2006

[48] Z-Y Shen W-Y Shen M-H Chen J Shen and Y ZengldquoReactive oxygen species and antioxidants in apoptosis ofesophageal cancer cells induced by As

2O3rdquo International Jour-

nal of Molecular Medicine vol 11 no 4 pp 479ndash484 2003[49] Y T Wu S B Wu and Y H Wei ldquoMetabolic reprogramming

of human cells in response to oxidative stress implications inthe pathophysiology and therapy of mitochondrial diseasesrdquoCurrent Pharmaceutical Design vol 20 no 35 pp 5510ndash55262014

[50] F Tchantchou M Graves D Ashline et al ldquoIncreased tran-scription and activity of glutathione synthase in response todeficiencies in folate vitamin E and apolipoprotein Erdquo Journalof Neuroscience Research vol 75 no 4 pp 508ndash515 2004

[51] I Germanakis K Tsarouhas P Fragkiadaki et al ldquoOxidativestress and myocardial dysfunction in young rabbits after shortterm anabolic steroids administrationrdquo Food and ChemicalToxicology vol 61 pp 101ndash105 2013

[52] C Tsitsimpikou M Tzatzarakis P Fragkiadaki et alldquoHistopathological lesions oxidative stress and genotoxiceffects in liver and kidneys following long term exposure ofrabbits to diazinon and propoxurrdquo Toxicology vol 307 pp109ndash114 2013

[53] A Zafiropoulos K Tsarouhas C Tsitsimpikou et al ldquoCar-diotoxicity in rabbits after a low-level exposure to diazinonpropoxur and chlorpyrifosrdquo Human amp Experimental Toxicol-ogy vol 33 no 12 pp 1241ndash1252 2014


[54] Y M Go J R Roede D I Walker et al ldquoSelective targetingof the cysteine proteome by thioredoxin and glutathione redoxsystemsrdquo Molecular and Cellular Proteomics vol 12 no 11 pp3285ndash3296 2013

[55] L Michelet M Zaffagnini V Massot et al ldquoThioredoxinsglutaredoxins and glutathionylation new crosstalks to explorerdquoPhotosynthesis Research vol 89 no 2-3 pp 225ndash245 2006

[56] T Hayashi Y Ueno and T Okamoto ldquoOxidoreductive regula-tion of nuclear factor 120581 B Involvement of a cellular reducingcatalyst thioredoxinrdquo The Journal of Biological Chemistry vol268 no 15 pp 11380ndash11388 1993

Submit your manuscripts athttpwwwhindawicom

Stem CellsInternational

Hindawi Publishing Corporationhttpwwwhindawicom Volume 2014


MEDIATORSINFLAMMATION

of


Behavioural Neurology

EndocrinologyInternational Journal of



Disease Markers


BioMed Research International

OncologyJournal of



Oxidative Medicine and Cellular Longevity


PPAR Research

The Scientific World JournalHindawi Publishing Corporation httpwwwhindawicom Volume 2014

Immunology ResearchHindawi Publishing Corporationhttpwwwhindawicom Volume 2014

Journal of

ObesityJournal of



Computational and Mathematical Methods in Medicine

OphthalmologyJournal of


Diabetes ResearchJournal of



Research and TreatmentAIDS


Gastroenterology Research and Practice


Parkinsonrsquos Disease

Evidence-Based Complementary and Alternative Medicine

Volume 2014Hindawi Publishing Corporationhttpwwwhindawicom


The impact of microsized particles on a living organismis fundamentally different from that of large-scale pollutants[4] One of themainmechanisms of toxic action bymicropar-ticles is linked with their ability to induce the productionof reactive oxygen species (ROS) Moderate levels of ROSmodulate cell signaling proliferation and gene expressionThe increase in ROS levels reduce the cellular antioxidantcapacity destroy the cell antioxidant defense system andlead to oxidative stress development [8] Oxidative stresscauses direct or indirect damage to key cell componentssuch as lipids proteins and nucleic acids and also inhibitsDNA repair [9] Cell competency in resisting pathogenicmicrosized xenobiotics mainly depends on the efficiency ofthe individual repair mechanisms

