European Hot Spot of Air Pollution by PM2.5 and Bap: Ostrava, Czech Republic

Hindawi Publishing CorporationISRN Public HealthVolume 2013 Article ID 416701 12 pageshttpdxdoiorg1011552013416701

Research ArticleThe European Hot Spot of B[a]P and PM25 ExposuremdashTheOstrava Region Czech Republic Health Research Results

Radim J Sram1 Miroslav Dostal1 Helena Libalova1 Pavel Rossner Jr1

Andrea Rossnerova1 Vlasta Svecova1 Jan Topinka1 and Alena Bartonova2

1 Institute of Experimental Medicine AS CR Videnska 1083 142 20 Prague 4 Czech Republic2 NILUmdashNorwegian Institute for Air Research 2027 Kjeller Norway

Correspondence should be addressed to Radim J Sram srambiomedcascz

Received 9 March 2013 Accepted 2 April 2013

Academic Editors A R Mawson and A Zaborskis

Copyright copy 2013 Radim J Sram et al This is an open access article distributed under the Creative Commons Attribution Licensewhich permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited

TheOstrava Region in the Czech Republic is a heavily polluted industrial area Concentrations of PM10 PM25 and benzo[a]pyrene

(B[a]P) significantly exceed limit values To investigate the impact of these levels on human health epidemiological molecularepidemiology and in vitro studies were done in 2008ndash2011 Morbidity of children was followed in 10 pediatric districts In the mostpolluted district children suffered higher incidence of acute respiratory diseases in the first year of life and higher prevalence ofasthma bronchiale Gene expression was studied in children from Ostrava and from a control rural area Genes specific to asthmabronchiale differed suggesting a different molecular phenotype in children in the polluted region compared to children in thecontrol area A molecular epidemiology study showed adverse effect of the Ostrava exposures but also an increased expression ofXRCC5 which probably protects these exposed subjects against the degree of genetic damage that would otherwise be expectedIn vitro studies clearly related concentration of B[a]P from PM

25extracts to induced PAH-DNA adducts These studies clearly

demonstrate that under the present local environmental conditions the health of the population is severely impaired and will likelyremain so for a significant period of time

1 Introduction

The Moravian-Silesian Region (MSR) is a heavily popu-lated industrial area situated in the easternmost part of theCzech Republic (CR) covering 5 427 km2 with 125 millioninhabitants [1] The MSR is situated in a basin borderedby mountains from west east and partially from southwith frequent temperature inversions in winter Since the2nd half of the 18th century the region is characterizedby coal mining processing of coal and metallurgy TheMSR administrative structure consists of six districts (fromthe west Bruntal Opava Novy Jicın Ostrava city Karvinaand Frydek-Mıstek) The Karvina district is one of themost densely populated districts of the Czech Republic (789inhabitantskm2) The most important current industriesare metallurgy steel coke ovens coal mining and powergeneration The population density in the MSR is alsoassociated with high-intensity local vehicular transport andlocal heating Almost fifty percent of the inhabitants use

central heating 34 natural gas 10 coal 3 electricity and3 wood [2]

This paper provides an overview of air pollution levels inthe Ostrava Region (OSTR city of Ostrava and the districtof Karvina) for the period (2002ndash2011) and a summary offindings fromhealth effects studies and in vitro investigationsdone in the region in years 2008ndash2011 In addition we reviewrelevant results from earlier investigations and studies donein the bordering similarly polluted region in Poland

2 Air Pollution Situation in OSTR

Figure 1 shows the relative burden of PM10(particulatematter

with aerometric diameter lt 10 120583m) in OSTR compared tothe whole Czech Republic (CR) in 2011 For PM

10 the

concentrations were continuously above 40120583gm3 annualaverage in 2002ndash2011 (Figure 2) and considerably higherthan urban background in the largest city of CR PragueConcentrations higher than 50120583gm3 PM

10were recorded

2 ISRN Public Health

Classification of stationsUrban backgroundSuburban backgroundRuralTrafficIndustrial

Ostrava

Prague

leLAT(LAT UATgt

30 LVgt

gtLV

385235851340403

RegionsAgglomerations

Prachatice

Ustı n L

Concentration (120583gmiddotmminus3)le10le

gt10ndash14gt14ndash20gt20ndash30gt30ndash40gt40ndash45gt45

(UAT 20gt(20 30gt

Figure 1 Field of annual average concentrations of PM10in ambient

air in 2011 (source CHMI [3])

(120583g

m3)

70

60

50

40

30

20

10

0

Ostrava-RadvaniceBartoviceOstrava-PřiacuteozOstrava-Poruba

KarvinaacutePrague-Libuš

Limityear

2002 2003 2004 2005 2006 2007 2008 2009 2010 2011

Figure 2 Annual average concentrations of PM10in the ambient air

on selected monitoring stations in OSTR and Prague years 2002ndash2011 ([3])

during the year 2011 for 100 days at two stationarymonitoringstations in MSR Karvina and Ostrava-Radvanice

Similarly to PM10 population in this region is exposed

to high concentrations of PM25

(particulate matter withaerometric diameter lt 25 120583m) that are higher than thoseobserved on a background station in Prague (Figure 3) Inthe period 2004ndash2011 the limit of 25120583gm3yearwas exceededon all three PM

25stationary monitoring stations in OSTR

(Figure 4)Concentrations of benzo[a]pyrene (B[a]P) in OSTR are

the highest in all of the Czech Republic (Figure 5) Thehighest concentrations were detected in Ostrava-Radvanice


Ostrava

Prague

LAT(LAT UAT

142441391161


Prachatice

Ustı n L

Concentration (120583gmiddotmminus3)le12

gt12ndash17gt17ndash25gt25ndash30gt30 gt30)

(UAT TVgt

(TV 30)

Figure 3 Field of annual average concentrations of PM25

inambient air in 2011 (source CHMI [3])

Limityear

2006 2007 2008 2009 2010 2011

20

30

40

50

25

35

45

2002 2003 2004 200505

1015

Ostrava-RadvaniceBartovice Ostrava-Poruba

Ostrava-Přiacuteoz Prague-Libuš

(120583g

m3)

Figure 4 Annual average concentrations of PM25

in ambient air onselected monitoring stations in OSTR and Prague years 2002ndash2011[3]

(Figure 6) The limit of 1 ngm3year B[a]P was exceededon all OSTR monitoring stations in all years 2004ndash2011In the city of Karvina comparing period 2002ndash2005 with2009-2009 shows that B[a]P concentrations increased Itis surprising that comparing years 2010 and 2011 inOstrava-Radvanice andKarvina concentrations of both PM

10

and PM25

decreased while B[a]P increasedmdashin Ostrava-Radvanice by 40 in Karvina by 20

Other pollutants benzenemdashthe limit of 5120583gm3year iscontinually exceeded in Ostrava-Privoz nitrogen dioxide(NO2) concentrations were lower on all measuring points

in the period 2006ndash2011 than the limit of 40 120583gm3year

ISRN Public Health 3


Ostrava

Prague

(UAT 08

(TV 2

44512215

14622


Prachatice

leLAT(LAT UATgt

Ustı n L


gt04ndash06gt06ndash08gt08ndash1gt1-2gt2

(08 TVSgt

gt2

115

Figure 5 Field of annual average concentrations of B[a]P in ambientair in 2011 (source CHMI [3])

0

2

4

6

8

10

12

14

Limityear

2002 2003 2004 2005 2006 2007 2008 2009 2010 2011

Ostrava-RadvaniceOstrava-PřiacuteozOstrava-Poruba

KarvinaacutePrague-LibušŠrobaacuterovaacute

(ng

m3)

Figure 6 Annual average concentrations of B[a]P in ambient air onselected monitoring stations in OSTR and Prague years 2002ndash2011[3]

arsenic (As) determined in PM10was lower than the limit of

6 ngm3year on all monitoring stations in the period 2006ndash2011

Air pollution concentrations are available from the CzechHydrometeorological Institute website starting 1997 [3] Acomparison can be made between the highly polluted Ostr-ava-Radvanice and Ostrava-Poruba considered as a cleanpart of Ostrava In 1997ndash2007 only PM

10was monitored in

Ostrava-Radvanice Average concentrations of PM10were in

Ostrava-Radvanice 36 120583gm3 in Ostrava-Poruba 32 120583gm3 in1997ndash2000 in years 2001ndash2004 47 120583gm3 versus 40 120583gm3

and in years 2006-2007 65 120583gm3 versus 34 120583gm3 respec-tively PM

10concentrations increased by 80 in the period

2006-2007 compared to 1997ndash2000 in Ostrava-Radvanicebut not in Ostrava-Poruba It is likely that these differencesin concentrations of PM

