This article was downloaded by:[Cirla, Piero Emanuele][Cirla, Piero Emanuele]

On: 11 July 2007Access Details: [subscription number 778651021]Publisher: Taylor & FrancisInforma Ltd Registered in England and Wales Registered Number: 1072954Registered office: Mortimer House, 37-41 Mortimer Street, London W1T 3JH, UK

Journal of Occupational andEnvironmental HygienePublication details, including instructions for authors and subscription information:http://www.informaworld.com/smpp/title~content=t713657996

Assessment of Exposure to Polycyclic AromaticHydrocarbons (PAH) in Italian Asphalt Workers

First Published on: 01 January 2007To cite this Article: Cirla, Piero Emanuele, Martinotti, Irene, Buratti, Marina,Fustinoni, Silvia, Campo, Laura, Zito, Epifania, Prandi, Enzandrea, Longhi, Omar,Cavallo, Domenico and Foà, Vito , (2007) 'Assessment of Exposure to PolycyclicAromatic Hydrocarbons (PAH) in Italian Asphalt Workers', Journal of Occupationaland Environmental Hygiene, 4:1, 87 - 99To link to this article: DOI: 10.1080/15459620701354325URL: http://dx.doi.org/10.1080/15459620701354325

PLEASE SCROLL DOWN FOR ARTICLE

Full terms and conditions of use: http://www.informaworld.com/terms-and-conditions-of-access.pdf

This article maybe used for research, teaching and private study purposes. Any substantial or systematic reproduction,re-distribution, re-selling, loan or sub-licensing, systematic supply or distribution in any form to anyone is expresslyforbidden.

The publisher does not give any warranty express or implied or make any representation that the contents will becomplete or accurate or up to date. The accuracy of any instructions, formulae and drug doses should beindependently verified with primary sources. The publisher shall not be liable for any loss, actions, claims, proceedings,demand or costs or damages whatsoever or howsoever caused arising directly or indirectly in connection with orarising out of the use of this material.

© Taylor and Francis 2007

Dow

nloa

ded

By:

[Cirl

a, P

iero

Em

anue

le] A

t: 17

:53

11 J

uly

2007

Journal of Occupational and Environmental Hygiene, 4(S1): 87–99ISSN: 1545-9624 print / 1545-9632 onlineCopyright c© 2007 JOEH, LLCDOI: 10.1080/15459620701354325

Assessment of Exposure to Polycyclic AromaticHydrocarbons (PAH) in Italian Asphalt Workers

Piero Emanuele Cirla,1 Irene Martinotti,1 Marina Buratti,1 Silvia Fustinoni,1

Laura Campo,1 Epifania Zito,2 Enzandrea Prandi,3 Omar Longhi,1

Domenico Cavallo,4 and Vito Foa1

1Department of Occupational and Environmental Health, University of Milan and Department ofOccupational Health, I.R.C.C.S. Foundation Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena ofMilan, Milan, Italy2Department of Prevention, Local Health Unit of Lodi, Lodi, Italy3Department of Prevention, Local Health Unit of Milan City, Milan, Italy4Department of Chemical and Environmental Sciences, University of Insubria at Como, Como, Italy

The purpose of the work was the assessment of exposureto Polycyclic Aromatic Hydrocarbons (PAH), a family ofubiquitous pollutants of which some are carcinogens, in 100Italian asphalt workers (exposed to bitumen fumes and dieselexhausts) and in a reference group of 47 ground constructionoperators (exposed only to diesel exhausts, reference group).The protocol included interview via questionnaires, environ-mental air-monitoring (active personal sampling during thework shift), dermal contamination measures (six pads placedon worker’s wrist, neck, arm, chest, thigh, and ankle), andbiological monitoring (determination of 1-hydroxypyrene inurine spot samples collected three at different moments: base-line after two days of vacation, before shift, and at end shift on aday in the second half of the week). Analysis of the most relevantPAH, according to the American Environmental ProtectionAgency, EPA, was performed by High Performance LiquidChromatography (HPLC) by fluorimetric detector. Medianairborne levels of PAH ranged from 426 to below 0.03 ng/m3.Vapor-phase PAH, apart from naphthalene, were significantlyhigher in asphalt workers than in the reference group. Particle-phase PAH were similar and very low (<1 ng/m3) in bothexposure groups. Exposure levels did not vary in differentwork-tasks. Excretion of urinary 1-hydroxypyrene (expressedby ng/g creatinine) showed a significant increase at differentsampling moments in asphalt workers, smokers, and non-smokers: baseline was lower than at the beginning of theworkshift, and values were even higher in the end workshiftsample. Comparing the two groups, a significant difference inthe levels of metabolite does not appear, whereas this trendcan be viewed observing the non-smokers. All body regionsmonitored by pads showed equivalent values levels of DermalDeposition Density in both exposure groups. The measuredamount of dermal contamination was significantly higher inasphalt workers than in ground construction operators. Inasphalt workers, skin contamination was significantly higherduring asphalt paving than during asphalt mixing. DermalExposure Rate was calculated about threefold higher thanAirborne Exposure Rate; whereas considering toxicokineticalinformation (Kp, lag time, experimental dermal absorptiondata) and hygienistic data (particle size of bitumen fume),

the relevance of dermal absorption is lower than respiratory.The results of this study demonstrate that asphalt workersexperience slight occupational exposure to PAH, both byinhalatory and dermal routes, resulting in a significant increaseof urinary 1-hydroxypyrene during the workweek.

Keywords polycyclic aromatic hydrocarbons, asphalt workers,bitumen fumes, 1-hydroxypyrene, dermal exposure, airmonitoring

Address correspondence to Piero Cirla, Department of Occupa-tional and Environmental Health, University of Milan, Via S. Barnaba8, I-20122 Milan, Italy; e-mail: piero.cirla@gruppocimal.it

INTRODUCTION

I n Italy, the National Research Center (CNR) defines asphalt(or bituminous concrete) a “mixture of mineral matter

(crushed stone, grit, sand and filler) and bituminous binder”(1,2)

In the United States, the common term is “asphalt mix”for bituminous concrete; on the contrary, the word “asphalt”means “bitumen.”(3) Bitumen is a binder of natural originor a by-product of petroleum processing, containing OrganicAromatic Compounds, traces of sulphur, nitrogen, oxygen,nickel, iron, and vanadium. In Italy bitumen is derived onlyfrom a visbreaking process, whereas is possible to obtainbitumen derived from a cracking process from other Europeancountries. “Tar” is viscous matter, derived from destructivedistillation of coal, and containing several classes of organiccompounds among the many PAH.(1,4,5) The correct meaningof words is an important starting point to focus on the problemof Polycyclic Aromatic Hydrocarbons (PAH) exposure in theasphalt industry. In fact, the terms “asphalt,” “bitumen,” and

Journal of Occupational and Environmental Hygiene Supplement 2007 87

Dow

nloa

ded

By:

[Cirl

a, P

iero

Em

anue

le] A

t: 17

:53

11 J

uly

2007

“tar” really have very different meanings, whereas frequentlythey are used interchangeably.

The different composition of bitumen and tar determinestheir different chemical properties and toxicological relevancy.The International Agency for Research on Cancer (IARC)classifies tar as a “carcinogenic to humans” substance (Group1), while bitumen is a substance “not classifiable as carcino-genic to humans” (Group 3).(6) This difference is ascribedmostly to PAH contents; in fact, bitumen fumes can containca. 1% PAH, tar fumes may be able to contain ca. 90% PAHand especially high molecular weight compounds.(3,4) CurrentIARC reviews assessing potential carcinogenicity of PAH alsoempathize origin of the products; in fact, the reviews of thesecompounds were divided based upon their source, that is coalor petroleum.(7)

PAH are a large family of similar compounds made upof high molecular weight aromatic hydrocarbons, whosemolecule is made up of two or more condensed benzenicring structures so as to have two or more carbon atomsin common.(8,9) They are divided into two categories: lowmolecular weight compounds (128–166 a.m.u.) composed offewer than four rings and high molecular weight compoundsof four or more rings (202–278 a.m.u.). In general, PAH withthree rings exist predominately in the vapor phase (boilingpoint between 217 and 295◦C), while those with four rings canexist in both the vapor and particulate phases, and those withfive or more rings exist predominately in the particulate phase(boiling point >375◦C).

PAH are common contaminants, discharged into the envi-ronment from natural, industrial, and urban sources (volcanoes,forest fires, industrial plants, motor vehicle traffic, residentialheating with fossil fuels, etc.), and can also be found intobacco smoke, charbroiled meats, and smoked foods.(8,10–12)

Therefore, people may be exposed to PAH through multiplemedia, including air, soil, food, water, and their jobs. Roadconstruction workers are exposed to additional sources ofPAH; in fact these substances are emitted from heated asphalt,bitumen emulsion (bitumen mixed with water to form anemulsion), and vehicle exhausts from surrounding traffic androad paving equipment.(13)

According to experimental and monitoring studies, the PAHshowed they might be absorbed through different pathways,namely respiratory, dermal, and gastrointestinal route. Toevaluate total PAH uptake into the body from any source,biological monitoring, that is the quantification of PAH andof their metabolites in biological fluids, is usually performed.Urinary 1-hydroxypyrene (OH-Py), a metabolite of pyrene,has been proposed as biological marker of exposure toPAH since pyrene is always present in PAH mixtures andgood correlations have been found between OH-Py and bothairborne pyrene and total airborne PAH in many industrialsettings.(14)

Scientific literature reports PAH may have irritant effects;moreover, some of these have been recognized as proba-bly or possibly carcinogenic to human by the InternationalAgency for Research on Cancer, the European Union, and

other institutions.(6,7,15,16) In particular, attention is focusedon some of the four-six ring PAH, but a notable exceptionis naphthalene, a smaller and more volatile PAH recentlyclassified as possibly carcinogenic to humans by the IARC(Group 2B).(16,17)

An epidemiological study carried out by the IARC in 2000suggested that pulmonary cancer risk is slightly higher thanexpected in road paving workers.(18) The reasons for thisobservation are not completely clear, and there are indirectpieces of evidence which suggest that confounding factorslike tobacco smoking and possible occupational exposure tocoal tar in the past, could play a key-role. In particular, therelative risk of lung cancer associated with bitumen exposureis reduced by restriction of the analysis to a tar-free sub cohortand by adjustment for tar exposure. However the tar exposureassessment suffered from a greater degree of misclassificationthan bitumen exposure, resulting in imperfect adjustment ofan underlying confounding effect.(19)

In Italy, asphalt production per inhabitant and year is about0.7 tons (United States over 2 tons, Europe 0.7 tons, Chinabelow 0.2 tons), with a total volume of approximately 200million tons.(20) The PPTP-POPA Study of Lombardy Region(Northern Italy), resulting from the fusion of the Preventionof Professional Tumors Project (PPTP) and the Project forOperative Protection of Asphalt Workers (POPA), was aimedto achieve new data from the asphalt industry, a field inItaly where rather few hypotheses are available. Many occu-pational and toxicological experts (occupational physicians,industrial hygienists, analytical chemists, prevention techni-cians, and laboratory technicians), and all those operating inthe factory prevention systems (employer, manager of theprevention and protection service, factory physician, work-ers and their representatives), were actively involved in thestudy.

