Marc Fadel
email: marc.fadel@net.usj.edu

Frédéric Ledoux

Charbel Afif

Dominique Courcot
email: dominique.courcot@univ-littoral.fr

Human health risk assessment for PAHs, phthalates, elements, PCDD/Fs, and DL-PCBs in PM2.5 and for NMVOCs in two East-Mediterranean urban sites under industrial influence

Keywords: PM2.5, NMVOCs, carcinogenic risk, exposure pathways, non-carcinogenic risk

ou non, émanant des établissements d'enseignement et de recherche français ou étrangers, des laboratoires publics ou privés.

Introduction

According to the World Health Organization (WHO), air pollution is responsible for about 11% of the worldwide deaths annually, and therefore considered as the biggest environmental threat to human health [START_REF] Who | Ambient air pollution : a global assessment of exposure and burden of disease[END_REF]. The international Agency for Research on Cancer (IARC) classified outdoor air pollution as well as different chemicals found in the atmosphere (chromium (VI), arsenic, cadmium, nickel, benzo[a]pyrene, benzene, 1,3-butadiene, 2,3,4,7,8-pentachlorodibenzofuran, and 2,3,7,8tetrachlorodibenzo-para-dioxin) as Group I "carcinogenic to humans" [START_REF] Loomis | The carcinogenicity of outdoor air pollution[END_REF].

Inhalation, oral ingestion, and dermal absorption are the three major routes of both intentional and accidental exposure to atmospheric chemicals. Vapor-phase and fine respirable particulate matter can travel into the respiratory system by adhering to the walls of the respiratory tract or penetrating deep into the lungs [START_REF] Díaz | Health risk by inhalation of PM2.5 in the metropolitan zone of the City of Mexico[END_REF]. However, the non-respirable particulates usually enter the human body via the oral ingestion route. The dermal absorption is possible for different physical forms. Particles -especially fine and ultrafine ones (having an aerodynamic diameter less than 2.5 and 0.1 µm, respectively) -exposure to the respiratory tract has been associated with various health problems such as asthma, chronic obstructive pulmonary disease, cardiovascular diseases and lung cancer [START_REF] Alkoussa | Extracellular vesicles as actors in the air pollution related cardiopulmonary diseases[END_REF][START_REF] Cochard | Atmospheric fine particulate matter and epithelial mesenchymal transition in pulmonary cells: state of the art and critical review of the in vitro studies[END_REF][START_REF] Goldberg | A systematic review of the relation between long-term exposure to ambient air pollution and chronic diseases[END_REF][START_REF] Thurston | A joint ERS/ATS policy statement: what constitutes an adverse health effect of air pollution? An analytical framework[END_REF].

Health risk assessment studies aim at evaluating the potential health effects resulting from human exposure to any source of risk or particular hazard (DoHA, 2012). This approach can be applied in a qualitative or quantitative way. In order to evaluate the severity of the exposure, it takes generally into account several factors such as the dose or intake, the characteristics of the exposed individuals, the duration and the frequency of the exposure, and other parameters related to the harmfulness of the compounds on human health. The evaluation of the health risks associated with exposure to atmospheric pollutants is of utmost importance as it can lead to developing effective risk management policies and strategies for a population [START_REF] Chen | Assessment of heavy metal pollution characteristics and human health risk of exposure to ambient PM2.5 in Tianjin, China[END_REF][START_REF] Samet | Health Effects Associated With Exposure to Ambient Air Pollution[END_REF].

The East Mediterranean is the third region with the highest ambient and household air pollution attributable death rate (age-standardized), scoring an average of 125 per 100,000 population in 2016, after Africa (181) and South East Asia (166), while this number could tend to rise in the future with the increase of the aerosol concentrations due to climate change [START_REF] Lelieveld | Model projected heat extremes and air pollution in the eastern Mediterranean and Middle East in the twenty-first century[END_REF]. Lebanon, an East Mediterranean country, faces extensive urbanization with heavy traffic, installation of diesel private generators within neighborhoods with no law enforcement, dust events, open waste burning, along with emissions from different types of industries [START_REF] Waked | An atmospheric emission inventory of anthropogenic and biogenic sources for Lebanon[END_REF]. The air quality in the country is considered unsafe as exceedances in PM2.5 concentrations above WHO guidelines of 25 µg/m 3 are recorded [START_REF] Moe | Lebanon's National Strategy for Air Quality Management for[END_REF] with more than 170 days in 2014 in Greater Beirut area. In order to evaluate the impact of air quality on human health in Lebanon, different approaches were tackled. Epidemiological studies were carried out to determine the association between outdoor air quality and different diseases such as chronic obstructive pulmonary diseases, chronic bronchitis, cardiovascular diseases and lung cancer [START_REF] Aoun | Lung cancer correlates in Lebanese adults: a pilot case-control study[END_REF][START_REF] Kobrossi | Respiratory health effects of industrial air pollution on children in North Lebanon[END_REF][START_REF] Nakhlé | Short-term relationships between emergency hospital admissions for respiratory and cardiovascular diseases and fine particulate air pollution in Beirut, Lebanon[END_REF][START_REF] Nasser | Outdoor air pollution and cardiovascular diseases in Lebanon: a case-control study[END_REF][START_REF] Salameh | Exposure to outdoor air pollution and chronic bronchitis in adults: a case-control study[END_REF]. These studies were based on questionnaires filled by hospital patients and air quality data. More recently, studies dealing with PM2.5 from different areas in Lebanon [START_REF] Abbas | In vitro evaluation of organic extractable matter from ambient PM2.5 using human bronchial epithelial BEAS-2B cells: Cytotoxicity, oxidative stress, proinflammatory response, genotoxicity, and cell cycle deregulation[END_REF][START_REF] Badran | Toxicity of fine and quasi-ultrafine particles: Focus on the effects of organic extractable and non-extractable matter fractions[END_REF][START_REF] Borgie | Comparison between ultrafine and fine particulate matter collected in Lebanon: Chemical characterization, in vitro cytotoxic effects and metabolizing enzymes gene expression in human bronchial epithelial cells[END_REF][START_REF] Melki | Physicochemical characteristics, mutagenicity and genotoxicity of airborne particles under industrial and rural influences in Northern Lebanon[END_REF] evidenced, on pulmonary cells in vitro, toxic effects of PM depending on the size and the composition of the particles.