10also corresponded to significantly

different exposures to PM25

and PAHs (polycyclic aromatichydrocarbons) Another specificity of Ostrava-Radvanice hasbeen high concentrations of B[a]P Considering general infor-mation about sources of PAH [4] this specific situation couldbe associated with the steelwork complex operating cokeovens located approximately 2 km from Ostrava-Radvanicewith prevailing winds goingmostly just to this part of the city[5]

3 Prior Evidence of Health Risks Related tothe Observed Pollution Levels

The pollution levels observed in OSTR give rise to severeconcerns regarding health risks Two main sources of infor-mation allow us to identify possible health risks prior tocarrying out own studies the WHO assessments and airquality guidelines that provide general guidance and researchthat documents possible human biological effects of airpollution in areas with similar source profiles

WHO [6] recommends to use concentrations of PM25

asan indicator of health risk The association between PM

25

(resulting from eg incomplete combustion inmobile aswellas stationary sources) and health effects such as increasedcardiovascular morbidity and mortality has already beenestablished

PM25

acts as a carrier of complex mixtures containingcarcinogenic PAHs (c-PAHs) These compounds formed byincomplete combustion of organic material as oil petrol gascoal and wood are adsorbed on the fine particulate fractionIt has been shown that health impact of PM

25is related

directly to content of reactive oxidative species (ROS) [7] andc-PAHs inducing oxidative damage and inflammation [8 9]

Using 32P-postlabeling and HPLC analysis of DNAadducts in in vitro acellular assay Binkova et al [10] observedthat in the extract from PM10 50 of total radioactivityfrom all DNA adducts corresponded to PAH-DNA adductsderived from c-PAHs Regarding health effects of air pollutedwith high concentrations of c-PAHs other effects than cancerwere observed only during the last twenty years molecularepidemiology studies indicate that air pollution with concen-trations higher than 1 ngm3 B[a]P affects genetic material(DNA) by increasing genomic frequency of translocations[11 12] micronuclei in peripheral lymphocytes [13] andDNA fragmentation in sperm [14] Elevated exposure toB[a]P has been associated with higher level of PAH-DNAadducts urinary 1-hydroxypyrene DNA strand breaks andDNA repair capacity [6] Increased concentrations of c-PAHswere associated with elevated risk of intrauterine growthretardation (IUGR) and low birth weight (LBW) during thefirst gestationalmonth of pregnancy (B[a]P gt 28 ngm3) [15]Figure 7 illustrates the impact of B[a]P levels in the year2011 in districts Ostrava-Radvanice and Ostrava-Poruba [3]Ambient PAHs and fine particles were associated with early-life susceptibility to bronchitis Associationswere stronger for


Monthly concentrations of benzo[a]pyrene (2011)

Impact on pregnancy outcome

RadvanicePoruba

75

28

Impact on DNA fragmentation in spermLimityear 1ngm3 (31122012)

0

5

10

15

20

25

30

35

40

(ng

m3)

Jan Feb Mar Apr May Jun Jul Aug Sept Oct Nov Dec

Figure 7 Monthly concentrations of B[a]P in 2011 in Ostrava-Radvanice and Ostrava-Poruba impact to pregnancy outcome andDNA fragmentation in sperm ([3 14 15])

longer pollutant-averaging periods and among children gt2years of age for PAHs compared to fine particles [16] Allthese data indicate that air pollution by B[a]P poses a verysignificant health risk in the Ostrava Region

It is surprising that there is no published informationabout the impacts of air pollution in OSTR except forLeonardi et al [17] They carried out a cross-sectional studyin four areas in Ostrava in school children aged 7ndash11 years in1996 In 1996 prevalence of pediatrician-diagnosed asthmain Ostrava-Radvanice was 30 asthma or asthmatic spas-tic or obstructive bronchitis 108 compared do Ostrava-Poruba with frequency 25 and 88 respectively Laterdata are available from the National Institute of Public Healthnationwide monitoring of allergic diseases in children aged5ndash17 years for 2006 Kratenova and Puklova [18] observeda prevalence of asthma 100 versus 79 in the OstravaRegion (119873 = 1189) versus other cities in the Czech Republicwith the highest prevalence of asthmatic children in Ostrava-Radvanice (308)

Signs of a possible impact of air pollution were observedby a pediatrician in Ostrava-Radvanice (pediatric districtwith approx 1 200 children) During the period 2001ndash2007the incidence of diagnosed asthma increased from 10 to30 in children aged up to 17 years from which 60 ofchildren were under the age of 35 years (Figure 8) We didnot find any authors that report similar high incidence ofasthma It may be a coincidence but PM

10increased from

392 120583gm3 to 654 120583gm3 in the period 2003ndash2007 Thesedata were obtained using ICD-10 (International StatisticalClassification of Diseases and Related Health Problems 10threvision) prior to the new recommendations in 2008 forboth diagnostics and treatment of asthma in children under

Asthmatic and allergic childrenOstrava-Radvanice 2001ndash2007

0

5

10

15

20

25

30

35

40

()

AsthmaticAllergic

2001 2003 2005 2007

Figure 8 Newly diagnosed asthma bronchiale and allergy cases inchildren in Ostrava-RadvaniceBartovice in years 2001ndash2007

five proposing to use the term wheezing instead of asthmabronchiale for such young children [19]

4 Program Ostrava

To elucidate situation in OSTR Program Ostrava wasdesigned to investigate the impact of air pollution on humanhealth in this region It was funded by the Ministry of theEnvironment and the Ministry of Education of the CzechRepublic [25] The aim was to evaluate if air pollutantsadsorbed on fine particles (c-PAHs carcinogenic polycyclicaromatic hydrocarbons) as well as VOC (volatile organiccompounds) affect human health and if new information canbe obtained using genomics methods

Program Ostrava consisted of 4 projects (1) morbidityin children (2) asthma bronchiale in children (3) molecularepidemiology study impact of air pollution on geneticdamage and (4) in vitro study mechanisms of toxic activitiesof chemicals adsorbed on respirable particulate matter

5 Morbidity in Children

In 10 pediatric districts in OSTR morbidity was followedin children born 2001ndash2004 up to 5 years of age (119873 =1888) The pediatricians abstracted medical records in ICD-10 codes Comparisons of detailed age-specific morbidity of1655 children born and living in the district of Ostrava-Radvanice (R and B) showed significantly higher incidenceof acute illnesses than in children in other parts of OstravaThey suffered higher incidence of acute respiratory diseasesin the first year of life (Figure 9) and higher prevalence ofasthma bronchiale (371119873 = 170) compared to other partsof Ostrava (102ndash132119873 = 1287) [26] Prenatal exposure toPAHs may be associated with altered lymphocyte immuno-phenotypic distribution in cord blood andpossible changes incord serum immunoglobulin E levels as proposed by Hertz-Picciotto et al [27] We can hypothesize that high concen-trations of PAHs affect maturation of the immune system


0 1st 2nd 3rd 4th 5th 6thYears of age

0

1

2

3

4

5

6

7

Inci

denc

ech

ild

M O (413)Hrab (595)Zabr (348)

Por (313)R and B (154)

Children respiratory morbidity(URI + bronchitis + laryngitis + pneumonia

+ tonsillitis + otitis media)

Figure 9 Morbidity of children in Ostrava 2001ndash2009 [26] (Ostr-ava districts MOmdashMoravian Ostrava HrabmdashHrabuvka ZabrmdashZabreh PormdashPoruba R and BmdashRadvanice and Bartovice)

Therefore children from amore polluted region suffer higherrespiratory morbidity especially during the first year of theirlife

6 Asthma Bronchiale in Children

In order to investigate specific effects on the origin and devel-opment of asthma bronchiale we have analyzed the impact ofair pollution inOSTR on gene expressionmicronuclei (MN)and oxidative damage in children Specifically we used geneexpression profiling technique to study changes in transcriptlevels in leukocytes of asthmatic children compared withthose in children without asthma in a group of 200 childrenliving in Ostrava-Radvanice (100 asthmatic and 100 healthychildren age 6ndash15 years) and in a control group of 200children living in Prachatice (rural district of SouthernBohemia) (100 asthmatic and 100 healthy children) [28]

Gene expression changes were analyzed in 368 bloodsamples using HumanHT-12 v3 BeadChips (Illumina) con-taining probes for more than 48K transcripts Samples werestatistically evaluated according to disease and locality(Ostrava-asthma Ostrava-control Prachatice-asthma andPrachatice-control) A comparison of both Ostrava groupsversus both Prachatice groups revealed 64 differentiallyexpressed genes (119875 value lt 001 fold change gt 15) corre-sponding to the effect of locality

