Lung cancer risk from PAHs emitted from biomass combustion Dimosthenis Α. Sarigiannis a,b,n , Spyros P. Karakitsios a,b , Dimitrios Zikopoulos a , Spyridoula Nikolaki a , Marianthi Kermenidou a a Aristotle University of Thessaloniki, Department of Chemical Engineering, Environmental Engineering Laboratory, 54124 Thessaloniki, Greece b Centre for Research and Technology Hellas, Chemical Process and Energy Resources Institute, Natural and Renewable Resource Exploitation Laboratory, 57001 Thessaloniki, Greece article info Article history: Received 13 November 2014 Received in revised form 9 December 2014 Accepted 11 December 2014 Keywords: PAH exposure Biomass burning Human respiratory tract deposition model- ing Internal dose Lung cancer risk Children susceptibility abstract This study deals with the assessment of the cancer risk attributable to PAH exposure, attributable to the increased use of biomass for space heating in Greece in the winter of 2012–2013. Three fractions of particulates (PM1, PM2.5 and PM10) were measured in two sampling sites (urban/residential and traffic- influenced) followed by chemical analysis of 19 PAHs and levoglucosan (used as a biomarker tracer). PAH-induced lung cancer risk was estimated by a comprehensive methodology that incorporated human respiratory tract deposition modelling in order to estimate the toxic equivalent concentration (TEQ) at each target tissue. This allowed us to further differentiate internal exposure and risk by age groups. Results showed that all PM fractions are higher in Greece during the cold months of the year, mainly due to biomass use for space heating. PAH and levoglucosan levels were highly correlated, indicating that particles emitted from biomass combustion are more toxic than PM emitted from other sources. The estimated lung cancer risk was non-negligible for residents close to the urban background monitoring site. Higher risk was estimated for infants and children, due to the higher bodyweight normalized dose and the human respiratory tract (HRT) physiology. HRT structure and physiology in youngsters favor deposition of particles that are smaller and more toxic per unit mass. In all cases, the estimated risk (5.7E 07 and 1.4E 06 for the urban background site and 1.4E 07 to 5.0E 07 for the traffic site) was lower to the one estimated by the conventional methodology (2.8E 06 and 9.7E 07 for the urban background and the traffic site respectively) that is based on Inhalation Unit Risk; the latter assumes that all PAHs adsorbed on particles are taken up by humans. With the methodology proposed herein, the estimated risk presents a 5–7 times difference between the two sampling sites (depending on the age group). These differences could not have been identified had we relied only on conventional risk as- sessment method. Consequently, the actual cancer risk attributable to PAHs on PM emitted from biomass burning would have been significantly underestimated. & 2014 Elsevier Inc. All rights reserved. 1. Introduction Several epidemiological studies have shown the adverse health effects of airborne particulate matter deposited in the human respiratory tract (HRT) (Kennedy, 2007; Pope III and Dockery, 2006). HRT deposition of a particular particle depends on its aerodynamic diameter (d p ). Particulate matter can be divided to coarse particles (d p 42.5 μm), which are mainly deposited in the Contents lists available at ScienceDirect journal homepage: www.elsevier.com/locate/envres Environmental Research http://dx.doi.org/10.1016/j.envres.2014.12.009 0013-9351/& 2014 Elsevier Inc. All rights reserved. Abbreviations: 2-MeN, 2-methylnapthalene; Ace, acenaphthene; Acy, acenapthylene; B[a]P, benzo[a]pyrene; B[a]Peq, equivalent concentration of benzo[a]pyrene, ng/m 3 ; BaA, benzo[a]anthracene; BeP, benzo[e]pyrene; BgP, benzo[g,h,i]perylene; BPDE, benzo[a]pyrene diol-epoxide; BW i , body weight of age group i, kg; CEPA, California En- vironmental Protection Agency; Chr, chrysene; DbA, dibenzo[a,h]anthracene; DCM, dichloromethane; DF, deposition fraction; d p , particle diameter, μm; EPA, US Environ- mental Protection Agency; Fla, fluoranthene; Flu, fluorene; FRC, functional residual capacity; GC, gas chromatography; HRT, human respiratory tract; IARC, International Agency for Research on Cancer; ICR, inhalation cancer risk; ICR, inhalation cancer risk; IDL, instrumental detection limit; Ind, indeno[1,2,3-cd]pyrene; IR i , weighted average daily inhalation rate i,m 3 /day; IUR, inhalation unit risk; IUR B[a]P , inhalation unit risk for B[a]P, m 3 /μg; LOQ, limit of quantification; MPPD, multiple path particle deposition model; MS, mass spectroscopy; MSD, mass spectroscopy detector; PAH, polycyclic aromatic hydrocarbon; Per, perylene; PM, particulate matter; PTFE, polytetra- fluoroethylene; Pyr, pyrene; RV, residual volume; TB, tracheobronchial region; TEF, toxic equivalent factors; TEQ, toxic equivalencyconcentration; TLC, total lung capacity; TV, tidal volume; URT, upper respiratory tract; VC, vital capacity; Νap, naphthalene; Ρ, pulmonary region n Correspondence to: Environmental Engineering Laboratory, Department of Chemical Engineering, Aristotle University of Thessaloniki, University Campus, Bldg. D, Rm 201, 54124 Thessaloniki, Greece. E-mail address: denis@eng.auth.gr (D.Α. Sarigiannis). Environmental Research 137 (2015) 147–156