PM atmospheric concentration is a widely used indicator of the air quality level.

However, a high share of PM mass consists of compounds with low toxicity such as ammonium, sulfate, nitrate, sea salt, and crustal dust elements [START_REF] Borm | Oxidant generation by particulate matter: from biologically effective dose to a promising, novel metric[END_REF]. On the other hand, species that barely contribute to PM mass such as transition metals and organic species can have a major impact on the aerosols' toxicity [START_REF] Bandowe | Nitrated polycyclic aromatic hydrocarbons (nitro-PAHs) in the environment -A review[END_REF][START_REF] Chen | Effects of Metals within Ambient Air Particulate Matter (PM) on Human Health[END_REF]. Among organic species, phthalates and PCDD/Fs are considered toxic to humans and were identified as endocrine disruptors and contributing to reproductive toxicity [START_REF] Marquès | Concentrations of PCDD/Fs in Human Blood: A Review of Data from the Current Decade[END_REF][START_REF] Tsatsakis | Phthalates: Exposure and Health Effects[END_REF]. [START_REF] Rengarajan | Exposure to polycyclic aromatic hydrocarbons with special focus on cancer[END_REF] reported that the long-term exposure to mixtures of PAHs can increase the risks of mainly lung and skin, but also bladder and gastrointestinal cancers. That is why it is important to evaluate the risk of exposure to PM not as whole but based on its chemical composition. Therefore, most of the studies found in the literature focused on the evaluation of the health risk related to the exposure to a specific family of compounds in PM such as elements, PAHs, and phthalates [START_REF] Bai | Pollution characteristics, sources and health risk assessment of polycyclic aromatic hydrocarbons in PM2.5 in an office building in northern areas, China[END_REF][START_REF] Murari | Source apportionment and health risk assessment of airborne particulates over central Indo-Gangetic Plain[END_REF][START_REF] Zhang | PM2.5 bound phthalates in four metropolitan cities of China: Concentration, seasonal pattern and health risk via inhalation[END_REF] or for Volatile Organic Compounds (VOCs) [START_REF] Dhaini | Quantitative cancer risk assessment and local mortality burden for ambient air pollution in an eastern Mediterranean City[END_REF].

Therefore, the aims of this work were as follow: (1) evaluate the cancer and non-cancer health risks based on a one-year PM2.5 and NMVOCs field campaign in two urban industrial areas, (2) compare the risks associated with the different exposure pathways and different age categories, and (3) compare the risks associated with the different classes of compounds such as polycyclic aromatic hydrocarbons (PAHs), phthalates, major and trace elements, non-methane volatile organic compounds (NMVOCs), dioxins, furans, and dioxin-like polychlorobiphenyls. This study will be a first evaluating the health impact of the different classes of compounds (organic and inorganic) from particulate and gas phases for the different exposure pathways and for different age categories.

Materials and methods

Site description and sample collection

The description of the sampling sites was detailed elsewhere [START_REF] Fadel | PM2.5 characterization of primary and secondary organic aerosols in two urban-industrial areas in the East Mediterranean[END_REF] and will be shortly presented here. PM2.5 and NMVOC samples were collected in two urbanindustrial sites in Lebanon: Zouk Mikael (33˚57'57.07''N 35˚37'09.46''E) at a rooftop of a 15 m-residential building, and Fiaa in Chekka region (34˚20'47.8''N 35˚47'14.0''E) collocated with the ambient air quality monitoring station of the Lebanese Ministry of Environment. The locations of the sites were chosen taking into account the topography, the existence of residents, micro siting (buildings, traffic, etc.) to represent the air quality background in the study areas.

The Zouk Mikael site (ZK) is characterized by a high residential density (4,200 inhabitants/km 2 ) along with the biggest power plant in Lebanon which runs on Heavy Fuel Oil (HFO), an important number of private generators, and traffic. The Fiaa site (FA) is less populated (250 inhabitants/km 2 ) with moderate traffic activity and some private generators. The major industrial activities around FA site are related to three cement industries (distant between 5 and 7 km from the sampling site) in the region along with their corresponding quarries and a sulfuric acid and phosphate fertilizer industry (15 km from the sampling site) in Selaata (Fig. 1).

Fig. 1 Location of the two sampling sites: Zouk Mikael (ZK) and Fiaa (FA) and the position of the nearby industries A total of 98 and 95 PM2.5 samples were collected on a 24-hour basis every third day at ZK and FA, respectively from the 13 th of December 2018 to the 15 th of October 2019. The sampling was carried out using high volume samplers operating at 30 m 3 /h, onto 150 mm pure quartz microfibers filters. Prior to sampling, the filters were heated for 12 hours at 550˚C to remove the organic impurities.

In addition, non-methane VOCs (NMVOCs) were collected using passive radial diffuse samplers (Radiello-Code 120) and by following the guidelines of the manufacturer of Radiello diffusive passive sampler (Fondazione Salvatore Maugeri, IRCCS, Padova, Italy).

The samples were placed for 4 weeks at both sites (11 samples per site). The cartridges were then kept at 4°C away from solvent until the analysis.

As for the 1,3-butadiene, the compound was trapped using Carbopack X diffusion tubes from Gradko International (Winchester, England) also over 4 weeks and a total of 9 samples per site were collected. Once the sampling completed, the tubes were returned to the company for the analysis.

Analysis of NMVOCs

NMVOCs were chemically extracted from cartridge by adding 2 mL of CS2 and 100 µL of 2-fluorotoluene as internal standard in the Radiello glass tube without drawing out the cartridge. The solution was stirred from time to time for 30 min before discarding the cartridge, then filtered using PTFE Whatman filter (0.2 µm). 2 µL of the solution was injected in the GC-MS (ISQ 7000, Thermo Scientific, United States of America) operating in the split mode with a split ratio of 25. The GC was equipped with a 100% dimethyl polysiloxane column (50 m x 0.2 mm x 0.5 µm, Supelco, United States of America). The column temperature program consisted of an injection at 35˚C hold for 5 min, a ramp of temperature corresponding to 1˚C/min up to 135˚C followed by another ramp of temperature of 5˚C/min up to 250 ˚C and finally an isothermal hold step at 250 ˚C for 7 min. The GC was interfaced to an ion trap MS with an external electron ionization (EI) source (220 ˚C, 70 eV). The identification of the compounds was made by comparing their retention times and their mass spectrum (full scan mode, range 25-350 m/z) to the authentic standards. The concentrations of the compounds (in ng/m 3 ) were calculated using Eq.1 provided by the manufacturer of Radiello diffusive passive sampler (Fondazione Salvatore Maugeri-IRCCS, Padova, Italy):

= × × 10 ( . 1)
Where C is the average concentration in µg/m 3 , m is the mass of analyte in µg, t is the exposure time in minutes, and Qk is the sampling rate expressed in mL/min.