Comparison of asthma groups with their correspond-ing controls within each locality (Ostrava-asthma versusOstrava-control and Prachatice-asthma versus Prachatice-control) showed 12 differentially expressed genes for OstravaRegion and 17 differentially expressed genes for Prachaticeregion Surprisingly deregulated genes specific to asthmain Ostrava and asthma in Prachatice completely differ no

transcript was observed simultaneously in both localities InOstrava MAPK (mitogen-activated protein kinases) signal-ing pathway (119875 lt 001 15-fold) and in Prachatice cytokine-cytokine receptor interaction pathway (119875 lt 001 15-fold)were affected (Figure 10)

In asthmatic children living in Ostrava the results showan increased gene expression related to the nonallergicimune response (DEFA4mdashrelationship to the presence ofneutrophils neutrophilic inflammation is associated withthe non-allergic type of asthma) and a response to hypoxia(AHSPmdashstabilization of haemoglobin 120572HBG2mdashpart of fetalhaemoglobin (subunits 2120572 and 2120574 higher affinity for oxy-gen))On the other hand in asthmatic children fromPrachat-ice we observed increased expression of SIGLEC8 trans-membrane protein involved in the apoptosis of eosinophilsRecently the association between sequence variants ofSIGLEC8 and total levels of serum IgE has been suggestedindicating the role of this gene in the susceptibility to asthma[29] Enhanced expression of other genes (CLC CCL23and CACNG6) having a relationship with the presence ofeosinophils has also been observed Eosinophilic inflamma-tion is related to allergic immune response and thus corre-sponds to the allergic phenotype of asthma These resultssuggest a different phenotype of asthma in children living inthe industrial Ostrava Region as compared to children livingin rural Prachatice

This study is unique because for the first time wholegenome chips were used to analyze the relationship betweenair pollution and asthma bronchiale Comparing expressionon profiles of children from both regions we observedderegulation of 64 genes which affect biological processesand metabolic pathways Rossnerova et al [30] studied DNAmethylation in the same childrenThey observed significantlydifferentmethylation pattern in 58CpG sites in children fromOstrava compared to children in PrachaticeThemethylationof all these 58CpG sites was lower in children from Ostravawhich indicates a higher gene expression in comparisonwith the control Prachatice region The patterns of methy-lation in asthmatic children differed similarly between bothregions

Studying gene expression and DNA methylation in chil-dren is a new approach that allows us to better understandthe effects of air pollution on human health and to evaluatethe significance of induced changes for morbidity of childrenas well as morbidity in adulthood [31]

To investigate if asthma bronchiale is related to biomark-ers of genetic damage a subset of the same Ostrava cohort(119873 = 175) was followed in November 2008 when the meandaily concentration of B[a]P measured by stationary moni-toring was 114 plusmn 98 ngm3 (samples taken every 6 days)The frequency of micronuclei (MN) in binucleated cellsmeasured by automated image analysis as well as markersof oxidative damage to DNA lipids and proteins was notassociated with asthma Higher levels of MN were associ-ated with increased levels of protein carbonyl groups Thefrequency of MN does not differ between asthmatic andcontrol children A hypothesis that asthmatic children maybe more affected by exposure to B[a]P was not confirmed[32]


Genesspecific

to asthmain Ostrava

No asthmaversus asthma

Ostrava


Ostrava

No genescommonfor bothregions



8981

304

73 13

255

1

10

00

0

12

16

No asthmaversus asthmacontrol region


Genesspecific

to asthmain Prachatice

119875 value le001119875 value le001Fold change ge15

Figure 10 Comparison of ldquono asthmardquo versus ldquoasthmardquo t-test results (In the Venn diagrams shown the t-test results obtained using allexperiments either with a 119875 value cutoff of 001 or a 119875 value cutoff of 001 and at least a 15-fold change are compared)

Table 1 DNA adducts in subjects from Prague and Ostrava Region in winters 2009 and 2010 [20] (data for controls are unexposed subjectsfrom [21])

DNA adductsDNA adducts108 nucleotides

119873 B[a]P (ngm3) B[a]Pmdashldquolikerdquo Total2009 2010 2009 2010 2009 2010

Prague 64 080 plusmn 055 286 plusmn 187 021 plusmn 006 025 plusmn 012 130 plusmn 041 137 plusmn 047Ostrava 98 273 plusmn 260lowast 148 plusmn 133lowast 028 plusmn 008lowast 016 plusmn 006lowast 137 plusmn 037 103 plusmn 033lowast

Controls 42 080 plusmn 062 010 plusmn 003 076 plusmn 020lowast119875 lt 005

7 Molecular Epidemiology Studies

We investigated the impact of high level of environmentalair pollution on selected biomarkers Exposure wasmeasuredas follows PM

25by stationary monitoring c-PAHs (B[a]P)

and VOC (benzene) by personal and stationary monitoringPersonal exposure to c-PAHs was defined using outdoorconcentration ETS exposure indicator of home heating bycoal wood or gas frequency of exhaust fan use cookinghabits and commuting by a car [23]

Cotinine in plasma triglycerides total HDL and LDLcholesterols and vitamins A C E were used as lifestyleindicators The following parameters were analyzed DNAadducts by 32P-postlabeling as biomarkers of effect chro-mosomal aberrations by FISH (fluorescent in situ hybridiza-tion) MN as biomarkers of effect 8-oxo-78-dihydro-21015840-deoxyguanosine (8-oxodG) as a marker of oxidative DNAdamage 15-F2t-isoprostane (15-F2t-IsoP) as a marker oflipid peroxidation protein carbonyls as a marker of proteinoxidation and genetic polymorphisms as biomarkers ofsusceptibility Sampling was done in winter 2009 summer2009 and winter 2010 Volunteers were recruited from officeworkers in Ostrava city city policemen from Havirov andKarvina (119873 = 98) and in 2010 also from general populationof Ostrava-Radvanice (119873 = 28) City policemen from Prague(119873 = 65) served as a control group

During all sampling periods the study subjects fromOSTR were exposed to significantly higher concentrationsof B[a]P and benzene than subjects in Prague as measuredby personal monitoring Taken separately B[a]P levels werelowest in Prague in 2009 Prague winter 2010 concentrationswere about equal to the lower Ostrava 2009 levels and levelsin Ostrava in winter 2010 were 5-fold higher Despite higherB[a]P air pollution in OSTR during all sampling periods thelevels of B[a]P-like DNA adducts per 108 nucleotides weresignificantly higher in the Ostrava subjects only in winter2009 (mean plusmn SD 021 plusmn 006 versus 028 plusmn 008 adducts108nucleotides 119875 lt 0001 for Prague and Ostrava subjectsrespectively) (Table 1 data for controls are unexposed sub-jects from [21]) During the other two sampling periods thelevels of B[a]P-like DNA adducts were significantly higherin the Prague subjects (119875 lt 0001) Multivariate analysesdone separately for subjects from Ostrava and from Praguecombining all sampling periods in each location revealedthat exposure to B[a]P and PM

25significantly increased

levels of B[a]P-like DNA adducts only in the Ostrava subjects[20]

Despite severalfold higher concentrations of air pollu-tants in the Ostrava Region the levels of stable aberrations(genomic frequency of translocations per 100 cells (119865G100)percentage of aberrant cells ( ABC) were comparable


Table 2 Chromosomal aberrations in peripheral lymphocytes by FISH in subjects from Prague and OSTR in winters 2009 and 2010 [22](data for controls are unexposed subjects from [12] ABC percentage of aberrant cells 119865G100 genomic frequency of translocations100cells)

Genomic frequency of translocations (FISH)

119873B[a]P (ngm3) ABC 119865G100

2009 2010 2009 2010 2009 2010Prague 60 080 plusmn 055 286 plusmn 187 027 plusmn 018 025 plusmn 015 143 plusmn 115 139 plusmn 103Ostrava 98 273 plusmn 260 148 plusmn 133lowast 026 plusmn 019 022 plusmn 018 144 plusmn 123 125 plusmn 118Controls 42 080 plusmn 062 021 plusmn 016 113 plusmn 101lowast119875 lt 005

Table 3 Lipid peroxidation in subjects from Prague and OstravaRegion in winters 2009 and 2010 [22]

Oxidative stress 15-F2t-isoprostane (pgmL)

119873B[a]P (ngm3) 15-2Ft-lsoP

2009 2010 2009 2010Prague 60 080 plusmn 055 286 plusmn 187 1659 plusmn 417 2565 plusmn 1047lowast

Ostrava 98 273 plusmn 260lowast 148 plusmn 136lowast 2793 plusmn 3036lowast 2795 plusmn 1245lowast119875 lt 005