The study targets were to evaluate the asphalt industrytechnological cycle (with analysis of critical points via reviewsof the literature, investigation on road yard and asphalt plant),to set up and to carry out an investigation to asses PAH exposure(by means of environmental-air monitoring and biologicalmonitoring), and to set the risk assessment criteria at work,to evaluate the adopted and adoptable preventive solutions, toset up an epidemiological survey.

To investigate the workers’ exposure to PAH in the roadconstruction industry, we carried out a comprehensive studywhere ambient, dermal, and biological exposure measurementswere conducted for assessing levels and routes of exposureto asphalt emissions among a group of asphalt workers incomparison to a group of ground construction operators. Boththe two groups are exposed to vehicle exhausts coming fromdiesel powered working machines, but only the first group isexposed to bitumen emissions. We used active samplers toquantify contaminants in breathing air and pads to measurethe mass of substance deposited on skin; both inhalatoryand dermal exposure to PAH from a variety of sources,including bitumen, were assessed by the determination of1-hydroxypyrene in urine.

88 Journal of Occupational and Environmental Hygiene Supplement 2007

Dow

nloa

ded

By:

[Cirl

a, P

iero

Em

anue

le] A

t: 17

:53

11 J

uly

2007

MATERIAL AND METHODS

Study Design

The study was conducted during spring-summer 2003 inurban, suburban, and rural areas of northern Italy.(21,22) Theprotocol included the investigation at work with interviewsvia questionnaires (occupational, physiological and pathologichistory, working environment, personal clothing and protectionequipment), environmental monitoring (active personal sam-pling via membrane and vials, application of six cutaneouspads), and biological monitoring (urine). Airborne exposure,skin contamination monitoring, and biological monitoringwere performed during the same workday for each subject.The characteristics of the paving operations and the weatherconditions were measured and recorded on a standardizedform. All the subjects gave their written informed consent toparticipate.

We investigated 147 road constructions workers divided intotwo wide groups: 100 asphalt workers (exposed to bitumenfumes and diesel exhausts), employed in different tasks,described by the following job titles, i.e., 9 asphalt mixingemployees (5 plant operators and 4 loaders), 11 transport truckdrivers (lorry driver), 11 paver operators, 13 roller drivers,56 rakermen (8 mastic asphalt pavers, 37 concrete asphaltrakermen, 11 screed men); 47 ground construction operators(exposed only to diesel exhausts) employed in soil removal,carpentry, and application of cement. The definition of thesejob classes is consistent with those used in the IARC study ofthe asphalt industry.(23) The subjects were male with a mean ageof 42 (range 19–75) and 40 (range 20–63) years, respectively,for asphalt workers and ground construction operators. About50% of the workers involved were smokers with a median of 20cigarettes/day (44% and 64%, respectively, for asphalt workersand ground construction operators).

The study was performed at paving sites characterized bylight, surrounding car traffic. Both groups were exposed todiesel exhausts coming from working machines. Only theasphalt workers were exposed to bitumen fumes from asphaltcontaining petroleum-based bitumen, 4–6% for concrete as-phalt and 6–10% for mastic asphalt; typical applications are1,200–2,500 quintals (temperature at 120–160◦C), and 200–300 quintals (210–260◦C), respectively. Concrete asphalt isan asphalt mix in which the aggregate mineral particles arecontinuously graded or gap-graded to form an interlockingstructure, whereas mastic asphalt is a gap-graded asphalt mixcomposed of a coarse, crushed, aggregate skeleton boundwith a mastic mortar. In Italy, mastic asphalt is used onlyfor sidewalk paving in some cities (i.e., Milan). In our study,only few workers used bitumen from cracking process formastic asphalt, but not are distinguished in the data elaborationbecause no significant differences in exposure were found.

Paving machines were not equipped with a cabin or aventilation system. All workers neither wore respiratory masksnor used any barrier cream, but they were provided withprotective gloves and shoes. The management never gave themunderwear (undershirt and underpants), socks, or laundering

facilities for these items. They wore work cotton clotheswithout extra protective garments such as PVC or Tyvek suits.Work clothes were water-washed weekly. Showering facilitieswere not available at workplaces, so, workers showered athome.

As for the meteorological parameters, atmospheric pressurewas middle-high (mean 1002 mbar) and ambient temperaturesvaried between 5◦–31◦C (with a reduced excursion of 11◦–30◦C during exposure to bitumen fumes and vapors). The windspeed ranged from 0.2 to 4.4 m/sec.

Assessment of Work-Related Symptoms

Standardized interviews were performed for each subject atthe beginning and the end of shift, during the same workdaywhen of environmental and biological monitoring was done(after two or more consecutive workdays with asphalt mix).The anamnesis was supported by an individual questionnaireaimed at categorizing acute health effects and subjectivesymptoms (i.e., throat irritation, eyes irritation, cough). Oc-cupational, physiological, and pathological histories were alsoinvestigated. The same occupational health doctor collectedthe data from all the subjects involved in the study. Resultswere elaborated separately for smokers and non smokers, andalso for other variables like age, number of working hours theprevious week, and work experience.

Assessment of Airborne Exposure

Personal exposure to PAH was assessed in both asphaltworkers and ground construction operators by personal activesamplers, worn by each worker in the respiratory zone duringthe first part of a work shift (typically 7:00 am–11:00 am).Particulates and gaseous PAH were collected respectivelyon Teflon filters (37 mm diameter, 2 μm porosity, Zefluorfilter, Supelco, Milan, Italy), and backed tubes filled withAmberlite XAD-2 resin (200 mg, ORBO 42 LG, Supelco,Milan, Italy), according to NIOSH method n.5506.(24) Airwas pumped through the samplers at a nominal flow rate of 2L/min. Sampling time ranged from 226 to 455 minutes (mean240 minutes). Samples were preserved by degradation fromsunlight, transported in coolers, and refrigerated at 2–8◦C untilextraction which was performed within 48 hours of samplereceipt.

Assessment of Dermal Exposure

Skin contamination to PAH was assessed by six pads foreach subject, using a modification of the dermal samplingmethods described by Jongeneelen and Van Rooij.(25–27) Eachpad, consisted of a 37 mm diameter polypropylene membrane(GH Polypro, Pall Corporation, Milan, Italy), stuck to the skinby means of an adhesive plaster. The exposed outer surface hadan area of 7 cm2. At the beginning of shift, pads were placed onthe skin in six different locations (neck, shoulder, upper arm,wrist, groin, ankle). At the end of the exposure period, whichranged from 5 to 10 hours (mean 8), pads were removed, andthe exposed portion stored in a vial at –20◦C. To prevent biasin the measurement of skin contamination, at withdrawal pads

Journal of Occupational and Environmental Hygiene Supplement 2007 89

Dow

nloa

ded

By:

[Cirl

a, P

iero

Em

anue

le] A

t: 17

:53

11 J

uly

2007

were examined carefully for visible stain; these cases wereregistered in standardized form. We also registered types ofclothing and protective disposals worn during the workday,and which pads were covered (inner) and not covered (outer)by garments.

Analysis of PAH

Organic Soluble Matter (OSM), including PAH, wereextracted from filters and XAD-2 by sonication at 40◦C with2 ml acetonitrile for 30 minutes and quantified by means of aUV spectrophotometric method (UV2 spectrometer—Unicam,Milan, Italy). Separation and identification of individual PAHwas afforded in the above-mentioned extraction solutions byhigh-performance liquid chromatography (HPLC) with fluori-metric detection.(28) The HPLC system included a gradientcontroller and high-pressure pump (Waters 600), an autosampler (Waters 715), a UV-visible detector (Waters 486), anda multi-programmable fluorescence detector (Waters 2475—Waters, Milan, Italy). A reversed-phase column (SupelcosilLC-PAH, 100 × 4.6 mm ID, 3 μm particle size—Supelco)was used for separation of PAH congeners. The flow-injectionsystem for fluorescence analysis (FIA-FL) was the same as theHPLC system, except that the chromatographic column wasremoved.