Field blanks and laboratory blanks were analyzed following the the same procedures as the sampling cartridges. The regression coefficient for the calibration curves was in the range of 0.96 -0.99 for the different compounds.

1,3-butadiene quantification was achieved by the Gradko International company (Winchester, England). The analysis has been carried out in accordance with in-house method GLM 13-6 under UKAS fixed scope accreditation using a thermal desorption-gas chromatography coupled to a mass spectrometer (TD-GC-MS).

Chemical characterization of PM2.5

PAHs and phthalates were extracted by a mixture of acetone/dichloromethane and analyzed by GC/MS (ISQ 7000, Thermo Scientific, United States of America) using the method described in [START_REF] Fadel | PM2.5 characterization of primary and secondary organic aerosols in two urban-industrial areas in the East Mediterranean[END_REF]. Major and trace elements were extracted by a mixture of HNO3/HF/HClO4 and quantified using Inductively Coupled Plasma-Atomic Emission Spectrometry (ICP-AES, iCAP 6000 series, Thermo Scientific, United Kingdom)

for Al, Ba, Fe, Mn, Ni, Sr, Zn and Pb, and ICP-Mass Spectrometry (ICP-MS, Agilent 7900, Varian, United States of America) for elements such as As, Cd, Co, Sn, Cu, Cr, Sb, V, La, and

Tl. The method is detailed in [START_REF] Kfoury | PM2.5 source apportionment in a French urban coastal site under steelworks emission influences using constrained non-negative matrix factorization receptor model[END_REF][START_REF] Ledoux | Characterization of iron and manganese species in atmospheric aerosols from anthropogenic sources[END_REF] [START_REF] Borgie | Comparison between ultrafine and fine particulate matter collected in Lebanon: Chemical characterization, in vitro cytotoxic effects and metabolizing enzymes gene expression in human bronchial epithelial cells[END_REF]. The apparatus used is a high-resolution gas chromatography coupled to a highresolution mass spectrometer (HRGC/HRMS).

2.4 Toxic equivalent concentrations for PAHs and PCDD/Fs and DL-PCBs 2.4.1 2,3,7,8-TCDD equivalents 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) is known to be a human carcinogen, highly persistent and widespread environmental contaminant (NTP, 2016). A toxic equivalent factor (TEFi) was introduced to assign toxicity values for the different congeners (PCDD/Fs and DL-PCBs) based on the toxicity of 2,3,7,8-TCDD reported as 1 (Van den [START_REF] Van Den Berg | The 2005 World Health Organization reevaluation of human and Mammalian toxic equivalency factors for dioxins and dioxin-like compounds[END_REF]. The toxic equivalent "TEQ" representing an equivalent concentration of 2,3,7,8-TCDD is calculated following Eq. 2 by summing the product of the congeners' concentration (Ci) multiplied by its corresponding TEF values (TEFiunitless) (Table S1).

TEQ = C × TEF (Eq. 2)

Benzo[a]pyrene equivalents

Among the different PAHs, benzo[a]pyrene has been classified as group I "Carcinogenic to humans" by the IARC. Upon that, the B[a]P equivalent concentration (B a P "# ) is often used to characterize the level of toxicity associated with PAHs. It is calculated as follows:

B a P "# = C $ × TEF $ $ (Eq. 3)
Where & is the concentration of the PAHs (ng/m 3 ) and TEF $ (unitless) is the corresponding Toxic Equivalency Factor for each PAH compared to B[a]P (TEF for B[a]P is 1) proposed by [START_REF] Nisbet | Toxic equivalency factors (TEFs) for polycyclic aromatic hydrocarbons (PAHs)[END_REF] and listed in Table S2.

Health Risk assessment

The health risk assessment was based on the Human health evaluation guidelines proposed by the United States Environmental Protection Agency (USEPA, 1989(USEPA, , 1991(USEPA, , 2011) ) and was performed for different age categories: newborns (0 to <1 year), children

(1 to <12 years), adolescents (12 to <18 years) and adults (18 to 70 years), and for three exposure pathways: inhalation, ingestion, and dermal absorption on exposed skin when data were available. The average concentrations of the species on the sampling period were considered for the health risk assessment assuming that they represent a typical yearly concentration of the pollutants in the atmosphere of the considered sites.

Non-cancer risk assessment

The assessment of the non-carcinogenic risk resulting from exposure to a chemical was based on the comparison between the exposure estimate such as the average daily dose (ADDi) to the reference dose (RfDi) both expressed in mg/kg/day or the comparison of the exposure concentration in air (ECi) to the reference concentration for inhalation (RfCi) expressed in mg/m 3 . These ratios are known as hazard quotients (HQi) and are calculated following one of the formulas of Eq. 4 depending on the availability of RfDi or RfCi in the literature (USEPA, 1989(USEPA, , 1991(USEPA, , 2011)):

' ( = )** ( +,* ( -. ' ( = ( +, ( ( . 4)
With ADDi for the different exposure pathways and ECi for inhalation estimated as follows (Eq. 5 to Eq. 8):

)** (0(123435(61 = ( × 7+ (12 × * × 8 × 10 0 9: × ); ( . 5)

)** (0(1=>?5(61 = ( × 7+ (1= × * × 8 × 10 0 9: × ); ( . 6)

)** (0A>BC34 = ( × D) × )8 × )9D × * × 8 × 10 0 9: × ); ( . 7) ( = ( × ; × 8 × * × 10 0 ); ( . 8)
Detailed information of each parameter used in the different formulas is given in Table 1 for newborns, children, adolescents, and adults. Values for RfDi and RfCi are presented in Table S3 for the different exposure pathways.