(Table 2 controls are unexposed subjects from [12]) Thefrequency of unstable aberrations measured as number ofmicronuclei was unexpectedly significantly lower in theOstrava Region subjects in both seasons of 2009 Urinaryexcretion of 8-oxodG did not differ between locations ineither season Lipid peroxidation measured as levels of 15-F2t-IsoP in blood plasmawas elevated in theOstrava subjectssampled in 2009 similarly increased in Prague samples in2010 (Table 3) Multivariate analyses conducted separatelyfor subjects from Prague and Ostrava showed a negativeassociation between the frequency of micronuclei and con-centrations of B[a]P and PM

25in both regions A positive

relationship was observed between lipid peroxidation and airpollution [22]

In contrast to the above results changes were observedin a group of 4 subjects from Prague who spent 3 weeksin Ostrava just in the period of inversion in winter 2010when the average daily concentration of B[a]P reported bystationary monitoring was 147 plusmn 133 ngm3 The frequencyofmicronuclei in peripheral lymphocytes in those individualsincreased approximately 50 (Table 4) [24] and similarincrease was observed for genomic frequency of transloca-tions

The relationship between exposure to B[a]P and the levelof DNA adducts and chromosomal aberrations in winter2010 in Ostrava inhabitants was surprising as the results didnot correspond with the expected dose-effect relationshipTherefore we put forward a hypothesis about a possibleadaptive response indicating that this outcome may beaffected by DNA repair

This hypothesis was tested by Rossner et al [33] who fur-ther investigated in 64 subjects from Prague and 75 subjectsfromOstrava the levels of oxidative stress markers (8-oxodG15-F2t-IsoP protein carbonyls) and cytogenetic parameters[119865G100 ABC and acentric fragments (ace)] and their

Table 4 The frequency of micronuclei in peripheral lymphocytesin subjects from Prague after 3-week stay in Ostrava in January 2010[24]

Frequency of micronuclei

Groups Sampling 119873

(6000 cperson)

ABC with MN MN1000

Controls (i) 4 081 plusmn 015 832 plusmn 163(ii) 4 080 plusmn 014 847 plusmn 155

Exposed (i) 4 074 plusmn 043 796 plusmn 492(ii) 4 114 plusmn 055 1291 plusmn 649lowast

lowast119875 lt 005

relationship with the expression of genes participating inbase excision repair (BER) and nonhomologous end joining(NHEJ) by quantitative PCR Multivariate analyses revealedthat subjects living in Ostrava had increased odds of havingabove-median levels of XRCC5 expression (OR 95 CI 333103ndash108 q = 0046) Above-median levels of 8-oxodG wereassociated with decreased levels of vitamins C (OR 95CI 037 016ndash083 119875 = 0016) and E (OR 95 CI 025008ndash075 119875 = 0013) which were elevated in subjectsfrom Ostrava They suggest that air pollution by c-PAHsaffects XRCC5 expression which probably protect subjectsfrom Ostrava against the induction of a higher frequency oftranslocations elevated vitamin C and E levels in the Ostravasubjects decrease the levels of 8-oxodG Such changes in geneexpression were not observed in the 4 subjects from Pragueafter 3-week-stay in Ostrava their reaction differed fromsubjects with long residence time in OSTR

For the first time this study measures the levels ofbiomarkers in subjects exposed to air pollutants Simulta-neous assessment of oxidative stress markers chromosomalaberrations and measurement of DNA repair gene expres-sion is a new approach that can bring more clarity to themechanisms of pollution effects

8 In Vitro Studies

A wide variety of in vitro systems was developed in orderto study the genotoxicity of chemicals and their mixturesincluding complex mixtures of environmental pollutantsadsorbed onto respirable air particles (PM

25) Complex mix-

tures of organic compounds to which humans are exposedthrough air pollution are only partially characterized with


PM25Locality (m3)

Volume of air

29900

Karvinaacute 042009 47400 188 121Třeboň 11-122008 44700 114

na

111

816

Filter from Ostrava-Bartovice

Ostrava-RadvaniceOstrava-Poruba

Monthand year

of collection032009032009

B[a]P(120583gm3) (120583gm3)

367

258

c-PAH(ngm3)

35200

136

428 272

792

Figure 11 Characteristics of PM25

particles collected in winter 2008-2009 in Ostrava-RadvaniceBartovice Ostrava-Poruba Karvina andTrebon [38]

0 05 1 15 2 25

B[a]P (ngm3)

0

4

8

12

16

20

0

4

8

12

16

20

Addu

cts10

8nu

cleot

ides

m3

Addu

cts10

8nu

cleot

ides

m31198772 = 0779

DNA adduct versus B[a]P

1198772 = 0762

DNA adduct versus c-PAHs

2 4 6 8 10 12

c-PAHs (ngm3)

Figure 12The relationship between the PAH-DNA adducts versus concentrations of B[a]P and c-PAHs in extracts from PM25

from samplesfrom Ostrava-RadvaniceBartovice Ostrava-Poruba Karvina and Trebon [38]

respect to their chemical composition due to difficulties withchemical analysis of the individual components Thereforealternative assays based on biological effects of complexmixture components may be a suitable alternative to acircumstantial chemical analysis Using rat liver microsomalfraction (S9) it has been repeatedly shown that PAHs formedDNA adducts after metabolic activation by P450 enzymes todiol epoxides This activation system may be used in acel-lular assay coupled with 32P-postlabeling to assess genotoxicpotential of complex environmental mixtures via the analysisof DNA forming activity of the mixtures in native DNA [34ndash37]

PM25

particles were collected by high-volume samplersin MSR (localities Ostrava-RadvaniceBartovice Ostrava-Poruba andKarvina) and in the locality exhibiting a low levelof air pollutionmdashTrebonmdasha small town in the nonindustrialregion of Southern Bohemia (Figure 11) PM

25was extracted

(extractable organic mattermdashEOM) and c-PAHs contentsin the EOMs were determined DNA adduct levels and

oxidative DNA damage levels (8-oxodG) induced by EOMsin an acellular assay of calf thymus DNA coupled with 32P-postlabeling (DNA adducts) and ELISA (8-oxodG) in thepresence and absence of microsomal S9 fraction were usedas markers of genotoxic potential Twofold higher DNAadduct levels (172 adducts108 nucleotidesm3 versus 85adducts108 nucleotidesm3) were induced by EOM fromOstrava-Bartovice (immediate proximity to heavy industry)compared with that from Ostrava-Poruba (mostly trafficemissions) PAH-DNA adducts are highly correlated with thecontent of B[a]P and c-PAHs in EOM (Figure 12) OxidativeDNA damage induced by EOM from Ostrava-Bartovicewas more than fourfold higher than damage induced byEOM from Trebon (8-oxodG108 dGm3 0131 versus 0030for Ostrava-Bartovice versus Trebon respectively) c-PAHcontents in EOMs were the most important factors relatingto their genotoxic potential [38]

These results clearly demonstrated that EOM extractedfrom PM

25induces bulky DNA adducts as well as oxidative


777675747372716968676665

Life expectancy in MSR Prague CBand the Czech Republic-males

Age

(yea

rs)

MSR-pollutedMSR-cleanPrague

CB

Year

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008

Figure 13 Life expectancy in two sub-regions of MSR (ldquopollutedrdquoldquocleanrdquo) Prague Coal Basin compared to average life expectancy forthe Czech Republic (males)

DNA damage as measured by the levels of 8-oxodG Botheffects are enhanced by metabolic activation by microsomalcytochrome P-450 enzymes Since PM

25particles collected

in various localities differ in their c-PAHs content andc-PAHs significantly contribute to genotoxicity and DNAoxidative damage it may be suggested that monitoring ofPM25

levels is not a sufficient basis to assess genotoxicity ofrespirable aerosols This further indicates that the industrialemissions prevailing in Ostrava-Bartovice represent a sub-stantially higher genotoxic risk than traffic-related emissionsin Ostrava-Poruba B[a]P and c-PAH contents in EOMs arethe most important factors for their genotoxic and DNAoxidative potential

9 Regional Studies Outside Program OstravaAir Pollution and Mortality

Impact of air pollution on life expectancy was repeatedlyestablished in USA [39 40] as well as in the mining districtof Usti Region in the Czech Republic (coal basin CB) [41]A long-term study done in the period 1982ndash2008 shows asignificant increase of life expectancy in the Czech Republicstarting around 1990 when major measures were taken toreduce emissions from the districtrsquos most prominent sources(brown coal fired power plants) This increase was approx7 years for males and 6 years for females These trends aresimilar also in the CB but 2 years lower for each genderwhen we assess the whole period 1990ndash2008 In 1990 MSRlife expectancy of males living in MSR-polluted districts was1 year shorter to the national average in 2008 life expectancyof males was 2 years shorter for females it corresponded withthe trends in the Czech Republic (Figures 13 and 14) [42]

The association between daily cardiovascular and res-piratory mortality in men and women and increase of100 120583gm3 PM