Redox systems are one of universal intracellular unitsmediating ROS regulatory functions They are presentedmainly by glutathione (GSH) and thioredoxin (TRX) [10]the most sensitive to oxidative stress systemsThey effectivelyrestore disulfide bonds in proteins through the activationof specific enzymatic systems For the glutathione systemthis is NADPH-dependent glutathione reductase and for theTRX system NADPH-dependent TRX-reductase (TrxR) Bymodulating the transcription factorsrsquo activity particularly inthe case of NF-120581B the TRX system plays a key role in the pro-tection of the cell components from the destructive effect ofvarious manifestations of oxidative stress [11] Different TRXsystem agents affect the activity of DNA repair endonucleaseaccording to shifts in the cell redox balance [12]

TRX and GSH systems participate in the regulation ofproinflammatory cytokines expression and apoptosis [1314] In addition to its function as a key regulator of theoxidative stress-associated redox processes thioredoxin playsan important role in protein folding the regulation ofnitrosative stress [15] cell growth and differentiation [1315 16] Interaction between glutathione and thioredoxinredox cell systems proceeds in particular through thioredoxinglutathionylation [17 18]

At the end of the last century (1979) suspended particleswere included within a number of polluting substances con-sideredwithin the ldquoConvention on long-range transboundaryair pollutionrdquo by the Economic Commission for Europe of theUnited Nations (UNECE) whose tasks include the qualitymanagement of atmospheric air as well as the regulationand control of emissions of polluting substances in theatmosphere in Europe

The impact of atmospheric microsized particles on theurban population under different environmental loads andthe assessment of the organismsrsquo response are importantresearch problems in this new century

Based on all the mentioned above the aim of the presentresearchwas to assess the contents and qualitative structure ofatmosphericmicroparticles and their role in the developmentof oxidative stress in healthy residents of the industrial city

2 Methods and Materials

21 Area and Particles Sample Collection Vladivostok thelargest city in the Far Eastern Federal District of Russia

and the largest Russian seaport on the Pacific Ocean islocated in the southern extremity of a peninsula that jutsfar out into the sea In Vladivostok there are relatively fewindustrial enterprises but the road traffic is quite intensiveThis determined our choice of it as an object for studyinga background of natural and anthropogenic atmosphericsuspensions in the city and its suburban area

Snow samples were collected during snowfall periodsfrom2010 to 2014 in 13 districts ofVladivostok [19]Theupperlayer (5ndash10 cm) of fresh snow from a 1m2 area was collectedinto 3 L sterile containers that had been prewashed withdouble-distilled water This collection method was chosen toavoid secondary contamination by anthropogenic aerosols

22 Particles Sample Analysis From each sample we took60mL of melted snow and analyzed it using a laser particlesizer analyzer Analysette 22 NanoTec (Fritsch Germany)During a single measurement set we determined the sizedistribution and shape of the particles

To obtain dry samples directly from the air we usedan LSV 31 sampler (Derenda Germany) with MGG filter(microglass fibre paper) with a diameter of 47mm (MunktellGermany) In work we used a reference device to collectparticulates from outdoor air in compliance with the CEN12341 (PM

10) standard We dried the filters prior to the

measurement in the thermostat at 40∘C and thenweighed thefilters on scales (Shimadzu AW-220 Japan) 10 times beforeand after the measurements

Substantial analysis was performed using a NikonSMZ1000 light microscope and a Hitachi S-3400N scanningelectron microscope with an Ultra Dry (Thermo ScientificUSA) energy-dispersive spectrometerThe sample depositionfor the electron microscopy was made with platinum

A high resolution inductively coupled plasma mass spec-troscopy (HR-ICP-MS) employing Element XR (ThermoFisher Scientific USA) was used to assess the Me in the col-lected snow PM samples The liquid part of the samples wasstored at 40∘C before evaporation and analyzed according totechnique CV 31805-2005 [20]

Our long-term observations (2010ndash2014) and laser parti-cle size electronmicroscopy andmass spectrometry analyses[19] allowed us to select 2 model points for this work from13 studied points the park area (the coast of Russky IslandVladivostok suburb) and the industrial area (the largesttransport hub in the city the continental part of Vladivostok)

Studies were conducted with use of the equipment of theInterdepartmental Center of Analytical Control of a State ofEnvironment of Far Eastern Federal University

23 Biomedical Study Subjects and Sample Collection Thestudy was approved by the Committee on Biomedical Ethicsand performed in 2012-2013 in Primorsky Krai (RussianFederation)