Total HQi is defined as the non-carcinogenic risk for a certain compound in the different exposure pathways assuming additive effects (Eq. 9) and calculated as follows:

;-GH ' ( = ' (0(123435(61 + ' (0(1=>?5(61 + ' (0A>BC34 ( . 9)

On the other hand, a receptor may be exposed to a specific family of chemicals associated with non-carcinogenic effects. Accordingly, a hazard index (HI) for a family of chemicals is defined as the total non-carcinogenic hazard for each exposure pathway and calculated as follows (Eq.10): Finally, in order to evaluate the total non-carcinogenic risk for a specific family for the combined exposure pathways, the total hazard index (THI) is calculated as follows (Eq.

11):

;-GH '7 = ; '7 = '7 (123435(61 + '7 (1=>?5(61 + '7 A>BC34 ( . 11) Generally, the higher the HQi, total HQi, HI and Total HI values above 1, the greater is the level of concern and the higher the probability of occurrence for hazardous noncarcinogenic effects (USEPA, 2011).

Cancer risk assessment

The risk estimates of carcinogenic chemicals represent the incremental probability that an individual might develop cancer over a lifetime as a result of a specific exposure to a carcinogenic chemical. The risks for inhalation and other pathways are calculated following (Eq. 12). CSFi is the cancer slope factor for a chemical in a specific exposure pathway expressed in kg•day/mg. IURi is the inhalation unit risk for a chemical expressed in m 3 /mg used to calculate the cancer risk associated with the inhalation pathway (USEPA, 1997). CSFi and IURi values are presented in Table S3.

+ (0(123435(61 = ( × 7L+ ( -.
+ (0(1=>?5(61/A>BC34 = M)** ( × D8 ( ( . 12)

When considering carcinogenic species, the exposure period during which the dose is averaged is usually lifetime or 70 years. Accordingly, the lifetime average daily dose (LADDi) calculation equations for the different exposure pathways take the form of (Eq. 5 to 8) with lifetime (25,500 days) replacing the average timing (ED x 365 days) (USEPA, 1989(USEPA, , 2011)).

To estimate the carcinogenic risk for a certain compound for the three exposure pathways, total CRi was calculated as follows (Eq.13):

;-GH + ( = + (0(123435(61 + + (0(1=>?5(61 + + (0A>BC34 ( . 13)

The total cancer risk for a specific family of chemicals associated with an exposure pathway is estimated as follows (Eq.14):

+ (

Results and discussion

Atmospheric concentrations of the compounds

The average concentrations of PAHs, phthalates, and elements in PM2.5 and NMVOCs are presented in Table 2 for ZK and FA sites. The concentrations of individual PAHs as well as phthalates were presented in details in [START_REF] Fadel | PM2.5 characterization of primary and secondary organic aerosols in two urban-industrial areas in the East Mediterranean[END_REF]. Finally, for NMVOCs, the highest concentrations are observed for benzene, toluene, ethylbenzene and xylenes. Between these compounds, toluene showed the highest concentrations at both sites and 1,3-butadiene showed the lowest concentrations at ZK and was not detected at FA (Table 2).

These species have been used for the evaluation of the carcinogenic and the noncarcinogenic risk due to their adverse health effects and the availability of reference values (RfD, RfC, CSF, and IUR) in the literature (Table S3).

Health risk evaluation

The hazard quotient (HQi) and the cancer risk (CRi) associated with each species in the three exposure pathways for the different age categories are reported in Table S4 and Table S5 for ZK and FA, respectively. Furthermore, the total hazard index (THI) and the cumulative cancer risk (CCR) for PAHs and TCDD equivalents along with total HQi and total CRi for phthalates, elements, and NMVOCs were summarized for ZK in Table S6 and for FA in Table S7.

Polycyclic Aromatic Hydrocarbons

The PAHs in this study were only analyzed in the particulate phase. Even though PAHs concentrations are usually higher in the gas phase according to the literature in other Mediterranean sites such as in Turkey and Greece [START_REF] Akyüz | Gas-particle partitioning and seasonal variation of polycyclic aromatic hydrocarbons in the atmosphere of Zonguldak, Turkey[END_REF][START_REF] Gaga | Gas-particle partitioning and health risk estimation of polycyclic aromatic hydrocarbons (PAHs) at urban, suburban and tunnel atmospheres: Use of measured EC and OC in model calculations[END_REF][START_REF] Vasilakos | Gasparticle concentration and characterization of sources of PAHs in the atmosphere of a suburban area in Athens, Greece[END_REF] The non-cancer risk for PAHs was evaluated for ingestion and inhalation pathways.

Exposure to PAHs via inhalation exhibited the highest risk for the different age categories contributing to more than 80% of the total HI (Tables S4 andS5). At both sites, the total HI value related with the exposure to the PM2.5-bound PAHs was <1 (acceptable risk), with a higher value for adolescents (0.43 at ZK and 0.11 at FA) then adults (0.42 at ZK and 0.10 at FA), then come the newborns (0.37 at ZK and 0.10 at FA) and the children (0.34 at ZK and 0.09 at FA) (Tables S6 andS7).

The cumulative cancer risk associated with exposure to PM2.5-bound PAHs via ingestion, inhalation and dermal contact were evaluated (Tables S6 andS7). The results showed that the values exceeded the potential risk value recommended by USEPA (10 -6 ) except for newborns at FA with a trend of children (1.5 x 10 -5 at ZK and 4.1 x 10 -6 at FA) > adults (1.4 x 10 -5 at ZK and 3.9 x 10 -6 at FA) > adolescents (3.8 x 10 -6 at ZK and 1.0 x 10 -6 at FA) > newborns (2.5 x 10 -6 at ZK and 7 x 10 -7 at FA), showing a potential cancer risk at these PAHs concentration exposure levels (Fig. 2). The cumulative cancer risk values reported for children and adults at both sites were higher than those reported for a site in Thailand (6.1 x 10 -9 -7.7 x 10 -9 for children and 1.3 x 10 -8 -1.4 x 10 -8 for adults)