Fifteen priority PAH, listed by the U.S. EnvironmentalProtection Agency (EPA), were quantified (naphthaleneNAP, acenaphthene ACN, fluorene FLE, phenanthrene PHE,anthracene ANT, fluoranthene FLT, pyrene PYR, chryseneCHR, benzo[a]anthrancene BaA, benzo[k]fluorantheneBkF, benzo[b]fluoranthene BbF, benzo[a]pyrene BaP,dibenzo[a,h]anthracene dBA, benzo[g,h,i]perylene BPE, andindeno[1,2,3-cd]pyrene IPY); acenaphthylene was omittedbecause it does not fluoresce. Analytical limits of detection(LOD), calculated for a 4 hour sampling period with anaverage air volume collection of 0.48 m3, are reported inTable II. The methods of sample preparation and analysisused for pads were the same used for air filters. Becauseof the slight identification of ACN, CHR, BaA, dBA, BPE,and IPY in pads (these six PAH were above the limit ofdetection in less than 10% pads), we consider in the analysisof data only the remaining nine PAH (ANT, BaP, BbF,BkF, FLE, FLT, NAP, PHE, PYR), also as sum (�9PAH).NAP concentration values were considered approximateestimates, possibly inaccurate because of the low affinity ofthe adopted polypropylene material towards that compoundand also because of unpredictable losses of NAP due to theevaporation step before the determination of PAH depositedonto pads. However, we included this PAH in our considerationbecause of the high amount on pads and the toxicologicalrelevancy.

OSM determination was performed on pads worn on 32ground construction operators and on all the asphalt workers,while only a smaller selection of pads, which were wornon a group of 53 asphalt workers, were analyzed for PAH.Analytical limits of detection (LOD) for dermal exposure are

respectively 0.1 ng/cm2 (NAP), 0.03 ng/cm2 (PHE, ANT, FLT,PYR), 0.01 ng/cm2 (FLE, BbF), and 0.003 ng/cm2 (BkF, BaP).

Biological Monitoring

Spot urine samples were collected from each worker in threedifferent moments of the same workweek: a baseline sampleon Monday morning (around 7:00 am), before-shift (around7:00 am) and end-shift (around 5:00 pm), and after 2 or moreconsecutive workdays (same day of air and dermal sampling).Specimens collected in the morning were obtained fromthe second urination of the day. Samples were immediatelyrefrigerated, and stored in polyethylene tubes at −20◦C untilanalysis.

PAH are present in common foods at concentration between<0.1 μg/Kg and 400 μg/Kg.(10,29) To prevent the possibleinterference of diet on biological monitoring, the eveningbefore the sampling and on the day of the sampling, subjectswere asked to abstain from food containing PAH:(30,31) i.e.,smoked foods (concentration range of BaP 0.01–18 μg/Kg),grilled foods (0.3–212 μg/Kg), mussels (0.2–12 μg/Kg), andcrustaceans (0.1–5.3 μg/Kg). Particular attention was paidto the influence of tobacco smoke(32) in the level of urinarymetabolites (concentration range of BaP 20–200 ng/cigarette).

Analysis of Urine

Urinary OH-Py was analyzed by HPLC with fluorimetricdetection according to a published method.(28) Briefly, urinesamples (1 ml) were diluted with 1 ml of acetate buffer (0.2M, pH 5.0), containing 250 U of β-glucoronidase and 20 U ofsulphatase and incubated for 16 h at 37◦C. Samples were thenpurified by extraction with 3 ml of ethyl acetate, the organicphase (2.5 ml) was transferred into a glass vial and taken todryness at 40◦C under a nitrogen stream. The residue wasdissolved with 200 μl of mobile phase (acetonitrile-water-acetic acid 30:69.5:0.5) and 40 μl-aliquots of the resultingsolution were injected into a chromatograph equipped with areverse-phase Supelcosil-DP column (50 mm length, 4.6 mminternal diameter, 5 μm particle size). The flow of the mobilephase was 4 ml/min. The wavelengths used for quantificationwere 340 nm for excitation and 390 nm for emission. TheLOD of the method is 50 ng/L. Creatinine was determinedusing Jaffe’s colorimetric method.

Investigation of Dermal Exposure

Assuming that each pad represents a skin region with acertain surface area, the contamination data on each exposurepad were extrapolated to the corresponding area to have anassessment of the total daily contamination on the skin. Thesurface areas of the different skin regions were calculated byPopendorf’s human dermal surface area model,(33) adaptedto anatomical dimension (height 174.58 cm, weight 70 Kg)of 50th percentile Italian men.(34) The relevance of differentanatomic regions, corresponding to each pad, is reported inTable III as percentage of total body surface.

We have used the term exposure to indicate the contactbetween PAH and a target (lung or skin), and the term dose

90 Journal of Occupational and Environmental Hygiene Supplement 2007

Dow

nloa

ded

By:

[Cirl

a, P

iero

Em

anue

le] A

t: 17

:53

11 J

uly

2007

to define the amount of agent that enters a target by crossingan exposure surface. Dermal Deposition Density is given fromtotal mass of contaminant found during analysis, divided bythe surface area of the pad (μg/cm2 for OSM, ng/cm2 for PAH).Since the shift length in this study varied from 4 to 10 hours,skin monitoring data was corrected for exposure duration,calculating also Dermal Exposure Rate (or nominal dermalexposure), which is Dermal Deposition Density multiplied bythe area of the body part represented by each pad and dividedby sampling time (μg/hr for OSM, ng/hr for PAH). Total bodyDermal Exposure Rate is calculated as the sum of DermalExposure Rate of the six different body parts and indicates themass of contaminant deposited on the total body surface areaper unit time.

To compare exposure via skin with the exposure viarespiratory tract, we also calculated Respiratory Exposure Rate(or nominal airborne exposure; ng/hr), which is the airborneconcentration multiplied by the respiratory minute volume (1.8m3/hr for moderate work). To compare the amount enteringthe body by the two routes (dermal and respiratory), and theirrelative contribution to internal dose we calculated dermal andrespiratory uptake. In fact, it is not appropriate to comparedermal exposure and respiratory exposure directly, since theuptake or absorption by these two routes is usually quitedifferent. Based on the relevant toxicokinetical data (Kp, lagtime, experimental dermal absorption data), we held that asuitable and cautious approximation is to consider dermaluptake as 20% of total body dermal exposure. Instead, forrespiratory uptake we can assume an absorption factor of 70%for both gaseous and particulate PAH.

Statistical Analysis

Statistical analysis was performed using the SPSS 12.0 andthe Excel XP package for Windows. The exposure variablesare presented with the median because this measure of centrallocation is more representative of a skewed distribution ofdata than the arithmetic mean. Data were log transformed toassure normal distribution (Kolmogorov-Smirnov test). Pairedt-test was applied to determine the significance of intra-groupsdifferences (repeated measures of Urinary OH-Py), while t-testfor independent samples was used for inter-groups comparison.To evaluate the relationships between both inhalatory anddermal exposure results, and urinary biomarker levels, andto identify significant predictors of absorbed dose, simpleand multiple regression analyses were conducted. The Chi-square test was used for discontinuous variables inter-groupscomparison. A p-value below 0.05 was considered statisticallysignificant. Data below the detection limit were processed ashaving the numeric value of half of the detection limit.

In some cases, small stains of black material on the padsworn on worker’s ankle or wrist occurred during work. Wesupposed that extrapolating the chemical mass deposited onthe stained pad to the represented body part could causean overestimation of whole body dermal exposure. So wecompared the Dermal Deposition Density of PAH in clean anddirty pads for each location in the group of asphalt workers,

and found a significantly tenfold increased of toxic amounts inthe dirty pads. This observation provides one of the criteria forsample rejection: 3% of pads were excluded from statisticalanalysis because macroscopically contaminated. Then weelaborated the data of 92 asphalt workers for OSM and 53for PAH.

RESULTS

T o help understand findings, the information in this sectionis organized by symptoms, and then by external exposure

(inhalation, dermal) and biological monitoring results.

Work-Related Symptoms

At the beginning of shift, no acute health symptoms werereported by any of the subjects involved, whereas at endalmost 30% of workers reported one or more symptomsin association with their work exposures during the survey(Figure 1). The most frequently reported symptoms wereeye irritation and coughing. The results showed the absenceof a significant difference in the incidence of work-relatedsymptoms (headache, throat irritation, eyes irritation, cough)in asphalt workers versus ground construction operators. Amoderate prevalence of coughing was reported by smokers.No influence appears linked to other background variables,such as age, number of hours worked the previous week, andwork experience.

Airborne Monitoring

Data on personal exposure to airborne PAH were previouslypartially reported(21,22) and are here shown completely andexplained. Air concentration values of single PAH monitored,most important for carcinogenicity, in particular BaP, fell intothe range of averages (ten year annual averages) that can beobserved in Italian urban areas (Table I).

The results of personal airborne monitoring are presentedaccording to job title in Table II and show a moderate exposure

FIGURE 1. Prevalence of work-related symptoms in asphaltworkers (white) and ground construction operators (gray) at theend of shift

Journal of Occupational and Environmental Hygiene Supplement 2007 91

Dow

nloa

ded

By:

[Cirl

a, P

iero

Em

anue

le] A

t: 17

:53

11 J

uly

2007

TABLE I. Airborne Levels (ng/m3) of Most Relevant PAH Regarding Carcinogenicity (Toxicity EquivalenceFactors—TEFs, According to the U.S. EPA was Shown), Among Asphalt Workers Investigated by PPTP—POPAStudy and in Italian Urban Areas (Ten Year Annual Averages)

PPTP–POPA Study Urban areas

PAH EPA TEF Average (S.D.) Median (5th–95th percentile) Minimum Maximum

NAP — 489 (347) 426 (155–1,185) — —CHR 0.01 0.79 (1.60) <0.08 (<0.08–1.64) 0.1 7.0BaA 0.1 0.74 (2.36) <0.08 (<0.08–3.71) — —BkF 0.1 0.73 (2.65) 0.14 (<0.03–1.76) 0.1 1.1BbF 0.1 1.6 (3.3) 0.8 (<0.2–5.2) 0.2 4.8BaP 1.0 (Index compounds) 1.45 (5.24) 0.33 (<0.03–3.47) 0.2 9.6dBA 1.0 0.51 (1.87) <0.07 (<0.07–1.13) — —IPY 0.1 0.7 (0.9) <0.3 (<0.3–2.5) 0.1 1.4

to investigated PAH (as sum of vapor and particulate phases),with values similar to those of ground construction operators.The partitioning of PAH was such that 99% was detectedin the vapor phase (low-boiling compounds) and 1% in theparticulate phase (high-boiling compounds). Median airbornelevels during the workshift of fifteen PAH, from Naphthaleneto Indeno(1,2,3-cd)pyrene, ranged from 426 to below 0.03ng/m3. In asphalt workers 4 out of 15 PAH were found tobe the most representative: NAP (detected above the LOD in100% of samples; median value: 426 ng/m3; 77% of the totalamount), PHE (99%; 52 ng/m3; 9%), FLE (96%; 34 ng/m3;6%), and PYR (100%; 26 ng/m3; 5%).