10was studied in MSR Usti region (coal basin

8281807978777675747372

Life expectancy in MSR Prague CBand the Czech Republic-females

Age

(yea

rs)


CBYear

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008

Figure 14 Life expectancy in two sub-regions of MSR (ldquopollutedrdquoldquocleanrdquo) Prague Coal Basin compared to average life expectancy forthe Czech Republic (females)

CB) and Prague for the period 1997ndash2009 [43] The step of100 120583gm3 reflects the observed variability of daily concen-trations In men the daily total mortality increases (4 daysmean) significantly with association with 100120583gm3 PM

10by

83 in MSR 59 in CB and 79 in Prague This increasewas higher in men older than 65 years (132 in MSR84 in CB and 85 in Prague) The relationship betweendaily mortality and PM

10was stronger for cardiovascular

mortality (129 in MSR 90 in CB 97 in Prague) andeven more pronounced in men older than 65 years (184MSR 128 CB and 105 Prague) In women the results arequite different No increase of daily total and cardiovascularmortality associated with 100 120583gm3 increase of PM

10was

observed It may be proposed that other factors are moreimportant for example differences in exposure to otherpollutants in occupational ambient and home environmentsmoking habits diet education and economical status

10 Regional Studies Outside Program OstravaLong-Term Effect of Air Pollution

Dejmek et al [15] observed for the first time the effectof increasing concentrations of c-PAHs in polluted air onintrauterine growth retardation (IUGR) and low birth weight(LBW lt2500 g) Today this is interpreted as the effect ofpregnant mothers being exposed to c-PAHs that inducesDNA damage and histone modification [44] PAH-DNAadducts were detected in cord and maternal blood [45] andplacentas [46] due to exposure to c-PAHs from polluted airExposure to c-PAHs during pregnancy is associated withthe toxic effect to fetus inducing IUGR LBW [15 47] andpremature birth [47] When those children were followeduntil the school age it was observed that prenatal exposureto c-PAHs impaired neuropsychic development [48] andincreased the incidence of asthma bronchiale [44]


Choi et al [49] published results of a study on pregnantmothers from Cracow Poland which is a region borderingMSR and similar in its industrial status The air is pollutedby local heating and power plants using coal Personal expo-sure to B[a]P in the first trimester was during March-May211 ngm3 during December-February 721 ngm3 [50] (thisconcentration corresponds with environmental burden inOstrava-Poruba in 2011 [25])This study showed a significantnegative impact of c-PAHs on growth of fetus during the firsttrimester

Epidemiologic studies indicate that the growth of fetus isprogrammed already in the very early stages of pregnancyand that impairment in the first trimester results causes alarger deficit of growth during further gestation [51ndash53] Theconsequence of these changes in children with IUGR or LBWis a higher risk to delay neurodevelopment [54] affect lungfunctions [55] increase asthmatic symptoms in childhood[56] and increase of cardiovascular diseases [57] and diabetes[58] in adulthood

Study byChoi et al [49] confirms the data byDejmek et al[15] about the impact of increased c-PAHs concentrations inpolluted air on fetusrsquo unfavorable development and the long-term effect of such burden

It is already recognized that pregnancy outcome andDNAdamage are affected by the child genotype genetic poly-morphisms [59] This study indicates that increased ambientconcentration of c-PAHs may induce more significant DNAdamage in children with certain genotypes (alleles) whichis expressed as the decrease of birth weight Therefore wemay expect that the quality of genome under a differentenvironmental stress may affect also the child morbidity

Miller et al [60] observed adverse effect of prenatalexposure to c-PAHs on respiratory symptoms for childrenaged 12ndash24 months especially asthmatic symptoms alreadyat concentrations 353 plusmn 281 ng c-PAHsm3 Jedrychowski etal [61] observed the effect of perinatal exposure to c-PAHs inCracow to increase respiratory symptoms as cough wheez-ing and ear infections They explain this observation byimmunotoxic activity of PAHs which impairs fetal immunefunctions and is later responsible for increased susceptibilityof newborns and preschool children to respiratory infectionsThese data suggest the risk of exposure to c-PAHs in veryearly age Low birth weight associated with impaired lungfunctions may increase the risk of inflammatory respiratorysymptoms or hyperreactivity of respiratory airways

11 Conclusions

The specific pollution situation observed in the Moravian-Silesian Region (especially in OSTR) is a result of highpopulation density and activities of heavy industries Com-bined evidence indicates that health impact of air pollutionis associated specifically with high concentrations of c-PAHsConcentrations of B[a]P have been exceeding the annual limitvalue of 1 ngm3 in the whole study period in some localitiesseveralfold These levels of air pollution and especially ofB[a]P significantly increase respiratorymorbidity in childrenof preschool age asthma bronchiale in children and car-diovascular mortality These levels have shown associations

with long-term biological effects manifesting themselves indifferent forms and ages from effects observable in foetus todecrease in life expectancy in adults

The health and biological effect studies clearly demon-strate that under the present environmental conditions inthe MSR the health of the population is severely impairedand will likely remain so for a significant period of timeRecent studies imply that B[a]P [62] and air pollution [63ndash65] induce gametic mutations It means that induced DNAdamage in human gametes is transferred to next generations[66] According to Barker [57] changes induced during thefetal growth increase in adults the risk of cardiovasculardiseases and diabetes It may be therefore postulated that theeffect of present air pollution in MSR will affect the health ofpopulation for the next several decades

The results presented here provide evidence of an asso-ciation between industrial pollution and deteriorated healthand point strongly at an urgent need to mitigate the pollutionin the region Considering that in 2011 levels of B[a]Pexceeding European limit values affected approximately 60of all Czech population [67] the results presented here shouldgive rise to a national concern

Acknowledgments

Writing of this review was supported by Grant Agency ofthe Czech Republic (P30113013458S) and by CITI-SENSE aCollaborative Project partly funded by the EU FP7-ENV-2012(no 308524)

References

[1] Czech Statistical Office 2010 httpwwwczsoczengredakcensfihome

[2] Czech Environmental Information Agency State of the Envi-ronment in Different Regions of the Czech Republic in 2009CENIA 2011

[3] Czech Hydrometeorological Institute CHMI February 2013httpportalchmiczfilesportaldocsuocoiskotab roctabroc ENhtml

[4] Y Zhang and S Tao ldquoGlobal atmospheric emission inventoryof polycyclic aromatic hydrocarbons (PAHs) for 2004rdquo Atmo-spheric Environment vol 43 no 4 pp 812ndash819 2009

[5] P Hapala Analysis of the Air Quality on the Territory of City ofOstrava and the Legislation on Air Protection 2008-2009 HealthInstitute in Ostrava Ostrava Czech Republic 2012

[6] World Health Organisation WHO Guidelines for Indoor AirQuality Selected Pollutants WHO European Centre for Envi-ronment and Health Bonn Office WHO Regional Office forEurope 2010

[7] F Mazzoli-Rocha S Fernandes M Einicker-Lamas and W AZin ldquoRoles of oxidative stress in signaling and inflammationinduced by particulate matterrdquo Cell Biology and Toxicology vol26 no 5 pp 481ndash498 2010

[8] W Xue and D Warshawsky ldquoMetabolic activation of polycyclicand heterocyclic aromatic hydrocarbons and DNA damage areviewrdquo Toxicology and Applied Pharmacology vol 206 no 1pp 73ndash93 2005


[9] T M Penning S T Ohnishi T Ohnishi and R G Har-vey ldquoGeneration of reactive oxygen species during the enzy-matic oxidation of polycyclic aromatic hydrocarbon trans-dihydrodiols catalyzed by dihydrodiol dehydrogenaserdquo Chem-ical Research in Toxicology vol 9 no 1 pp 84ndash92 1996

[10] B Binkova D Vesely D Vesela R Jelınek and R J SramldquoGenotoxicity and embryotoxicity of urban air particulatematter collected during winter and summer period in twodifferent districts of the Czech Republicrdquo Mutation Researchvol 440 no 1 pp 45ndash58 1999

[11] R J Sram O Beskid A Rossnerova et al ldquoEnvironmentalexposure to carcinogenic polycyclic aromatic hydrocarbonsThe interpretation of cytogenetic analysis by FISHrdquo ToxicologyLetters vol 172 no 1-2 pp 12ndash20 2007

[12] R J Sram O Beskid B Binkova et al ldquoChromosomal aber-rations in environmentally exposed population in relation tometabolic and DNA repair genes polymorphismsrdquo MutationResearch vol 620 no 1-2 pp 22ndash33 2007

[13] A Rossnerova M Spatova P Rossner Jr I Solansky and R JSram ldquoThe impact of air pollution on the levels of micronucleimeasured by automated image analysisrdquoMutation Research vol669 no 1-2 pp 42ndash47 2009