having lower B[a]Peq concentration (0.06-0.07 ng/m 3 ) [START_REF] Pongpiachan | Incremental Lifetime Cancer Risk of PM2.5 Bound Polycyclic Aromatic Hydrocarbons (PAHs) Before and After the Wildland Fire Episode[END_REF]. In terms of exposure pathways, ingestion and dermal contact were the main exposure routes leading to cancer risk (2.0 x 10 -6 and 3.8 x 10 -7 at ZK, 5.3 x 10 -7 and 1.0 x 10 -7 at FA, respectively), which were at least three times higher than the inhalation pathway (9.4 x 10 -8 at ZK and 2.5 x 10 -8 at FA) (Table 4, Table 5). The CR values from inhalation were lower than those reported for a site characterized by high traffic density and industrial activities (4 x 10 -7 -8.4 x 10 -5 ), but also an urban Indian site with values in the range of 10 -6 [START_REF] Fang | PM2.5-Bound Polycyclic Aromatic Hydrocarbons: Sources and Health Risk during Non-Heating and Heating Periods (Tangshan, China)[END_REF][START_REF] Kumar | Source identification and health risk assessment of atmospheric PM2.5-bound polycyclic aromatic hydrocarbons in Jamshedpur, India[END_REF]. These differences are mostly related to PM2.5bound PAHs concentrations (87-608 ng/m 3 ) that were at least 80 times higher than the ones at our study (2.56 ng/m 3 at ZK and 0.95 ng/m 3 at FA).

The lifetime cancer risk values for the exposure to PAHs were 1.4 x 10 -5 at ZK and 3.7 x 10 -6 and FA, exceeding the threshold limit of 10 -6 . PAHs can be metabolized and can react as electrophilic intermediates capable of forming PAH-DNA adduct, considered as biomarker of DNA damage and that has been linked to cancer [START_REF] Veglia | Bulky DNA adducts and risk of cancer: a metaanalysis. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research[END_REF]. The observed concentrations of these species at both sites were mainly attributed to combustion processes such as vehicular emissions, biomass burning, and power plants [START_REF] Fadel | PM2.5 characterization of primary and secondary organic aerosols in two urban-industrial areas in the East Mediterranean[END_REF]. These results show that exposure to these PAHs emitted from various anthropogenic activities could be responsible for 14 and 4 additional cancer cases per million habitats at ZK and FA, respectively. Reducing PAHs concentrations, especially from these combustion sources can largely reduce the CCR attributed to PAHs exposure for the inhabitants.

Phthalates

Among the analyzed phthalates, BEHP was classified by the IARC as possibly carcinogenic to humans (group 2B) due to sufficient evidence for carcinogenicity in the liver of animals but little evidence of possible association between BEHP and liver cancer in humans [START_REF] Rusyn | Mechanistic considerations for human relevance of cancer hazard of di(2-ethylhexyl) phthalate[END_REF]. On the other hand, butyl benzyl phthalate (BBP) was classified as non-carcinogenic (group 3), and other phthalate esters such as DBP were not assessed (IARC, 2004). As for the non-carcinogenic effects, asthma and allergies were reported to be linked to exposure to BEHP and BBP, respectively [START_REF] Jaakkola | The role of exposure to phthalates from polyvinyl chloride products in the development of asthma and allergies: a systematic review and meta-analysis[END_REF]. In this study, the cancer risk of BEHP and the non-cancer risk of DBP and BEHP were studied.

The total HI values, corresponding here to the HI value for ingestion as no RfCi or RfDi were found for these phthalates for inhalation or dermal contact, ranged between 10 -2 and 10 -3 for the different age categories at both sites resulting in a negligible non-cancer risk (<1).

As for the cancer risk, the only contributor was BEHP. CR values were higher for the ingestion pathway compared to inhalation: 6 times higher for an adult and 18 times higher for a newborn. Conversely, CR for inhalation, ingestion, and cumulative CR (inhalation + ingestion; no value for dermal) presented low cancer risk with values below 10 -6 . The CR values for inhalation at both sites (3.9 x 10 -9 at ZK and 5.2 x 10 -9 at FA) (Table 4, Table 5) were in the interval of estimated carcinogenic risk reported by Li et al. ( 2019) for a regional background site (8.9 x 10 -10 -7.4 x 10 -9 ). The cumulative CR values for BEHP found in this study were higher than the ones reported by Ma et al.

(2020) for a Chinese city (in the range of 10 -10 ). Although the concentration of BEHP (54.8 ng/m 3 ) in the latter study was close to those reported in ZK and FA, the exposure parameters were different especially for body weight that was reported as 15 kg for a child and 58.6 kg for an adult along with the inhalation rate (7.8 m 3 /day for a child and 12.8 m 3 /day for an adult). The lifetime cancer risk from exposure to BEHP was 3.8 x 10 -7

for ZK and 5.1 x 10 -7 for FA.

Phthalates are generally released into the atmosphere during open burning of plastics [START_REF] Simoneit | Combustion Products of Plastics as Indicators for Refuse Burning in the Atmosphere[END_REF]. Based on the total HI and the cumulative CR values, the risk associated with human exposure to PM2.5-bound phthalates were relatively low.

However, these compounds should be monitored by reducing open burning of plastics because the exposure to these species even at doses lower than the RfD might be linked to adverse health problems [START_REF] Chen | Phthalate exposure, even below US EPA reference doses, was associated with semen quality and reproductive hormones: Prospective MARHCS study 32 in general population[END_REF].

Dioxins, furans and dioxin-like polychlorobiphenyls

TEQ values were calculated for every class of compounds along with total TEQ (Table 3). Although contributions in terms of concentrations differ between the two sites, PCDFs were the largest contributors to the total TEQ accounting for 81% (ZK) and 87%

(FA) of the total TEQ values. 2,3,4,7,8-PeCDF contributed mostly to total TEQ with a percentage of 23.7% at ZK and 38.9% at FA. These findings were similar to those done in other industrial sites [START_REF] Chang | Sampling and analysis of ambient dioxins in northern Taiwan[END_REF]. DL-PCBs in ZK only contribute to 0.3% of total TEQ while in FA, they contribute to 6.5%. The main difference between the two sites was PCB 169 that was not detected in ZK and highly contributes to the PCB-TEQ at FA.

The total HI value calculated using the total TEQ shows that the non-cancer risk due to exposure to PCDD/Fs and DL-PCBs is negligible at both sites (Fig. 2). As for the cancer risk, both CRinhalation and CRingestion have values below 10 -6 with a higher CRingestion for adults (7-fold higher) and newborns (100-fold higher).