With regard to ground construction operators, the mostfrequently detected compounds were: NAP (100% of samples;371 ng/m3; 92% of the total amount), PHE (100%; 14 ng/m3;3%), and FLE (91%; 9 ng/m3; 2%); PYR contribution to thetotal PAH amount was in this case negligible (79%; 1 ng/m3;<1%). Median values of individual volatile PAH (NAP toPYR) observed in asphalt workers were higher than those inground construction operators, with major differences in PHEand FLE (4-fold higher), and PYR (30-fold higher). On thecontrary, the concentration of high-boiling PAH (BkF, BbF, andBaP) was similar in the two groups; their median levels werevery low (range 0.1–0.9 ng/m3) and no significant inter-groupsdifferences were appreciable, though considerable variabilitywas present among the subgroups of asphalt workers.

According to U.S. EPA Toxicity Equivalence Factors(TEFs) and considering BaP as an Index compound (see Table Iand Table II), the median exposure level to the weighed sum ofthe 7 most relevant, in regard to carcinogenicity, airborne PAHmonitored (W�7PAH) was 0.8 and 1.1 ng BaPeq /m3 in asphaltworkers and ground construction operators, respectively (nosignificant difference).

As regards asphalt workers, among different work-tasks(asphalt mixing employees, transport truck drivers, paveroperators, roller drivers, manual workers, screed man, concreteasphalt rakermen, and mastic asphalt pavers), there were no sta-tistically significant differences in air-environmental exposure,

but only an upward trend for mastic asphalt operators. Thistrend is due to high-boiling PAH and appears also consideringW�7PAH.

Dermal Monitoring

Data on personal exposure to PAH were also previouslypartially reported(21) and are here briefly summarized andfurther explained. Since the cutaneous monitoring did notshow a significant difference between the “covered” and“uncovered” pad in all body parts for both asphalt workersand ground construction operators, we decided not to considerthem separately in the following analysis. We did not findimportant differences in Dermal Deposition Density betweenpads located on different body parts, and the neck alwaysappears as “uncovered” and “clean.” The total body dermalexposure from OSM in asphalt workers in contact with bitumenduring their activity is significantly higher (p = 0.005) than thatof ground construction operators. In fact, the median valuesof total body Dermal Exposure Rate are, respectively, 995μg/hr in asphalt workers and 516 μg/hr in ground constructionoperators. We find a statistically significant difference betweenthe two groups in all these body sites (neck p < 0.001, shoulderp < 0.001, upper arm p < 0.001, wrist p = 0.002, groin p =0.018, ankle p < 0.001).

The cutaneous monitoring results were not significantlydifferent among different work-tasks in the asphalt workers,with the exception of asphalt mixing employees; an increasedtrend was detectable only for rakermen and paver operators.In fact, taking into account the five job classes we foundthat asphalt mixing employees have a total body DermalExposure Rate to OSM lower than transport truck drivers(p = 0.009), rakermen (p = 0.06), paver operators (p = 0.05),and roller drivers (p = 0.14), similar to ground constructionoperators. There was no other significant difference amongthe five job classes (p > 0.40) which have comparable dermalcontamination from OSM.

In asphalt workers, the total body Dermal Exposure Rate(see Table III) of representative PAH (�9PAH; calculated

92 Journal of Occupational and Environmental Hygiene Supplement 2007

Dow

nloa

ded

By:

[Cirl

a, P

iero

Em

anue

le] A

t: 17

:53

11 J

uly

2007

TA

BL

EII

.A

irb

orn

eP

AH

sL

ev

els

(ng

/m3)

Am

on

gA

sp

ha

ltW

ork

ers

(n=

10

0)

an

dG

rou

nd

Co

ns

tru

cti

on

Op

era

tors

(n=

47

).T

he

Nu

mb

er

of

Wo

rke

rsfo

rE

ach

Ac

tiv

ity

isR

ep

ort

ed

inth

eR

ela

tiv

eC

olu

mn

.R

ep

ort

ed

Va

lue

sa

reM

ed

ian

(5th

–9

5th

Pe

rce

nti

le),

an

dP

erc

en

tag

eo

fS

am

ple

sA

bo

ve

the

LO

D(i

tali

c)

ASP

HA

LTW

OR

KE

RS

PA

HL

OD

bT

ran

spo

rt

Tru

ckD

river

s

N.

11

bS

cree

d

Ma

nR

ak

erm

en

N.

11

bC

on

cret

eA

sph

alt

Ra

ker

men

N.

37

bM

ast

icA

sph

alt

Ra

ker

men

N.

8

bR

oll

er

Dri

ver

s

N.

13

bP

aver

Op

era

tors

N.

11

bA

sph

alt

Mix

ing

Em

plo

yee

s

N.

9

AL

L

N.1

00

Gro

un

dC

on

stru

ctio

n

Op

era

tors

N.4

7

NA

P2

399

(134

–149

0)36

4(1

62–4

46)

440

(187

–1,1

76)

454

(244

–724

)34

5(1

44–5

41)

493

(218

–1,3

80)

489

(90–

1,13

1)a42

6(1

55–1

,185

);99

a37

1(15

3–79

4);1

00A

CN

28

(2–2

3)24

(∗−3

2)18

(∗−1

22)

5(3

–16)

4(∗

−18)

16(∗

−200

)9

(2–1

85)

a9

(∗–1

99);

59a∗(

∗−∗);

0FL

E0.

230

.5(9

.2–9

5,7)

40.0

(18.

6–76

.6)

30.8

(6.7

–139

.0)

32.5

(2.5

–58.

5)26

.1(5

.7–5

6.5)

36.6

(19.

6–21

4.8)

39.3

(14.

0–62

.4)

a33

.6(6

.7–1

37.7

);96

a8.

6(∗

–47.

5);8

1PH

E1.

433

.6(1

7.9–

183,

8)45

.7(2

4.1–

313.

9)60

.7(1

3.2–

400.

9)15

1.1

(26.

9–25

7.1)

49.5

(12.

7–70

.3)

67.1

(28.

9–77

0.4)

22.2

(4.5

–83.

4)a51

.8(1

0.8–

360.

7);9

9a13

.3(4

.1–3

8.4)

;100

AN

T0.

40,

5(∗

−1.6

)0.

5(∗

−21.

6)0.

7(∗

−19.

8)27

.7(2

.6–5

9.9)

0.8

(∗−5

.8)

0.82

(∗−9

3.6)

0.6

(∗−3

.8)

a0.

7(∗

–39.

8);5

5a∗(

∗–1.

8);3

6FL

T0.

43.

4(1

.0–1

4.5)

3.3

(0.4

–33.

3)2.

0(∗

−40.

2)0.

9(0

.6–4

2.1)

2.4

(∗−1

8.8)

4.3

(1.6

–88.

7)2.

0(∗

−8.0

)a2.

8(∗

–37.

8);7

0a1.

3(∗

–2.9

);85

PYR

0.6

23.5

(6.1

–40.

2)29

.2(1

2.1–

58.9

)35

.8(4

.1–1

71.0

)31

.3(2

.8–9

8.9)

18.8

(11.

3–69

.7)

23.8

(14.

6–17

9.1)

25,7

(4.8

–226

.8)

a26

.3(4

.3–1

82.4

);10

0a1.

0(∗

–4.3

);79

CH

R0.

080.

10(∗

−0.3

3)0.

11(∗

−0.3

6)0.

11(∗

−0.9

4)5.

78(0

.47–

8.98

)0.

13(∗

−0.3

1)0.

09(∗

−0.7

4)0.

18(∗

−0.8

4)∗(

∗–1.

64);

330.

69(∗

–1.6

4);9

4B

aA0.

080.

10(∗

−0.7

4)0.

10(∗

−2.4

1)0.

11(∗

−1.2

0)0.

46(0

.18–

8.05

)0.

10(∗

−1.5

9)0.

09(∗

−2.8

5)0.

10(∗

−0.4

8)∗(

∗–3.

71);

280.

64(∗

–2.8

5);9

4B

kF0.

030.

11(0

.03–

0.31

)0.

21(0

.05–

0.58

)0.

13(0

.03–

0.64

)3.

01(∗

−18.

0)0.

17(0

.03–

1.49

)0.

11(0

.04–

0.76

)0.

26(0

.07–

0.37

)0.

14(∗

–1.7

6);7

40.

27(∗

–0.7

0);9

4B

bF0.

20.

6(∗

−1.3

)0.

8(∗

−2. 3

)0.

8(∗

−3.0

)3.

24(∗

–23.

4)0.

4(∗

−2.7

)0.

9(∗

−3.8

)1.

5(0

.3–3

.0)

0.8

(∗–5

.2);

690.

9(∗

–2.2

);82

BaP

0.03

0.22

(0.0

3–0.

44)

0.19

(0.0

5–0.

32)

0.27

(0.0

5–1.

16)

6.24

(0.2

6–36

.03)

0.48

(0.0

3–0.

91)

0.38

(0.1

1–0.

61)

0.43

(0.1

1−5.

51)

0.33

(∗–3

.47)

;84

0.61

(0.0

9–2.

07);

97dB

A0.

070.

07(∗

−0.9

2)0.

32(0

.08–

1.04

)0.

10(∗

−0.8

5)0.

20(0

.09–

12.2

9)0.

19(∗

–1.7

1)0.

11(0

.06–

1.18

)0.

32(∗

−0.7

4)∗(

∗–1.

13);

480.

16(∗

–0.4

7);5

8B

PE0.

30.

9(0

.3–2

.6)

0.6

(0.3

–0.5

)1.