[14] J Rubes R Rybar P Prinosilova et al ldquoGenetic polymorphismsinfluence the susceptibility of men to sperm DNA damageassociated with exposure to air pollutionrdquo Mutation Researchvol 683 no 1-2 pp 9ndash15 2010

[15] J Dejmek I Solansky I Benes J Lenıcek and R J Sram ldquoTheimpact of polycyclic aromatic hydrocarbons and fine particleson pregnancy outcomerdquo Environmental Health Perspectives vol108 no 12 pp 1159ndash1164 2000

[16] I Hertz-Picciotto R J Baker P S Yap et al ldquoEarly childhoodlower respiratory illness and air pollutionrdquo EnvironmentalHealth Perspectives vol 115 no 10 pp 1510ndash1518 2007

[17] G S Leonardi D Houthuijs B Nikiforov et al ldquoRespiratorysymptoms bronchitis and asthma in children of Central andEastern Europerdquo European Respiratory Journal vol 20 no 4pp 890ndash898 2002

[18] J Kratenova and V Puklova ldquoMonitoring of allergy diseasesin children in the Ostrava-Karvina region in 2006rdquo Alergiesupplement 2 pp 30ndash35 2011 (Czech)

[19] L B Bacharier A Boner K H Carlsen et al ldquoDiagnosis andtreatment of asthma in childhood a PRACTALL consensusreportrdquo Allergy vol 63 no 1 pp 5ndash34 2008

[20] P Rossner Jr V Svecova J Schmuczerova et al ldquoAnalysisof biomarkers in a Czech population exposed to heavy airpollutionmdashpart I bulkyDNAadductsrdquoMutagenesis vol 28 pp89ndash95 2013

[21] B Binkova I Chvatalova Z Lnenickova et al ldquoPAH-DNAadducts in environmentally exposed population in relation tometabolic and DNA repair gene polymorphismsrdquo MutationResearch vol 620 no 1-2 pp 49ndash61 2007

[22] P Rossner Jr A Rossnerova M Spatova et al ldquoAnalysis ofbiomarkers in a Czech population exposed to heavy air pollu-tionmdashpart II chromosomal aberrations and oxidative stressrdquoMutagenesis vol 28 pp 97ndash106 2013

[23] V Svecova J Topinka I Solansky P Rossner Jr and R JSram ldquoPersonal exposure to carcinogenic polycyclic aromatichydrocarbons in the Czech Republicrdquo Journal of ExposureScience amp Environmental Epidemiology 2013

[24] A Rossnerova M Spatova C Schunck and R J Sram ldquoAuto-mated scoring of lymphocyte micronuclei by the MetaSystems

Metafer image cytometry system and its application in studiesof human mutagen sensitivity and biodosimetry of genotoxinexposurerdquoMutagenesis vol 26 no 1 pp 169ndash175 2011

[25] R J Sram ldquoResults of air pollution studymdashnew knowledge2010rdquo Ochrana Ovzdusı vol 22 pp 3ndash7 2010 (Czech)

[26] M Dostal A Pastorkova S Rychlik V Svecova E Rychlikovaand R J Sram ldquoMorbidity of children in Ostrava 2001ndash2009rdquoOchrana Ovzdusı vol 23 pp 7ndash12 2011 (Czech)

[27] I Hertz-Picciotto H Y Park M Dostal A Kocan T Trnovecand R J Sram ldquoPrenatal exposures to persistent and non-persistent organic compounds and effects on immune systemdevelopmentrdquo Basic and Clinical Pharmacology and Toxicologyvol 102 no 2 pp 146ndash154 2008

[28] H LibalovaMDostal andR J Sram ldquoStudy of gene expressionin asthmatic children living in localities with different extent ofair pollutionrdquoOchrana Ovzdusı vol 23 pp 13ndash17 2011 (Czech)

[29] P S Gao K Shimizu A V Grant et al ldquoPolymorphisms inthe sialic acid-binding immunoglobulin-like lectin-8 (Siglec-8) gene are associated with susceptibility to asthmardquo EuropeanJournal of Human Genetics vol 18 no 6 pp 713ndash719 2010

[30] A Rossnerova E Tulupova N Tabashidze et al ldquoFactorsaffecting the 27K DNA methylation pattern in asthmatic andhealthy children from locations with various environmentsrdquoMutation Research vol 741-742 pp 18ndash26 2013

[31] R J Sram B Binkova M Dostal et al ldquoHealth impact ofair pollution to childrenrdquo International Journal of Hygiene andEnvironmental Health 2013

[32] A Rossnerova M Spatova P Rossner Jr Z Novakova ISolansky and R J Sram ldquoFactors affecting the frequency ofmicronuclei in asthmatic and healthy children from OstravardquoMutation Research vol 708 no 1-2 pp 44ndash49 2011

[33] P Rossner Jr K Uhlirova O Beskid A Rossnerova V Svecovaand R J Sram ldquoExpression of XRCC5 in peripheral bloodlymphocytes is upregulated in subjects from a heavily pollutedregion in the Czech Republicrdquo Mutation Research vol 713 no1-2 pp 76ndash82 2011

[34] S P Adams G M Laws R D Storer J G DeLuca and WW Nichols ldquoDetection of DNA damage induced by humancarcinogens in acellular assays potential application for deter-mining genotoxic mechanismsrdquo Mutation Research vol 368no 3-4 pp 235ndash248 1996

[35] M V Reddy G R Blackburn C A Schreiner and C R Mack-erer ldquoCorrelation of mutagenic potencies of various petroleumoils and oil coal tar mixtures with DNA adduct levels in vitrordquoMutation Research vol 378 no 1-2 pp 89ndash95 1997

[36] W A Smith J M Arif and R C Gupta ldquoEffect of cancerchemopreventive agents on microsome-mediated DNA adduc-tion of the breast carcinogen dibenzo[al]pyrenerdquo MutationResearch vol 412 no 3 pp 307ndash314 1998

[37] S K Pohjola M Lappi M Honkanen and K Savela ldquoCompar-ison of mutagenicity and calf thymus DNA adducts formed bythe particulate and semivolatile fractions of vehicle exhaustsrdquoEnvironmental andMolecularMutagenesis vol 42 no 1 pp 26ndash36 2003

[38] J Topinka P Rossner Jr A Milcova J Schmuczerova VSvecova and R J Sram ldquoDNA adducts and oxidative DNAdamage induced by organic extracts from PM

25in an acellular

assayrdquo Toxicology Letters vol 202 no 3 pp 186ndash192 2011[39] C A Pope III M Ezzati and D W Dockery ldquoFine-particulate

air pollution and life expectancy in the United StatesrdquoThe NewEngland Journal of Medicine vol 360 no 4 pp 376ndash386 2009


[40] A W Correia C A Pope III D W Dockery Y Wang MEzzati and F Dominici ldquoEffect of air pollution control on lifeexpectancy in theUnited States an analysis of 545US Countiesfor the period from 2000 to 2007rdquo Epidemiology vol 24 pp 23ndash31 2013

[41] F Kotesovec J Skorkovsky and J Brynda ldquoThe course of long-termmortality in the Czech Republic and in selected regions inthe period of 1982ndash2007rdquo Ochrana Ovzdusı vol 21 pp 23ndash262009 (Czech)

[42] J Skorkovsky F Kotesovec V Svecova J Brynda E Rychlikovaand R J Sram ldquoThe course of long-term mortality in twolocalities in Moravian-Silesian region with different levels of airpollutionrdquo Ochrana Ovzdusı vol 22 pp 28ndash34 2010 (Czech)

[43] J Skorkovsky E Rychlikova F Kotesovec andR J Sram ldquoDailymortality in three regions with different PM10 concentrationsin ambient airmdashCzech Republicrdquo Ochrana Ovzdusı vol 23 pp23ndash29 2011 (Czech)

[44] F Perera W Y Tang J Herbstman et al ldquoRelation of DNAmethylation of 51015840-CpG island of ACSL3 to transplacentalexposure to airborne polycyclic aromatic hydrocarbons andchildhood asthmardquo PLoS One vol 4 no 2 Article ID e44882009

[45] F Perera D Tang R Whyatt S A Lederman and W Jedry-chowski ldquoDNAdamage frompolycyclic aromatic hydrocarbonsmeasured by benzo[a]pyrene-DNA adducts in mothers andnewborns from Northern Manhattan the World Trade CenterArea Poland and Chinardquo Cancer Epidemiology Biomarkers andPrevention vol 14 no 3 pp 709ndash714 2005

[46] J Topinka B Binkova G Mrackova et al ldquoInfluence ofGSTM1 and NAT2 genotypes on placental DNA adducts inan environmentally exposed populationrdquo Environmental andMolecular Mutagenesis vol 30 no 2 pp 184ndash195 1997