PCDD/Fs were generally emitted from the incineration of hospital, municipal, and hazardous waste as well as during the manufacturing of chlorinated pesticides [START_REF] Zubair | Dioxins and Furans: Emerging Contaminants of Air[END_REF]. As for DL-PCBs, they were produced as industrial chemicals or generated unintentionally during incineration of waste [START_REF] Hogarh | Source characterization and risk of exposure to atmospheric polychlorinated biphenyls (PCBs) in Ghana[END_REF]. The lifetime cancer risk was found to be 4.0 x 10 -7 for both sites. These values can be decreased by reducing waste incineration. LCR values found in our study were lower than the ones reported near different factories in China such as sintering, aluminum and copper plants [START_REF] Sun | PCDD/Fs profile in ambient air of different types factories and human health risk assessment in Suzhou of Jiangsu province, China[END_REF][START_REF] Yang | Atmospheric occurrence and health risks of PCDD/Fs, polychlorinated biphenyls, and polychlorinated naphthalenes by air inhalation in metallurgical plants[END_REF]. This might be mainly due to reported values for both particulate and gas phase in the above-mentioned studies and reported equivalent TEQ that were at least 10 times higher compared to our study.

Major and trace elements

The populations living around the study sites are considered the main receptors of airborne elements. It is worth noting that the toxicity of Cr was mainly reported to the hexavalent state Cr(VI). Therefore, the Cr atmospheric concentration was scaled by a factor of 1/7, given the assumed Cr(VI)/Cr(III) concentration ratio of 1 to 6 (USEPA, 2004a). It was also assumed that the measured arsenic is totally inorganic [START_REF] Huang | Arsenic speciation in total contents and bioaccessible fractions in atmospheric particles related to human intakes[END_REF]. The HQi values for all the identified elements (As, Cd, Co, Cr, Cu, Mn, Ni, Pb, Zn, Ba, Al, V, Fe, Sr, Sn, Sb, La and Tl) were calculated for the different exposure pathways and age categories (Tables S4 andS5).

As and Zn exhibit higher HQi values for dermal contact and ingestion while for Sb, the main health risk is due to ingestion. For this latter route, As, Zn and Sb were more likely to have potential hazard for newborns and children (Table S5): these elements can be accumulated in soil and dust and transferred to children through ingestion [START_REF] Xue | A Meta-Analysis of Children's Hand-to-Mouth Frequency Data for Estimating Nondietary Ingestion Exposure[END_REF]. The total HQi value for these elements were far less than 1 for the different age categories at both sites; the potential carcinogenic risks were negligible and considered not harmful (Tables S6 andS7).

Fe, Sr, Sn, La and Tl were only considered via the ingestion pathway and exhibited HQi lower than the safe limit value of 1. For Ni, the health risk was mainly explained by dermal contact and inhalation. For the other elements, i.e., Cd, Co, Cr(VI), Cu, Mn, Pb, Ba, Al and V, the main risk was associated with the inhalation route at both sites.

Considering the three routes, i.e., total HQi values, the non-carcinogenic risk, from the highest to the lower value, was observed for Mn (highest risk), then Pb, Ni, Co, and V (lowest risk) ; for FA site, the order was as follows: Pb, then Mn, Ni, Co, and V. Even for these elements, Total HQi values were less than 1 for the different age categories implying that these elements do not seem to pose any non-carcinogenic health risk.

Mn and Pb contributed to more than 50% of the total HI. This is mainly due to their relatively high concentrations in air. When comparing the three exposure pathways, inhalation contributed the most to the non-cancer risk for the different age categories (77-93%).

However, when considering the total HI for elements, the value is close to 1 for children at ZK and FA and exceeding 1 for newborns while lower values were reported for adolescents and adults (Fig. 2). This could possibly be explained by the higher rate of exposure and the lower body weight of children and newborns compared to adolescents and adults. The total HI for elements in this study was higher than those presented by [START_REF] Murari | Source apportionment and health risk assessment of airborne particulates over central Indo-Gangetic Plain[END_REF] for an urban city in India (10 -4 -10 -3 ). The differences are mainly due to the choice made for exposure parameters and the variations in the concentrations of the elements specifically Pb, Mn and Co.

The cancer risk for the different exposure pathways was calculated for As, Cd, Co, Cr(VI),

Ni, Pb and V. As shown in Table S4 and Table S5, no values exceeded the average risk acceptance of 10 -6 /year for dermal contact and ingestion pathways at both sites.

However, for the inhalation route, adults were subjected to more carcinogenic risk from As, Co, Cr(VI), Ni and V at ZK since their CR values were 1.2 x 10 -6 , 1.9 x 10 -6 , 1.7 x 10 -6 , 1.5 x 10 -6 and 5.2 x10 -5 respectively, exceeding the safe limit of 10 -6 . Additionally, vanadium showed high cancer risk values of 8.1 x 10 -6 and 5.9 x 10 -6 for children and adolescents, respectively. While at FA, values exceeded the limit for As, Cr(VI) and V for adults and also V for children and adolescents. The cancer risks through the inhalation pathway for the elements were either in the same range or higher than the ones reported for a Romanian site (6.5 -7.2 x 10 -6 ), an urban site in China (7.1 x 10 -6 ), and an urban site in Colombia (3.1 x 10 -6 ) [START_REF] Galon-Negru | Size-resolved measurements of PM2.5 water-soluble elements in Iasi, north-eastern Romania: Seasonality, source apportionment and potential implications for human health[END_REF][START_REF] Liu | Emission control priority of PM2.5-bound heavy metals in different seasons: A comprehensive analysis from health risk perspective[END_REF][START_REF] Ramírez | Hazardous trace elements in thoracic fraction of airborne particulate matter: Assessment of temporal variations, sources, and health risks in a megacity[END_REF].