2(∗

−4.8

)0.

9(0

.7–1

.4)

1.4

(0.3

–3.6

)1.

4(0

.3–1

.8)

1.5

(0.5

–10.

7)1.

1(∗

–4.8

);69

0.8

(∗–1

.8);

61IP

Y0.

3∗(

∗−2.

6)0.

4(0

.3–2

.7)

0.4

(∗−1

.8)

0.7

(0.5

–0.9

)0.

4(∗

−0.8

)0.

4(∗

−1,9)

0.5

(0.3

–1.9

)∗(

∗–2.

5);1

20.

6(∗

–1.8

);55

�9 P

AH

n.a.

470

(192

–1,80

6)48

2(2

90–7

73)

641

(291

–1,72

8)75

5(2

86–1

,23

8)50

3(2

17–6

76)

620

(335

–2,56

4)53

5(2

22–1

,34

8)a55

1(1

78–1

,76

0)a40

1(1

93–8

63)

W�

7 PA

Hn.

a.0.

4(0

.1–0

.6)

0.6

(0.4

–1.9

)0.

8(0

.3–2

.0)

11.9

(0.6

–39.

1)0.

9(0

.2–2

.9)

0.6

(0.4

–2.3

)1.

4(0

.4–6

.4)

0.8

(0.2

–4.5

)1.

1(0

.3–2

.8)

∗ =D

ata

belo

wth

ede

tect

ion

limit

wer

epr

oces

sed

asha

ving

the

num

eric

valu

eof

LO

D/2

.N

AP

=na

phth

alen

e,A

CN

=ac

enap

hthe

ne,

FLE

=flu

oren

e,PH

E=

phen

anth

rene

,A

NT

=an

thra

cene

,FL

T=

fluor

anth

ene,

PYR

=py

rene

,C

HR

=ch

ryse

ne,

BaA

=be

nzo[

a]an

thra

ncen

e,B

kF=

benz

o[k]

fluor

anth

ene,

BbF

=be

nzo[

b]flu

oran

then

e,B

aP=

benz

o[a]

pyre

ne,d

BA

=di

benz

o[a,

h]an

thra

cene

,BPE

=be

nzo[

g,h,

i]pe

ryle

ne,I

PY=

inde

no[1

,2,3

-cd]

pyre

ne.

�9 P

AH

=N

AP,

FLE

,PH

E,A

NT,

FLT,

PYR

,BkF

,BbF

,BaP

.a

=si

gnifi

cant

diff

eren

cebe

twee

n“A

llas

phal

twor

kers

”an

d“G

roun

dco

nstr

uctio

nop

erat

ors”

grou

ps(t

-tes

tfor

inde

pend

ents

ampl

es,p

<0.

05).

b=

nosi

gnifi

cant

inte

r-gr

oups

diff

eren

ces

vers

usot

her

asph

altw

ork-

task

s(t

-tes

tfor

inde

pend

ents

ampl

es,p

>0.

05).

93

Dow

nloa

ded

By:

[Cirl

a, P

iero

Em

anue

le] A

t: 17

:53

11 J

uly

2007

TABLE III. Dermal Contamination to Σ9PAH (ng/h) Expressed as Dermal Exposure Rate, in Different Body Parts(%) and Total Body, During Five Different Activity Performed by Asphalt Workers. The Number of Workers forEach Activities is Reported in the Relative Column. Reported Values are Median (5th–95th Percentile)

Anatomic

regions

(%)

Transport

truck drivers

(n. 7)

Rakermen

(n. 25)

Roller

Drivers

(n. 6)

Paver

Operators

(n. 7)

Asphalt Mixing

Employees

(n. 8)

Neck (7%) 97 (60–537) 182 (68–2735) 162 (58–473) 192 (78–2,517) a66 (13–777)Shoulder (19%) 395 (175–1,177) 484 (115–1,517) 511 (154–607) 333 (224–1,346) a180 (36–495)Upper arm (13%) 191 (86–402) 306 (99–1,317) 489 (89–764) 380 (158–615) a176 (29–154)Wrist (14%) 197 (67–2,686) 633 (152–2,355) 495 (207–1,152) 502 (181–1,360) a290 (37–1,237)Groin (27%) 455 (276–2,582) 842 (355–2,533) 997 (330–2,508) 1,374 (476–3,796) a364 (93–1,284)Ankle (20%) 274 (161–1,882) 886 (257–2,039) 785 (406–1,543) 1459 (661–2,677) a865 (63–1,664)Total body (100%) 1,606 (959–8,559) 3,005 (1,496–12,023) 3,367 (1,389–6,619) 3,397 (1,945–12,129) a1,975 (290–5,595)

a = significant difference between “Asphalt mixing employees” and other asphalt work-tasks (t-test for independent samples, p < 0.05).b = no significant inter-groups differences versus other asphalt work-tasks (t-test for independent samples, p > 0.05).

as the sum of PAH Dose Rates of NAP, FLE, PHE, ANT, FLT,PYR, BkF, BbF and BaP) ranges from 1.6 μg/hr to 3.4 μg/hrand is about 300- to 1,000-fold lower than total body DermalExposure Rate of OSM. In regard to dermal exposure at �9PAH,we found that asphalt mixing workers have lower values thanthose employed in other activity and that there is no significantdifference among other asphalt workers subgroups.

Dermal and inhalatory exposure to PAH in asphalt workers,evaluated as total body Dermal Exposure Rate (ng/hr) andRespiratory Exposure Rate (ng/hr), is presented in Table IV.Data show that total body Dermal Exposure Rate is about

TABLE IV. Dermal and Airborne Exposure to PAHin Asphalt Workers (n = 53), Calculated as TotalBody Dermal Exposure Rate (ng/hr) and RespiratoryExposure Rate (ng/hr). Reported Values are Median

PAH

Gaseous Particulates Total Body Dermal Respiratory

Phase Phase Exposure Rate Exposure Rate

NAP 1,089# 720FLE 282 48PHE 1,169 64ANT 76 1FLT 72 4PYR 247 53

BkF ∗ 1BbF ∗ 2BaP ∗ 1

�9PAH 3, 116 915

∗Data below the detection limit were processed as having the numeric valueof LOD/2.#Approximate estimate.NAP = naphthalene, FLE = fluorene, PHE = phenanthrene, ANT =anthracene, FLT = fluoranthene, PYR = pyrene, BkF = benzo[k]fluoranthene,BbF = benzo[b]fluoranthene, BaP = benzo[a]pyrene.

threefold higher than Respiratory Exposure Rate. The profileof PAH found in pads is comparable to that found in air: in bothcases, the most relevant PAH are the volatile compounds. Abetter significant correlation was ascertained between airborneand dermal exposure, considering the total concentration ofrepresentative PAH (�9PAH) in asphalt workers (r = 0.55).The correlation was particularly good for FLE (p = 0.77) andFLT (p = 0.73).

Biological Monitoring

Results of urinary OH-Py, expressed by ng/g creatinine,were previously partially reported.(21) In good accordance withthe low levels of airborne PAH, also OH-Py levels found inthe present study are lower. Summarized statistics for urinaryOH-Py stratified by smoking habit are presented in Table V.The excretion of urinary 1-hydroxypyrene (Figure 2) showed asignificant increase among different sampling times in asphaltworkers, smokers and non-smokers: baseline after two daysof vacation lower than the beginning of the workshift, withthe higher values at the end of the workshift (p < 0.01). Inthe ground construction operators, a significant increase wasfound only between end-shift versus pre-shift or baseline insmokers, whereas intra-group differences not appeared in no-smokers. In the two groups, OH-Py was significantly higher insmokers compared to non-smokers at all sampling times (p ≤0.01).

Comparing the two groups, no significant difference in thelevels of metabolite appeared in baseline samples collected af-ter a weekend away from work. Also inter-group comparisonsusing OH-Py levels at the beginning or at the end of workshiftdid not show any significant differences, whether consideringall subjects or smokers (Figure 1B). Nevertheless, this trendcan be viewed when the confounding effect of smoking wasexcluded: in non-smokers, the amount of OH-Py was higherin asphalt workers than in ground construction operators,both in before- and end-shift samples (Figure 1A). When thestatistical analysis was performed using OH-Py expressed byng/L, similar results were obtained.(22)

94 Journal of Occupational and Environmental Hygiene Supplement 2007

Dow

nloa

ded

By:

[Cirl

a, P

iero

Em

anue

le] A

t: 17

:53

11 J

uly

2007

TABLE V. Urinary OH-Py (ng/g Creatinine) at Different Sampling Times in Asphalt Workers (Bold, n = 100)and Ground Construction Workers (Normal, n = 47), According to Smoking Habit. Reported Values are Median(5th–95th Percentile)

Sampling time

All

(n = 100)

(n = 47)

Non-smokers

(n = 56)

(n = 17)

Smokers

(n = 44)

(n = 30)

Baseline 155 (<50–630)

193 (<50–489)

b126(<50–584)b 87(<50–336)

b206(<50–694)b229(70–488)

Before-shift c233(<50–914)

176(<50–535)

a,b,c189 (<50–944)a,b 121(<50–306)

b,c288(100–946)b235(78–644)

End-shift c,d362(70–1263)

246(98–991)

a,b,c,d253 (55–1277)a,b171(69–395)

b,c,d392(152–1228)b,c,d349(151–1058)

a = inter-groups significant difference between “Asphalt workers” and “Ground construction workers” (t-test for independent samples, p < 0.05).b = inter-groups significant difference between “Non-smokers” and “Smokers” (t-test for independent samples, p < 0.05).c = intra-group significant difference versus “Baseline” sampling time (paired t-test, p < 0.05).d = intra-group significant difference versus “Before-shift” sampling time (paired t-test, p < 0.05).