[47] H Choi V Rauh R Garfinkel Y Tu and F P Perera ldquoPrenatalexposure to airborne polycyclic aromatic hydrocarbons andrisk of intrauterine growth restrictionrdquo Environmental HealthPerspectives vol 116 no 5 pp 658ndash665 2008

[48] F P Perera Z Li R Whyatt et al ldquoPrenatal airborne polycyclicaromatic hydrocarbon exposure and child IQ at age 5 yearsrdquoPediatrics vol 124 no 2 pp e195ndashe202 2009

[49] H Choi L Wang X Lin J D Spengler and F P PereraldquoFetal window of vulnerability to airborne polycyclic aromatichydrocarbons on proportional intrauterine growth restrictionrdquoPloS One vol 7 Article ID e35464 2012

[50] H Choi F Perera A Pac et al ldquoEstimating individual-level exposure to airborne polycyclic aromatic hydrocarbonsthroughout the gestational period based on personal indoorand outdoor monitoringrdquo Environmental Health Perspectivesvol 116 no 11 pp 1509ndash1518 2008

[51] G C S Smith ldquoFirst trimester origins of fetal growth impair-mentrdquo Seminars in Perinatology vol 28 no 1 pp 41ndash50 2004

[52] LNeufeldD L Pelletier and JDHaas ldquoThe timing hypothesisand body proportionality of the intra-uterine growth retardedinfantrdquo American Journal of Human Biology vol 11 no 5 pp638ndash646 1999

[53] S Milani A Bossi E Bertino et al ldquoDifferences in size at birthare determined by differences in growth velocity during earlyprenatal liferdquoPediatric Research vol 57 no 2 pp 205ndash210 2005

[54] A vanWassenaer ldquoNeurodevelopmental consequences of beingborn SGArdquo Pediatric Endocrinology Reviews vol 2 no 3 pp372ndash377 2005

[55] J Lipsett M Tamblyn K Madigan et al ldquoRestricted fetalgrowth and lung development a morphometric analysis of

pulmonary structurerdquo Pediatric Pulmonology vol 41 no 12 pp1138ndash1145 2006

[56] L Nepomnyaschy and N E Reichman ldquoLow birthweight andasthma among young urban childrenrdquo American Journal ofPublic Health vol 96 no 9 pp 1604ndash1610 2006

[57] D J P Barker ldquoAdult consequences of fetal growth restrictionrdquoClinical Obstetrics and Gynecology vol 49 no 2 pp 270ndash2832006

[58] M S Martin-Gronert and S E Ozanne ldquoExperimental IUGRand later diabetesrdquo Journal of Internal Medicine vol 261 no 5pp 437ndash452 2007

[59] R J Sram B Binkova J Dejmek I Chvatalova I Solansky andJ Topinka ldquoAssociation of DNA adducts and genotypes withbirth weightrdquo Mutation Research vol 608 no 2 pp 121ndash1282006

[60] R L Miller R Garfinkel M Horton et al ldquoPolycyclic aromatichydrocarbons environmental tobacco smoke and respiratorysymptoms in an inner-city birth cohortrdquo Chest vol 126 no 4pp 1071ndash1078 2004

[61] W Jedrychowski A Galas A Pac et al ldquoPrenatal ambientair exposure to polycyclic aromatic hydrocarbons and theoccurrence of respiratory symptoms over the first year of liferdquoEuropean Journal of Epidemiology vol 20 no 9 pp 775ndash7822005

[62] C L Yauk ldquoAdvances in the application of germline tandemrepeat instability for in situmonitoringrdquoMutation Research vol566 no 2 pp 169ndash182 2004

[63] C M Somers C L Yauk P A White C L J Parfett andJ S Quinn ldquoAir pollution induces heritable DNA mutationsrdquoProceedings of the National Academy of Sciences of the UnitedStates of America vol 99 no 25 pp 15904ndash15907 2002

[64] C M Somers and D N Cooper ldquoAir pollution and mutationsin the germline are humans at riskrdquoHuman Genetics vol 125no 2 pp 119ndash130 2009

[65] C M Somers ldquoAmbient air pollution exposure and damageto male gametes human studies and in situ lsquosentinelrsquo animalexperimentsrdquo Systems Biology in Reproductive Medicine vol 57no 1-2 pp 63ndash71 2011

[66] D M DeMarini ldquoDeclaring the existence of human germ-cellmutagensrdquo Environmental and Molecular Mutagenesis vol 53pp 166ndash172 2012

[67] J Ostatnicka and LMatouskova EdsAir Pollution in the CzechRepublic in 2011 Czech Hydrometeorological Institute PragueCzech Republic 2012

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



Ostrava

Prague

leLAT(LAT UATgt

30 LVgt

gtLV

385235851340403


Prachatice

Ustı n L

Concentration (120583gmiddotmminus3)le10le

gt10ndash14gt14ndash20gt20ndash30gt30ndash40gt40ndash45gt45

(UAT 20gt(20 30gt

Figure 1 Field of annual average concentrations of PM10in ambient

air in 2011 (source CHMI [3])

(120583g

m3)

70

60

50

40

30

20

10

0

Ostrava-RadvaniceBartoviceOstrava-PřiacuteozOstrava-Poruba

KarvinaacutePrague-Libuš

Limityear

2002 2003 2004 2005 2006 2007 2008 2009 2010 2011

Figure 2 Annual average concentrations of PM10in the ambient air

on selected monitoring stations in OSTR and Prague years 2002ndash2011 ([3])

during the year 2011 for 100 days at two stationarymonitoringstations in MSR Karvina and Ostrava-Radvanice

Similarly to PM10 population in this region is exposed

to high concentrations of PM25

(particulate matter withaerometric diameter lt 25 120583m) that are higher than thoseobserved on a background station in Prague (Figure 3) Inthe period 2004ndash2011 the limit of 25120583gm3yearwas exceededon all three PM

25stationary monitoring stations in OSTR

(Figure 4)Concentrations of benzo[a]pyrene (B[a]P) in OSTR are

the highest in all of the Czech Republic (Figure 5) Thehighest concentrations were detected in Ostrava-Radvanice


Ostrava

Prague

LAT(LAT UAT

142441391161


Prachatice

Ustı n L


gt12ndash17gt17ndash25gt25ndash30gt30 gt30)

(UAT TVgt

(TV 30)

Figure 3 Field of annual average concentrations of PM25

inambient air in 2011 (source CHMI [3])

Limityear

2006 2007 2008 2009 2010 2011

20

30

40

50

25

35

45

2002 2003 2004 200505

1015

Ostrava-RadvaniceBartovice Ostrava-Poruba

Ostrava-Přiacuteoz Prague-Libuš

(120583g

m3)

Figure 4 Annual average concentrations of PM25

in ambient air onselected monitoring stations in OSTR and Prague years 2002ndash2011[3]

(Figure 6) The limit of 1 ngm3year B[a]P was exceededon all OSTR monitoring stations in all years 2004ndash2011In the city of Karvina comparing period 2002ndash2005 with2009-2009 shows that B[a]P concentrations increased Itis surprising that comparing years 2010 and 2011 inOstrava-Radvanice andKarvina concentrations of both PM

10

and PM25

decreased while B[a]P increasedmdashin Ostrava-Radvanice by 40 in Karvina by 20

Other pollutants benzenemdashthe limit of 5120583gm3year iscontinually exceeded in Ostrava-Privoz nitrogen dioxide(NO2) concentrations were lower on all measuring points

in the period 2006ndash2011 than the limit of 40 120583gm3year



Ostrava

Prague

(UAT 08

(TV 2

44512215

14622


Prachatice

leLAT(LAT UATgt

Ustı n L



(08 TVSgt

gt2

115


0

2

4

6

8

10

12

14

Limityear

2002 2003 2004 2005 2006 2007 2008 2009 2010 2011



(ng

m3)





10was monitored in













25


PM25


25is related






RadvanicePoruba

75

28


0

5

10

15

20

25

30

35

40

(ng

m3)






10increased from



0

5

10

15

20

25

30

35

40

()

AsthmaticAllergic

2001 2003 2005 2007



4 Program Ostrava







0

1

2

3

4

5

6

7

Inci

denc

ech

ild

M O (413)Hrab (595)Zabr (348)

Por (313)R and B (154)















Genesspecific

to asthmain Ostrava


Ostrava


Ostrava




8981

304

73 13

255

1

10

00

0

12

16



Genesspecific





















119873B[a]P (ngm3) ABC 119865G100
















(6000 cperson)

ABC with MN MN1000



lowast119875 lt 005



8 In Vitro Studies


25) Complex mix-



PM25Locality (m3)

Volume of air

29900


na

111

816



Monthand year


B[a]P(120583gm3) (120583gm3)