The cumulative cancer risk for the three exposure pathways was assessed (Tables S6 andS7) and the problematic species were, from highest to lower values,

V > Cr(VI) > As > Co > Ni > Pb > Cd for FA and V > As > Cr(VI) > Co > Ni > Pb > Cd for ZK.
Hence, V, As, and Cr(VI) were the major carcinogenic toxic elements among these elements. Specifically, V was the top contributor to the cumulative CR with a contribution varying between 40 -90% according to the different age categories and the sites. The cancer risk associated to V was higher than 10 -6 at ZK and FA for all age categories, excepted newborn. The cancer risk values associated with adults were the highest between the different age categories (5.2 x 10 -5 at ZK and 2.6 x 10 -5 at FA). V, along with Ni, were generally considered as important tracers of HFO combustion, Cr and Co were mainly associated with industrial emissions and As was emitted from coal combustion [START_REF] Becagli | Evidence for heavy fuel oil combustion aerosols from chemical analyses at the island of Lampedusa: a possible large role of ships emissions in the Mediterranean[END_REF][START_REF] Chen | Source-specific health risk assessment of PM2.5bound heavy metals based on high time-resolved measurement in a Chinese megacity: insights into seasonal and diurnal variations[END_REF]. The exposure to high concentrations of V, Cr(VI), and As can lead to an increased risk of lung cancer according to epidemiological studies [START_REF] Deng | The Effect of Hexavalent Chromium on the Incidence and Mortality of Human Cancers: A Meta-Analysis Based on Published Epidemiological Cohort Studies[END_REF][START_REF] Hubaux | Molecular features in arsenic-induced lung tumors[END_REF][START_REF] Rondini | Vanadium pentoxide induces pulmonary inflammation and tumor promotion in a strain-dependent manner[END_REF].

When considering the cumulative cancer risk for the elements as a whole, it exceeded the average risk acceptance of 10 -6 per year for all age categories at ZK and the risk is higher for adults, followed by children, adolescents and finally newborns (Fig. 2). At FA, cumulative CR exceeded the limit of 10 -6 for all age categories except newborns and the risk occurs on the same order as ZK.

This shows that adults were subjected to more carcinogenic risks than the other age categories at both sites. The cumulative cancer risk (1.3 x 10 -6 -5.9 x 10 -5 for ZK and 8.0

x 10 -7 3.0 x 10 -5 for FA) was mostly found higher than the values presented for a dusty site in Nigeria for children and adults [START_REF] Sulaymon | PM2.5 in Abuja, Nigeria: Chemical characterization, source apportionment, temporal variations, transport pathways and the health risks assessment[END_REF]).

These differences were observed due to the higher concentrations of V (highest contributor to cumulative CR) recorded at ZK (25 ng/m 3 ) and FA (13 ng/m 3 ) compared to the Nigerian site (5-8 ng/m 3 ). The lifetime cancer risk for 70 years of exposure exceeded the safe limit of 10 -6 . Per million habitats, 44 and 25 additional cases of cancer were found based on the LCR calculations at ZK and FA, respectively. In order to decrease these numbers, the concentrations of the major contributor to the CCR, namely Vanadium, should be reduced. This can be done by replacing the energy production based on the combustion of heavy fuel oil used by cleaner energy. Children PAHs -3.3 x 10 -2 3.1 x 10 -1 3.2 x 10 -6 1.1 x 10 -5 6.7 x 10 -7 PCDD/Fs + DL-PCBs -3.0 x 10 -2 3.3 x 10 -5 -4.3 x 10 -7 7.9 x 10 -9 PAEs -9.5 x 10 -3 --4.1 x 10 -7 2.8 x 10 -8 Elements 4.4 x 10 -2 1.1 x 10 -1 6.3 x 10 -1 3.0 x 10 -7 6.3 x 10 -7 1.1 x 10 -5 NMVOCs -1.4 x 10 1 7.2 x 10 -2 -2.0 x 10 -4 1.8 x 10 -6 Adolescents PAHs -1.4 x 10 -2 4.1 x 10 -1 1.1 x 10 -6 2.5 x 10 -6 2.1 x 10 -7 PCDD/Fs + DL-PCBs -1.2 x 10 -2 4.4 x 10 -5 -9.6 x 10 -8 5.7 x 10 -9 PAEs -3.9 x 10 -3 --9.2 x 10 -8 8.6 x 10 -9 Elements 2.6 x 10 -2 4.7 x 10 -2 4.4 x 10 -1 9.9 x 10 -8 1.4 x 10 -7 6.5 x 10 -6 NMVOCs -5.7 x 10 0 9.6 x 10 -2 -4.4 x 10 -5 1.3 x 10 -6 Adults PAHs -5.7 x 10 -3 4.1 x 10 -1 3.4 x 10 -6 9.5 x 10 -6 1.6 x 10 -6 PCDD/Fs + DL-PCBs -5.2 x 10 -3 4.4 x 10 -5 -3.6 x 10 -7 5.1 x 10 -8 PAEs -1.7 x 10 -3 --3.5 x 10 -7 6.5 x 10 -8 Elements 9.5 x 10 -3 2.0 x 10 -2 3.9 x 10 -1 3.2 x 10 -7 5.2 x 10 -7 5.6 x 10 -5 NMVOCs -2.4 x 10 0 9.6 x 10 -2 -1.6 x 10 -4 1.1 x 10 -5 1.0 x 10 -7 5.3 x 10 -7 2.5 x -8 PCDD/Fs + DL-PCBs -6.0 x 10 -2 3.4 x 10 -5 -7.8 x 10 -8 7.4 x 10 -10 PAEs -2.4 x 10 -2 --9.7 x 10 -8 5.2 x -9 Elements 4.0 x 10 -2 1.7 x 10 -1 7.9 x 10 -1 3.6 x 10 -8 1.1 x 10 -7 6.6 x -7 NMVOCs -6.6 x 10 0 1.6 x 10 -2 -9.5 x 10 -6 4.7 x -8

Children PAHs -8.8 x 10 -3 8.3 x 10 -2 8.6 x 10 -7 3.0 x 10 -6 1.8 x -7 PCDD/Fs + DL-PCBs -3.1 x 10 -2 2.0 x 10 -5 -4.4 x 10 -7 8.1 x -9 PAEs -1.3 x 10 -2 --5.5 x 10 -7 3.7 x -8 Elements 3.1 x 10 -2 8.9 x 10 -2 5.3 x 10 -1 3.1 x 10 -7 6.2 x 10 -7 6.1 x -6 NMVOCs -3.4 x 10 0 1.6 x 10 -2 -5.5 x 10 -5 5.1 x -7 Adolescents PAHs -3.6 x 10 -3 1.1 x 10 -1 2.8 x 10 -7 6.8 x 10 -7 5.6 x -8 PCDD/Fs + DL-PCBs -1.3 x 10 -2 4.5 x 10 -5 -9.9 x 10 -8 5.9 x -9 PAEs -5.2 x 10 -3 --1.2 x 10 -7 1.2 x -8 Elements 1.8 x 10 -2 3.7 x 10 -2 3.5 x 10 -1 1.0 x 10 -7 1.4 x 10 -7 3.6 x -6 NMVOCs -1.4 x 10 0 2.2 x 10 -2 -1.2 x 10 -5 3.7 x -7