The study involved healthy residents of Vladivostok andRussky Island who had lived and worked for at least 5 yearswithin 1 km from model areas We surveyed 121 men and 134women with an age range from 28 to 54 years (mean age37 plusmn 6) All volunteers were fully informed about the goals





Rarelydrinking







3 Results





























Glutathione (GSH)





















carbon


highways






mdash mdash



(a)

2 4 6 8

(keV)

0

500

1000

1500

2000CO

Fe

Fe

FeMg

Na Al

Si

Cl K CaCr

Cr

klm-1-H

(b)


(a)

2 4 6 8

(keV)

0

0

500

1000

1500

2000

C

O

Na Al

Si

klm-1-H

(b)



















TRX 1 063p = 0004

PC 052p = 0027

TrxR 1 053p = 0022

minus058p = 0011


066p = 0002



GR 071p = 0001

minus062p = 0005

071p = 00001

GPx 054p = 0021

055p = 0017

051p = 0035

minus057p = 0002

GSH 053p = 0022

minus054p = 0022

minus054p = 0023

051p = 0006

minus055p = 0002












4 Discussion












5 Conclusions








Acknowledgments


References



































































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of




















Rarelydrinking







3 Results





























Glutathione (GSH)





















carbon


highways






mdash mdash



(a)

2 4 6 8

(keV)

0

500

1000

1500

2000CO

Fe

Fe

FeMg

Na Al

Si

Cl K CaCr

Cr

klm-1-H

(b)


(a)

2 4 6 8

(keV)

0

0

500

1000

1500

2000

C

O

Na Al

Si

klm-1-H

(b)



















TRX 1 063p = 0004

PC 052p = 0027

TrxR 1 053p = 0022

minus058p = 0011


066p = 0002



GR 071p = 0001

minus062p = 0005

071p = 00001

GPx 054p = 0021

055p = 0017

051p = 0035

minus057p = 0002

GSH 053p = 0022

minus054p = 0022

minus054p = 0023

051p = 0006

minus055p = 0002












4 Discussion












5 Conclusions








Acknowledgments


References



































































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of


































Glutathione (GSH)





















carbon


highways






mdash mdash



(a)

2 4 6 8

(keV)

0

500

1000

1500

2000CO

Fe

Fe

FeMg

Na Al

Si

Cl K CaCr

Cr

klm-1-H

(b)


(a)

2 4 6 8

(keV)

0

0

500

1000

1500

2000

C

O

Na Al

Si

klm-1-H

(b)



















TRX 1 063p = 0004

PC 052p = 0027

TrxR 1 053p = 0022

minus058p = 0011


066p = 0002



GR 071p = 0001

minus062p = 0005

071p = 00001

GPx 054p = 0021

055p = 0017

051p = 0035

minus057p = 0002

GSH 053p = 0022

minus054p = 0022

minus054p = 0023

051p = 0006

minus055p = 0002












4 Discussion












5 Conclusions








Acknowledgments


References



































































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of

















(a)

2 4 6 8

(keV)

0

500

1000

1500

2000CO

Fe

Fe

FeMg

Na Al

Si

Cl K CaCr

Cr

klm-1-H

(b)


(a)

2 4 6 8

(keV)

0

0

500

1000

1500

2000

C

O

Na Al

Si

klm-1-H

(b)



















TRX 1 063p = 0004

PC 052p = 0027

TrxR 1 053p = 0022

minus058p = 0011


066p = 0002



GR 071p = 0001

minus062p = 0005

071p = 00001

GPx 054p = 0021

055p = 0017

051p = 0035

minus057p = 0002

GSH 053p = 0022

minus054p = 0022

minus054p = 0023

051p = 0006

minus055p = 0002












4 Discussion












5 Conclusions








Acknowledgments


References



































































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of



















TRX 1 063p = 0004

PC 052p = 0027

TrxR 1 053p = 0022

minus058p = 0011


066p = 0002



GR 071p = 0001

minus062p = 0005

071p = 00001

GPx 054p = 0021

055p = 0017

051p = 0035

minus057p = 0002

GSH 053p = 0022

minus054p = 0022

minus054p = 0023

051p = 0006

minus055p = 0002












4 Discussion












5 Conclusions








Acknowledgments


References



































































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of


















4 Discussion












5 Conclusions








Acknowledgments


References



































































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of






















Acknowledgments


References



































































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of





























































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of
















Research Article Impact of Atmospheric Microparticles on ...

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