367

258

c-PAH(ngm3)

35200

136

428 272

792



0 05 1 15 2 25

B[a]P (ngm3)

0

4

8

12

16

20

0

4

8

12

16

20

Addu

cts10

8nu

cleot

ides

m3

Addu

cts10

8nu

cleot

ides

m31198772 = 0779


1198772 = 0762


2 4 6 8 10 12

c-PAHs (ngm3)




PM25


25was extracted






777675747372716968676665


Age

(yea

rs)


CB

Year

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008










8281807978777675747372


Age

(yea

rs)


CBYear

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008



10by




10was










11 Conclusions





Acknowledgments


References









































25in an acellular






































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of


















Ostrava

Prague

(UAT 08

(TV 2

44512215

14622


Prachatice

leLAT(LAT UATgt

Ustı n L



(08 TVSgt

gt2

115


0

2

4

6

8

10

12

14

Limityear

2002 2003 2004 2005 2006 2007 2008 2009 2010 2011



(ng

m3)





10was monitored in













25


PM25


25is related






RadvanicePoruba

75

28


0

5

10

15

20

25

30

35

40

(ng

m3)






10increased from



0

5

10

15

20

25

30

35

40

()

AsthmaticAllergic

2001 2003 2005 2007



4 Program Ostrava







0

1

2

3

4

5

6

7

Inci

denc

ech

ild

M O (413)Hrab (595)Zabr (348)

Por (313)R and B (154)















Genesspecific

to asthmain Ostrava


Ostrava


Ostrava




8981

304

73 13

255

1

10

00

0

12

16



Genesspecific





















119873B[a]P (ngm3) ABC 119865G100
















(6000 cperson)

ABC with MN MN1000



lowast119875 lt 005



8 In Vitro Studies


25) Complex mix-



PM25Locality (m3)

Volume of air

29900


na

111

816



Monthand year


B[a]P(120583gm3) (120583gm3)

367

258

c-PAH(ngm3)

35200

136

428 272

792



0 05 1 15 2 25

B[a]P (ngm3)

0

4

8

12

16

20

0

4

8

12

16

20

Addu

cts10

8nu

cleot

ides

m3

Addu

cts10

8nu

cleot

ides

m31198772 = 0779


1198772 = 0762


2 4 6 8 10 12

c-PAHs (ngm3)




PM25


25was extracted






777675747372716968676665


Age

(yea

rs)


CB

Year

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008










8281807978777675747372


Age

(yea

rs)


CBYear

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008



10by




10was










11 Conclusions





Acknowledgments


References









































25in an acellular






































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of



















RadvanicePoruba

75

28


0

5

10

15

20

25

30

35

40

(ng

m3)






10increased from



0

5

10

15

20

25

30

35

40

()

AsthmaticAllergic

2001 2003 2005 2007



4 Program Ostrava







0

1

2

3

4

5

6

7

Inci

denc

ech

ild

M O (413)Hrab (595)Zabr (348)

Por (313)R and B (154)















Genesspecific

to asthmain Ostrava


Ostrava


Ostrava




8981

304

73 13

255

1

10

00

0

12

16



Genesspecific





















119873B[a]P (ngm3) ABC 119865G100
















(6000 cperson)

ABC with MN MN1000



lowast119875 lt 005



8 In Vitro Studies


25) Complex mix-



PM25Locality (m3)

Volume of air

29900


na

111

816



Monthand year


B[a]P(120583gm3) (120583gm3)

367

258

c-PAH(ngm3)

35200

136

428 272

792



0 05 1 15 2 25

B[a]P (ngm3)

0

4

8

12

16

20

0

4

8

12

16

20

Addu

cts10

8nu

cleot

ides

m3

Addu

cts10

8nu

cleot

ides

m31198772 = 0779


1198772 = 0762


2 4 6 8 10 12

c-PAHs (ngm3)




PM25


25was extracted






777675747372716968676665


Age

(yea

rs)


CB

Year

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008










8281807978777675747372


Age

(yea

rs)


CBYear

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008



10by




10was










11 Conclusions





Acknowledgments


References









































25in an acellular






































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of


















0

1

2

3

4

5

6

7

Inci

denc

ech

ild

M O (413)Hrab (595)Zabr (348)

Por (313)R and B (154)















Genesspecific

to asthmain Ostrava


Ostrava


Ostrava




8981

304

73 13

255

1

10

00

0

12

16



Genesspecific





















119873B[a]P (ngm3) ABC 119865G100
















(6000 cperson)

ABC with MN MN1000



lowast119875 lt 005



8 In Vitro Studies


25) Complex mix-



PM25Locality (m3)

Volume of air

29900


na

111

816



Monthand year


B[a]P(120583gm3) (120583gm3)

367

258

c-PAH(ngm3)

35200

136

428 272

792



0 05 1 15 2 25

B[a]P (ngm3)

0

4

8

12

16

20

0

4

8

12

16

20

Addu

cts10

8nu

cleot

ides

m3

Addu

cts10

8nu

cleot

ides

m31198772 = 0779


1198772 = 0762


2 4 6 8 10 12

c-PAHs (ngm3)




PM25


25was extracted






777675747372716968676665


Age

(yea

rs)


CB

Year

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008










8281807978777675747372


Age

(yea

rs)


CBYear

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008



10by




10was










11 Conclusions





Acknowledgments


References









































25in an acellular






































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of

















Genesspecific

to asthmain Ostrava


Ostrava


Ostrava




8981

304

73 13

255

1

10

00

0

12

16



Genesspecific





















119873B[a]P (ngm3) ABC 119865G100
















(6000 cperson)

ABC with MN MN1000



lowast119875 lt 005



8 In Vitro Studies


25) Complex mix-



PM25Locality (m3)

Volume of air

29900


na

111

816



Monthand year


B[a]P(120583gm3) (120583gm3)

367

258

c-PAH(ngm3)

35200

136

428 272

792



0 05 1 15 2 25

B[a]P (ngm3)

0

4

8

12

16

20

0

4

8

12

16

20

Addu

cts10

8nu

cleot

ides

m3

Addu

cts10

8nu

cleot

ides

m31198772 = 0779


1198772 = 0762


2 4 6 8 10 12

c-PAHs (ngm3)




PM25


25was extracted






777675747372716968676665


Age

(yea

rs)


CB

Year

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008










8281807978777675747372


Age

(yea

rs)


CBYear

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008



10by




10was










11 Conclusions





Acknowledgments


References









































25in an acellular






































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of



















119873B[a]P (ngm3) ABC 119865G100
















(6000 cperson)

ABC with MN MN1000



lowast119875 lt 005



8 In Vitro Studies


25) Complex mix-



PM25Locality (m3)

Volume of air

29900


na

111

816



Monthand year


B[a]P(120583gm3) (120583gm3)

367

258

c-PAH(ngm3)

35200

136

428 272

792



0 05 1 15 2 25

B[a]P (ngm3)

0

4

8

12

16

20

0

4

8

12

16

20

Addu

cts10

8nu

cleot

ides

m3

Addu

cts10

8nu

cleot

ides

m31198772 = 0779


1198772 = 0762


2 4 6 8 10 12

c-PAHs (ngm3)




PM25


25was extracted






777675747372716968676665


Age

(yea

rs)


CB

Year

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008










8281807978777675747372


Age

(yea

rs)


CBYear

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008



10by




10was










11 Conclusions





Acknowledgments


References









































25in an acellular






































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of

















PM25Locality (m3)

Volume of air

29900


na

111

816



Monthand year


B[a]P(120583gm3) (120583gm3)

367

258

c-PAH(ngm3)

35200

136

428 272

792



0 05 1 15 2 25

B[a]P (ngm3)

0

4

8

12

16

20

0

4

8

12

16

20

Addu

cts10

8nu

cleot

ides

m3

Addu

cts10

8nu

cleot

ides

m31198772 = 0779


1198772 = 0762


2 4 6 8 10 12

c-PAHs (ngm3)




PM25


25was extracted






777675747372716968676665


Age

(yea

rs)


CB

Year

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008










8281807978777675747372


Age

(yea

rs)


CBYear

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008



10by




10was










11 Conclusions





Acknowledgments


References









































25in an acellular






































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of

















777675747372716968676665


Age

(yea

rs)


CB

Year

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008










8281807978777675747372


Age

(yea

rs)


CBYear

CR

1982

1983

1984

1985

1986

1987

1988

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

2006

2007

2008



10by




10was










11 Conclusions





Acknowledgments


References









































25in an acellular






































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of






















11 Conclusions





Acknowledgments


References









































25in an acellular






































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of
















































25in an acellular






































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of



















































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of





















of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of
















Documents

European Hot Spot of Air Pollution by PM2.5 and Bap: Ostrava, Czech Republic