The correlation between OH-Py (ng/g creatinine) andvarious indices of airborne exposure to PAH was limited tolow-boiling compounds and the sum of 15 PAH monitored.Subjects were considered all together or divided according tosmoking habit. A weak association was also found betweenend-shift OH-Py and PYR in all subjects (r = 0.26), in smokers(r = 0.30), and in non-smokers (r = 0.34). Higher correlationcoefficients were generally observed when a similar analysiswas performed using OH-Py expressed by ng/L.(22)

Considering within-subject variability, in all subjects sig-nificant correlations were observed between baseline OH-Pyand both before- and end-shift OH-Py (r = 0.48 and 0.42,respectively) as well as between before- and end-shift OH-Py(r= 0.79). These correlations generally improved when onlynon-smokers were considered.

DISCUSSION

E pidemiologic studies on asphalt workers showed con-tradictory results regarding the possible adverse health

effects due to occupational exposure to organic compoundsand especially to PAH.(3,12,13) A recent study, carried outby IARC in 2000, suggested that in road paving workers’pulmonary cancer risk is slightly higher than expected.(18) Thereasons for this observation are not completely clear; severalconfounding factors were present (like tobacco smoking orexposure to coal tar) and exposure data was lacking.(19) Hence,the epidemiologic evidence for an association between lungcancer and exposure to asphalt in paving is inconclusive at thistime. In the present study, we have focused on exposure toPAH, considering the toxicological relevance of some of thesecompounds and the importance of this occupational healthproblem.(3,6,35)

Acute health effects and subjective symptoms (i.e., eye,nose, laryngeal/pharyngeal irritation; fatigue; headaches; etc.)have been reported during several bitumen related work-ing activities and also in the asphalt industry.(3) Generally,symptoms increased with increasing asphalt temperature andincreasing concentrations of asphalt fumes.(36) There was noclear correlation between symptoms and total amounts of

FIGURE 2. Box-plot of urinary 1-hydroxypyrene (ng/g creatinine, white = asphalt workers, grey = ground construction operators, O = outliers)in non smokers (A) and smokers (B)

Journal of Occupational and Environmental Hygiene Supplement 2007 95

Dow

nloa

ded

By:

[Cirl

a, P

iero

Em

anue

le] A

t: 17

:53

11 J

uly

2007

volatile compounds, but a significant positive correlation wasdemonstrated between symptoms and some substances likePAH.(13,35,37)

Similarly to other experiences(3) and in disagreement witha cross-sectional study performed in Norway by Norsethet al.,(36) our results showed at the end-shift survey the absenceof a significant difference in the prevalence of work-relatedirritation symptoms (throat irritation, eye irritation, coughs),in asphalt workers versus ground construction operators. Likethe Norwegian study, we also took into account smokinghabits, age, number of hours worked the previous week, workexperience, weather conditions, and traffic density. Our resultsfor concentration of asphalt fumes exposure were lower, butthe analytical methods used by Norseth et al.(36) to evaluateexposure were not clearly defined (apparently as total organiccompounds).

Moreover, potential biases of the Norwegian study includethe use of self-administered questionnaires and the possiblepresence of coal-tar contamination. The limitations of ourevaluation include the lack of pre- and post-shift spirometrywith which to evaluate the effects of asphalt exposures onlung function more fully and the prevalence of smokers inthe control group.

The constant reduction of PAH exposure at work inthe last thirty years is comforting data shown in recentevaluations.(13,18,19) As we already reported,(21,22) PAH expo-sure in the Italian asphalt industry is some orders of magnitudelower than in other working environments.(12) In particular, airconcentration of BaP, dBa, and NAP results are much belowthe few existing Occupational Exposure Limits (Dutch TRK,Polish and Norwegian MPC), and the median BaP levels arebelow the Air Quality established by the Italian EnvironmentalOffice (1 ng/m3, average yearly value).

In good accordance with observations by otherauthors,(38–42) we registered the prevalence of low-boilingPAH, particularly NAP, recently classified as possiblycarcinogenic to humans.(16,17) The high-boiling PAH (CHRto IPY) were also present in the majority of the samples,their abundance being two to three orders of magnitudelower than the low-boiling ones. The airborne levels of singlePAH monitored, those most important for carcinogenicity,particularly BaP, reported on here, are in the same range ofthose found in Italian urban settlements.(29,43–45) However,toxicity criteria are not available for all the PAH and severalapproaches have been developed to allow the relative potencyof the different PAH to be considered in a specific riskassessment. The BaP Equivalent concentration is a methodproposed by the U.S. EPA to estimate the carcinogenicity ofa PAH mixture relative to the carcinogenicity of BaP. TheTEF can be used for estimating the relative carcinogenicity ofan environmental mixture with a known distribution of PAH.Specifically, the concentration of each carcinogenic PAHis multiplied by the appropriate TEF and then added up toprovide an estimate of the BaP Equivalent Concentration.(46)

Regarding the cancerogenic risk evaluation, in this study,we found no significant differences between asphalt workers

and ground construction operators or among different jobsin asphalt worker groups for BaP Equivalent concentration(W�7PAH), except for an upward trend in mastic asphaltoperators.

When the results of the present investigation are comparedwith those of other European studies conducted on asphaltworkers, the median levels of airborne exposure to PAH inItaly seem to be similar to those found in Norway, Sweden,and the United States,(39,42,47) but ten-fold inferior to thosefound in Finland.(38,40) The low levels of airborne PAH reportedhere could be explained by many reasons, for instance, asphaltcomposition, application technologies and, therefore, asphalttemperature. It has been observed that application temperatureis one of the most important factors in determining thechemical composition and concentration of asphalt fumes.(39)

In the present study concrete asphalt was applied, withtemperatures in the 120◦–160◦C range, with a median of130◦C.

Regarding the use of mastic asphalt, in Italy this is limited tosidewalk surfaces: though an application temperature of 230–260◦C was measured and the percentage of bitumen is higher,the amount of asphalt used is moderate. On the contrary, inFinnish studies, where mastic or remixed asphalt was applied,higher temperature ranges of 160◦–250◦C or 130◦–200◦C werereported.(38,40) Furthermore, differences in sampling and/oranalytical methods could as well contribute to some extentto the discrepancy observed. Moreover, most methods of PAHmeasurement in asphalt fumes are nonspecific, and their resultsshould be considered unreliable.(3)

In particular, sampling methods using only a membranefilter are not useful for asphalt fume PAH monitoring becauseair stripping can cause volatile fume components to be lost fromthe sampling medium. Also, the analysis performed by HPLCwith fluorimetric detection or GC/FID should not be used forbitumen fumes that contain many alkylated PAH in relativelyhigh concentration in comparison to the non-alkylated PAHinvolved because of the lack of resolution between compounds;an alternative method should be used to confirm the identity ofany suspected PAH (i.e., GC/MS).

Considering the importance of determining the total bodyburden,(41,48) we performed an evaluation of dermal exposureby six pads/man. No difference was found in the toxic contentbetween “covered” and “uncovered” pads, probably becausethe workers wore normal cotton clothes without extra protec-tive garments such as PVC or Tyvek suits.(49) The dermal con-tamination from OSM of asphalt workers is significantly higherthan those of the other group, probably owing to the use of bitu-men; moreover, it cannot be confirmed by a similar differencefor PAH contamination because this data is lacking for groundconstruction operators. According to the literature,(25) we donot find any significant difference in skin contamination, distin-guishing asphalt workers by specific tasks, except for asphaltmixing employees whose contamination is lower than in otheractivities.

The differences among body parts appear to be of smallextent, but adopting preventive measures to avoid bitumen

96 Journal of Occupational and Environmental Hygiene Supplement 2007

Dow

nloa

ded

By:

[Cirl

a, P

iero

Em

anue

le] A

t: 17

:53

11 J

uly

2007

splashes could be useful to prevent wider contaminationon wrist and ankle and to reduce cutaneous exposure. Itis difficult to estimate the quantitative implications of theabove-mentioned findings, considering some criticism of theuse of deposition pads as quantitative measures of dermalcontamination because they have a number of drawbacks (i.e.,location, material, area, etc.).

Concerns exist about a comparison between the effectivemagnitude of dose absorbed by respiratory tract and der-mal surface to determine occupational exposures to PAH.There is still no agreement on the quantitative distributionbetween the two routes and data are very limited. Of thefew authors who have carried out these determinations, mostconclude that skin contamination is the main determinant ofinternal dose, suggesting on average a contribution of 70%or more.(25,26,50–52) This is based in some cases on multipleregression analysis,(25,26) in other cases on the excreted hy-droxypyrene/inhaled pyrene ratio that exceeds the unity,(50)

or by complex models to evaluate effects of inhalation anddermal exposures on urinary metabolite excretion,(51) or finallyby study of urinary excretion of 1-hydroxypyrene, repeatingthe measures under different conditions of personal protectionequipment.(52)

But there are also studies that reduce these percentages to20–30%.(53,54) In fact, Breznicki et al.(53) estimate that underexperimental conditions the dermal absorption of airbornePYR may account for about 20% of the total absorbed dose;moreover Lafontaine et al.(54) conclude that the inhalatory trackis generally the main entrance route of pyrene for exposedpeople: the correlation was studied between pyrene inhaleddose (with assumed retention of 100%) and urinary escreted1-hydroxypyrene, taking in account the background level ofurinary metabolite concentrations that results from personallifestyle (diet and smoking).

To evaluate the potential contribution of the cutaneousroute to overall exposure, we compared Dermal Exposure Rateand Respiratory Exposure Rate. The pattern of PAH foundin pads was similar to that found in air, but data showedthat total body Dermal Exposure Rate is almost threefoldhigher than Respiratory Exposure Rate. This does not lead tothe conclusion that dermal uptake is the most relevant routeof exposure in asphalt workers. To estimate the real uptakefrom skin and lungs, it is necessary consider the toxicokineticdata (chemical specific permeability constant Kp, lag time,experimental dermal absorption data) and the hygienistic data(particle size of bitumen fume).

In particular, referring to dermal uptake, lag time is thefirst relevant parameter we must take into account when weevaluate dermal absorption during an eight hour work shift.Lag time is the time needed to achieve steady-state diffusionrate; based on data of an in vitro experiment using full thicknessmonkey skin as the membrane, but dispersing PAH into thematrix of different type lag time for percutaneous absorptionof PAH, it is in the order of 1–6 hours for naphthalene andfluorene and ranges from 10 to 31 hours for the other PAHconsidered.(55)

Moreover, available in vitro percutaneous studies haveglobally shown percutaneous absorption rate of PAH (singlecompounds or mixture) as very low after 6 hours achieving3% for naphthalene, 1% for fluorene, while for other PAHtested, lag time was longer than application time.(55) A studyconducted in vitro using human cadaver skin shows the greatestuptake for phenanthrene (absorption rate of 10% after 6 hoursand 33% after 24 hours) and for pyrene (2% after 6 hours and15% after 24 hours).(56) Sanders et al.(57) found an absorptionrate of 25% after 6 hours and 41% after 24 hours, afterapplication of a very high dose of Benzo(a)pyrene (125,000ng/cm2) and by measuring recovered radioactivity in mice.Yang et al.(58) estimated an absorption rate of 20% after 24hours from application of an anthracene dose equal to 9,300ng/cm2.

Respiratory uptake of gaseous PAH (such as naphthalene,fluorene, phenanthrene, anthracene, and pyrene) is certainlygreater and faster, so we can assume a resorption factor of70%; we can also imagine a similarly efficient absorption forparticulate PAH because a high rate of particles reaches thealveolar zone; in fact, some studies (conducted by measure-ments during field surveys and on fumes from the laboratorytest rig) have determined the particle size of bitumen fume,showing that 96–99.7% of the mass was below 12.5 μm andthat 68–89% was below 3.8 μm.(59,60)

Moreover, a study conducted in vivo on dogs revealed thatdiesel soot-absorbed Benzo(a)pyrene was absorbed throughthe alveolar epithelium quickly, in the order of minutes.(61)

Considering all this information, we believe that consid-ering dermal and respiratory uptake respectively as about20% and 70% of the dermal and respiratory exposure ratesis a suitable and cautious approximation. Based on thiswe concluded that, in the worst hypothesis, the amount ofabsorption ratio attributable to each of the two routes issimilar.

In good accordance with the low levels of airborne PAH,also OH-Py levels found in the present study are lowerthan those reported by other authors.(38,40,42,62) The post-shiftlevel of urinary OH-Py excretion in our bitumen-exposednon-smokers never exceeded the suggested no effect levelbenchmark.(63) While the creatinine adjustment can introducebiases and reduce precision due to creatinine variation with age,body mass index, physical activities and other physiologicalfactors, the results of urinary OH-Py reported in Table V andin Figure 2 are expressed in ng/g creatinine. In fact, to assessinternal exposure by a metabolite urinary concentration, thehydration state is important, mostly in presence of unfavor-able microclimatic conditions as in this case. Moreover, ourstatistical analysis showed similar results using corrected oruncorrected values.

The increase in OH-Py excretion during the workday andthe workweek, together with the observation of inter-groupdifferences at the beginning and at the end of workshift in no-smokers, suggests that OH-Py is a sensible biomarker, whichcan be used on a group basis to evidence exposure even at lowlevels of airborne PAH such as those found here.

Journal of Occupational and Environmental Hygiene Supplement 2007 97

Dow

nloa

ded

By:

[Cirl

a, P

iero

Em

anue

le] A

t: 17

:53

11 J

uly

2007

According to the literature, the other most relevant sourcesof PAH are diet and smoke.(29,64) To avoid unexpected peaksin excretion, we asked study subjects to refrain from PAH-rich food the evening before and the day of the sampling.This did not eliminate the background level due to widespreadconsumption of contaminated foods, which may be, at leastin part, responsible for the excretion of OH-Py observed inbaseline samples in either group. Moreover, this may explainthe significant correlation found between baseline OH-Py andeither before-shift or end-shift OH-Py. Also, in this study,urinary HO-Py was significantly affected by smoking habits,in accordance with the literature.(29,40,64) This effect was in thesame order of magnitude as the effect of occupational exposure.

CONCLUSION

T he results of this study show that the group of asphaltworkers studied and compared to a matched control group

experienced only slight occupational exposure to PAH. Inparticular, air concentration values of single PAH monitored,most important for carcinogenicity, showed values that canbe observed in Italian urban areas. The results of biologicalmonitoring suggest that OH-Py is a sensible biomarker, whichcan be used at low levels of PAH exposure.

ACKNOWLEDGMENTS

T his project was supported by the Italian Ministry ofEducation, University, and Research (MIUR) as a 2003

COFIN project, by the Italian Institute for Safety at Work(ISPESL, contract no. B/47/DML/03), and by the Associationfor Safety of Building Industry Workers (ASLE).

REFERENCES

1. Giua, M., and C. Lollini: Dizionario di chimica generale e industriale.Torino, Italy: Unione Tipografico Editrice Torinese, 1933.

2. Discacciati, M., and G. Filippucci: Le strade: progettazione,costruzione, manutenzione. Rome, Italy: La Nuova Scientifica, 1995.

3. National Institute for Occupational Safety and Health (NIOSH):

Hazard Review: Health Effects of Occupational Exposure to Asphalt.Cincinnati, Ohio: DHHS (NIOSH) Publication no. 2001-110, 2000.

4. CONCAWE: Bitumen and Bitumen Derivatives. Brussels: Productdossier no. 92/104, 1992.

5. Giavarini, C., and M. Scarsella: Struttura e composizione del bitume.La chimica & l’industria 75(11):754–764 (1993).

6. International Agency for Research on Cancer: IARC Monographs onthe Evaluation of Carcinogenic Risks to Humans. Overall Evaluationsof Carcinogenicity: An Updating of IARC Monographs volumes 1 to 42.Lyon, France: IARC Supplement 7, 1987.

7. International Agency for Research on Cancer: IARC Monographs onthe Evaluation of Carcinogenic Risks to Humans. Air Pollution, Part1: Some Non-Heterocyclic Polycyclic Aromatic Hydrocarbons and SomeRelated Exposures. Lyon, France: IARC Volume 92, 2005.

8. Canadian Environmental Protection Act (Government of Canada,

Environment Canada, Health Canada): Priority Substances List As-sessment Report: Polycyclic Aromatic Hydrocarbons. Ottawa, Canada:National Printers, 1994.

9. Dabestani, R., and I.N. Ivanov: A compilation of physical, spectroscopicand photophysical properties of polycyclic aromatic hydrocarbons. Pho-tochem. Photobiol. 70(1):10–34 (1999).

10. Buckley, T.J., and P.J. Lioy: An examination of the time course fromhuman dietary exposure to polycyclic aromatic hydrocarbons to urinaryelimination of 1-hydroxypyrene. Br. J.. Ind. Med. 49(2):113–24 (1992).

11. Menichini, E.: Urban air pollution by polycyclic aromatic hydrocarbons:levels and sources of variability. Sci. Total Environ. 116(1–2):109–135(1992).

12. Brandt, H., and W. Watson: Monitoring human occupational andenvironmental exposures to polycyclic aromatic compounds. Ann. Occup.Hyg. 47(5):349–78 (2003).

13. Burstyn, I., H. Kromhout, and P. Boffetta: Literature review of exposureto potential carcinogens and other agents in the road construction industry.AIHAJ. 61:715–726 (2000).

14. Jongeneelen, F.J., R.P. Bos, R.B. Anzion, J.L. Theuws, and P.T.

Henderson: Biological monitoring of polycyclic aromatic hydrocarbons.Metabolites in urine. Scand. J. Work Environ. Health 12(2):137–43 (1986).

15. Pott, P: Surgical Observations Relative to the Cataract, the Polypus ofthe Nose, the Cancer of the Scrotum, the Different Kinds of Ruptures, andthe Mortification of the Toes and Feet. London, England, 1775.

16. International Agency for Research on Cancer: IARC Monographs onthe Evaluation of Carcinogenic Risks to Humans. Some Traditional HerbalMedicines, Some Mycotoxins, Naphthalene and Styrene. Lyon, France:IARC Vol. 82 (2002).

17. National Toxicology Program (NTP): Toxicology and carcinogenesisstudies of naphthalene (case no. 91-20-3) in F344/N rats (inhalationstudies). National Toxicology Program Technical Report Series 500:1–173 (2000).

18. Boffetta, P., I. Burstyn, T. Partanen, et al.: Cancer mortality amongEuropean asphalt workers: an international epidemiological study. I.Results of the analysis based on job titles. Am. J. Ind. Med. 43:18–27(2003).

19. Boffetta, P., I. Burstyn, T. Partanen, et al.: Cancer mortality amongEuropean asphalt workers: an international epidemiological study. II.Exposure to bitumen fume and other agents Am. J. Ind. Med. 43:28–39 (2003).

20. SITEB (Associazione Italiana Bitume Asfalto Strade): Asphalt andInnovation in Europe, C. Giavarini (ed.). Rome, Italy: Artigiana Multi-stampa, 2004.

21. Cirla, P.E., I. Martinotti, E. Zito, et al.: Assessment of exposure toorganic aromatic compounds and PAH in asphalt industry: the PPTP-POPA Study results. G. Ital. Med. Lav. Ergon. 27:303–7 (2005).

22. Campo, L., M. Buratti, S. Fustinoni, et al.: Evaluation of exposure toPAHs in asphalt workers by environmental and biological monitoring.Ann. NYAS 1076:405–420 (2006).

23. Partanen, T.J., P. Boffetta, P.R. Heikkila, et al.: Cancer risk forEuropean asphalt workers. Scand. J. Work Environ. Health 21(4):252–8 (1995).

24. National Institute for Occupational Safety and Health (NIOSH):

Polynuclear aromatic hydrocarbons by HPLC:5506. In Manual of An-alytical Methods, 4th edition. Cincinnati, Ohio: NIOSH, 2002.

25. Jongeneelen, F.J., R.B. Anzion, P.T. Scheepers, et al.: 1-Hydroxypyrenein urine as a biological indicator of exposure to polycyclic aromatichydrocarbons in several work environments. Ann. Occup. Hyg. 32(1):35–43 (1988).

26. Van Rooij, J.G., J.G. De Roos, M.M. Bodelier-Bade, and F.J. Jonge-

neelen: Absorption of polycyclic aromatic hydrocarbons through humanskin: Differences between anatomical sites and individuals. J. Toxicol.Environ. Health 38(4):355–68 (1993).

27. Van Rooij, J.G., M.M. Bodelier–Bade, and F.J. Jongeneelen: Estima-tion of individual dermal and respiratory uptake of polycyclic aromatichydrocarbons in 12 coke oven workers. Br. J. Ind. Med. 50(7):623–32(1993).

28. Buratti, M., O. Pellegrino, C. Valla, F.M. Rubino, C. Verduci, and

A. Colombi: Polyurethane foam chips combined with liquid chro-matography in the determination of unmetabolized polycyclic aromatic

98 Journal of Occupational and Environmental Hygiene Supplement 2007

Dow

nloa

ded

By:

[Cirl

a, P

iero

Em

anue

le] A

t: 17

:53

11 J

uly

2007

hydrocarbons excreted in human urine. Biomed. Chromat. 20(9):971–978(2006).

29. Buratti, M., O. Pellegrino, G. Brambilla, and A. Colombi: Urinaryexcretion of 1-hydroxypyrene of exposure to polycyclic aromatic hydro-carbons from different sources. Biomarkers :368–381 (2000).

30. Dennis, M.J., R.C. Massey, G. Cripps, I. Venn, N. Howarth, and G.

Lee: Factors affecting the polycyclic aromatic hydrocarbon content ofcereals, fats and other food products. Food Addit. Contam. 517–30 (1991).

31. Bocca, B., R. Crebelli, and E. Menichini: Presenza degli idrocarburipoliciclici aromatici negli alimenti. Rome, Italy: Instituto Superiore diSanita Rapporti ISTAN n.03/22, 2003.

32. Hoffmann, D., and I. Hoffmann: The changing cigarette, 1950–1995. J.Toxicol. Environ. Health 50(4):307–64 (1997).

33. Popendorf, W.J., and J.T. Leffingwell: Regulating OP pesticide residuesfor farmworker protection. Residue Rev. 82:125–201 (1982).

34. Italian national statistic institute (ISTAT): Annuario statistico italiano2002. Roma: Instituto Poligrafico e Zecca dello Stato (ISBN 88 458 07169), (2002).

35. Wess, J.A., L.D. Olsen, and M.H. Sweeney (NIOSH): Asphalt (Bitu-men). Concise International Chemical Assessment Document 59. Geneva:WHO (2004).

36. Norseth, T., J. Waage, and I. Dale: Acute effects and exposure to organiccompounds in road maintenance workers exposed to asphalt. Am J. Ind.Med. 20(6):737–44 (1991).

37. Randem, B.G., S. Langard, J. Kongerud, et al.: Mortality from non-malignant diseases among male Norwegian asphalt workers. Am J. Ind.Med. 43:96–103 (2003).

38. Vaananen, V., M. Hameila, H. Kontsas, et al.: Air concentrations andurinary metabolites of polycyclic aromatic hydrocarbons among pavingand remixing workers. J. Environ. Monit. 5:739–746 (2003).

39. Burstyn, I., B. Randem, J.E Lien, et al.: Bitumen, polycyclic aromatichydrocarbons and vehicle exhaust: exposure levels and controls amongNorwegian asphalt workers. Ann. Occup. Hyg. 46:79–87 (2002).

40. Heikkila, P., R. Riala, M. Hameila, et al.: Occupational exposure tobitumen during road paving. AIHAJ. 63:156–165 (2002).

41. Hicks, J.B.: Asphalt industry cross-sectional exposure assessment study.Appl. Occup. Environ. Hyg. 10:840–848 (1995).

42. Jarvholm, B., G. Nordstrom, B. Hogstedt, et al.: Exposure to polycyclicaromatic hydrocarbons and genotoxic effects on nonsmoking Swedishroad pavement workers. Scand J. Work Environ. Health 25(2):131–136(1999).

43. Sciarra, G.: Valori di riferimento ambientali e biologici degli idrocarburipoliciclici aromatici. G. Ital. Med. Lav. Ergon. 25:83–93 (2003).

44. Minoia, C., S. Magnaghi, G. Micoli, et al.: Determination of environ-mental reference concentration of six PAHs in urban areas (Pavia, Italy).Sci. Total Environ. 198:33–41 (1997).

45. Pastorelli, R., M. Guanci, J. Restano, et al.: Seasonal effect onairborne pyrene, urinary 1-hydroxypyrene, and benzo(a)pyrene diolepoxide-hemoglobin adducts in the general population. Cancer Epidem.Biomarkers Prev. 8:561–565 (1999).

46. U.S. Environmental Protection Agency: Supplementary Guidance forConducting Health Risk Assessment of Chemical Mixtures. Washington,DC: U.S. EPA, 2000.

47. Watts, R.R., K.M. Wallingford, R.W. Williams, D.E. House, and

J. Lewtas. Airborne exposures to PAH and PM2.5 particles for roadpaving workers applying conventional asphalt and crumb rubber modifiedasphalt. J. Expo. Anal. Environ. Epidemiol. 8(2):213–29 (1998).

48. Vaananen, V., M. Hameila, P. Kalliokoski, et al.: Dermal exposure topolycyclic aromatic hydrocarbons among road pavers. Ann. Occup. Hyg.49:167–178 (2005).

49. Boogard, P.J., and N.J. van Sittert: Urinary 1-hydroxypyrene asbiomarker of exposure to polycyclic aromatic hydrocarbons in petrochem-ical industries: baseline values and dermal uptake. Sci. Total Environ.163:203–9 (1995).

50. Elovaara, E., P. Heikkila, L. Pyy, P. Mutanen, and V. Riihi-

maki: Significance of dermal and respiratory uptake in creosoteworkers: Exposure to polycyclic aromatic hydrocarbons and urinaryexcretion of 1-hydroxypyrene. Occup. Environ. Med. 52(3):196–203(1995).

51. McClean, M.D., R.D. Rinehart, L. Ngo, E.A. Eisen, K.T. Kelsey, and

R.F. Herrick: Inhalation and dermal exposure among asphalt pavingworkers. Ann. Occup. Hyg. 48(8):663–71 (2004).

52. Boogard, P.J., and N.J. van Sittert: Urinary 1-hydroxypyrene asbiomarker of exposure to polycyclic aromatic hydrocarbons in petrochem-ical industries: baseline values and dermal uptake. Sci. Total Environ.163(1–3):203–9 (1995).

53. Breznicki, S., M. Jakubowski, and B. Czerski: Elimination of 1-hydroxypyrene after human volunteer exposure to polycyclic aro-matic hydrocarbons. Int. Arch. Occup. Environ. Health 70:257–260(1997).

54. Lafontaine, M., J.P. Payan, P. Desault, and Y. Morele: Polycyclicaromatic hydrocarbon exposure in an artificial shooting Target factory:assessment of 1-hydroxypyrene urinary excretion as a biological indicatorof exposure. Ann. Occup. Hyg. 44:89–100 (2000).

55. Sartorelli, P., A. Cenni, G. Matteucci, et al.: Dermal exposure assess-ment of polycyclic aromatic hydrocarbons: In vitro percutaneous pene-tration from lubricating oil. Int. Arch. Occup. Environ. Health 72:528–32(1999).

56. Sartorelli, P., L. Montomoli, A.G. Sisinni, et al.: Dermal expo-sure assessment of polycyclic aromatic hydrocarbons: in vitro per-cutaneous penetration from coal dust. Toxicol. Ind. Health 17:17–21(2001).

57. Sanders, C.L., C. Skinner, and R.A. Gelman: Percutaneous absorptionof [7,10-14C]benzo(a)pyrene and [7,12-14C]dimethylbenz(a)anthracenein mice. Environ. Res. 33:353–60 (1984).

58. Yang, J.J., T.A. Roy, and C.R. Mackerer: Percutaneous absorption ofanthracene in the rat: comparison of in vivo and in vitro results. Toxicol.Ind. Health 2:79–84 (1986).

59. Calzavara, T.S., C.M. Carter, and C. Axten: Air sampling methodologyfor asphalt fume in asphalt production and asphalt roofing manufacturingfacilities: total particulate sampler versus inhalable particulate sampler.Appl. Occup. Environ. Hyg. 18:358–67 (2003).

60. Brandt, H.C.A., P.C. De Groot, M.K.B. Molyneux, and P.E. Tindle:

Sampling and analysis of bitumen fumes. Ann. Occup. Hyg. 29:27–80(1985).

61. Gerde, P., B.A. Muggernburg, M. Lundborg, and A.R. Dahl: The rapidalveolar absorption of diesel soot-adsorbed benzo(a)pyrene: bioavailabil-ity, metabolism and dosimetry of an inhaled particle-borne carcinogen.Carcinogenesis 22:741–9 (2001).

62. McClean, M.D., R.D. Rinehart, L. Ngo, et al.: Urinary 1-hydroxypyreneand polycyclic aromatic hydrocarbon exposure among asphalt pavingworkers. Ann. Occup. Hyg. 48(6):565–78 (2004).

63. Jongeneelen, F.J.: Benchmark guideline for urinary 1-hydroxypyrene asbiomarker of occupational exposure to polycyclic aromatic hydrocarbons:Ann. Occup. Hyg. 45:3–13 (2001).

64. Van Rooij, J.G., M.M. Veeger, M.M. Bodelier-Bade, and F.J. Joge-

neelen: Smoking and dietary intake of polycyclic aromatic hydrocarbonsas sources of interindividual variability in the baseline excretion of 1-hydroxypyrene in urine. Int. Arch. Occup. Environ. Health 66:55–65(1994).

Journal of Occupational and Environmental Hygiene Supplement 2007 99