Adults PAHs -1.5 x 10 -3 1.1 x 10 -1 9.0 x 10 -7 2.5 x 10 -6 4.2 x -7 PCDD/Fs + DL-PCBs -5.4 x 10 -3 4.5 x 10 -5 -3.7 x 10 -7 5.2 x -8 PAEs -2.2 x 10 -3 --4.6 x 10 -7 8.6 x -8 Elements 6.6 x 10 -3 1.5 x 10 -2 3.1 x 10 -1 3.2 x 10 -7 5.2 x 10 -7 3.1 x -5 NMVOCs -6.0 x 10 -1 2.2 x 10 -2 -4.6 x 10 -5 3.3 x -6 3.2.5 Non-methane Volatile organic compounds (NMVOCs)

The non-carcinogenic risk related with exposure to the eleven NMVOCs was investigated. Detailed results are shown in Table S4 and Table S5. The species were studied for inhalation and oral ingestion pathways since no RfDi or CSFi were found for dermal contact. The ingestion pathway appears as the major exposure route for the different species, contributing to more than 80% of the total HI values at both sites.

Heptane and cyclohexane show respectively the highest and the lowest noncarcinogenic risk.

A close examination considering the three routes together revealed that benzene is the second contributor to total HI. Benzene and heptane explain at least 78 to 94% of the total HI values for NMVOCs at both sites. The total HQi value for benzene and n-heptane exceeded the threshold limit of 1 for non-carcinogenic risk for all age categories at ZK and for newborns and children at FA (Table S6 andS7). Additionally, toluene gave total HQi value exceeding the limit at ZK for newborns (1.56). Other species such as tetrachloroethene, ethylbenzene and xylenes recorded total HQi values under the threshold limit meaning that these compounds could be associated with acceptable noncarcinogenic effects. The total HI for the NMVOCs class of compounds showed values higher than 1 for all the age categories at ZK and for newborns, children, and adolescents at FA. It ranged between 26.8 (newborns) and 2.9 (adults) at ZK, and between 6.6 (newborns) and 0.8 (adults) at FA (Fig. 2). Up to our knowledge, most of the studies focused mainly on BTEX and there have been no studies reporting hazard index values for both ingestion and inhalation pathways despite the higher contribution of the ingestion compared to the inhalation pathway as shown in this study. Considering

NMVOCs measured as a whole, the HI values presented in this study for the inhalation pathway (2 x 10 -2 -8 x 10 -2 ) were similar to the ones reported in Tehran, a Middle Eastern city (in the order of 10 -2 -10 -3 ) with a population of approximately 9 million [START_REF] Miri | Investigation of outdoor BTEX: Concentration, variations, sources, spatial distribution, and risk assessment[END_REF].

5 NMVOCs (1,3-butadiene, n-hexane, tetrachloroethene, benzene and ethylbenzene)

were considered for evaluating the cancer risk through two exposure pathways:

inhalation and oral ingestion (values in Tables S4 andS5). Among these compounds, 1,3-butadiene and benzene were classified as carcinogenic to humans according to the IARC causing leukemia. While tetrachloroethene was also classified by IARC as potential human carcinogen based on limited evidence and might cause bladder cancer. The carcinogenic risk values from the ingestion pathway were at least ten times higher than the inhalation route. Additionally, benzene was associated with the highest total CRi with values in the order of 10 -5 -10 -4 at ZK and 10 -6 -10 -5 at FA. These cancer risk values exceeded the acceptable USEPA threshold limit for both sites and for the different age categories. Furthermore, 1,3-butadiene and ethylbenzene also exhibited values higher than 10 -6 at ZK site with total CRi values for the different age categories in the following order: child (2.8 x 10 -5 for 1,3-butadiene and 2.6 x 10 -5 for ethylbenzene)> adult (2.4 x 10 -5 for 1,3-butadiene and 2.4 x 10 -5 for ethylbenzene)> adolescent (6.3 x 10 -6 for 1,3butadiene and 6.0 x 10 -6 for ethylbenzene)> newborn (4.9 x 10 -6 for 1,3-butadiene and 4.5 x 10 -6 for ethylbenzene). Ethylbenzene gave values higher than the threshold limit at FA for children and adults only (~4 x 10 -6 ). The lifetime cancer risk values at ZK for benzene (1.2 x 10 -4 ), 1,3-butadiene (2.3 x 10 -5 ) and ethylbenzene(2.2 x 10 -5 ) reported in this study were higher than the values reported for a suburban site in Lebanon during winter (1.3 x 10 -5 , 1.2 x 10 -5 , 6 x 10 -6 , for the same compounds respectively) and summer

(1.6 x 10 -5 , 8 x 10 -6 , 3 x 10 -6 ) [START_REF] Dhaini | Quantitative cancer risk assessment and local mortality burden for ambient air pollution in an eastern Mediterranean City[END_REF]. However, n-hexane and tetrachloroethene showed values lower than the acceptable threshold implying a moderate cancer risk for these species. The cumulative cancer risk for all NMVOCs measured exceeded the permissible risk level at both sites and for the different age categories and varied from 3.5 x 10 -5 for newborns to 1.8 x 10 -4 for adults and from 1 x 10 -5 for newborns to 6 x 10 -5 for children at ZK and FA, respectively. The lifetime cancer risk was 170 (1.7 x 10 -4 ) and 46 (4.6 x 10 -5 ) times higher than the USEPA limit at ZK and FA, respectively. This is mainly due to high concentrations of benzene and ethylbenzene at both sites, and additionally 1,3-butadiene at ZK. Benzene and 1,3-butadiene were known to be mainly generated from combustion sources leading to the assumption that fuel combustion emissions were considered as significant contributors to the cumulative cancer risk calculated for NMVOCs [START_REF] Salameh | Exploring the seasonal NMHC distribution in an urban area of the Middle East during ECOCEM campaigns: Very high loadings dominated by local emissions and dynamics[END_REF][START_REF] Who | Ambient air pollution : a global assessment of exposure and burden of disease[END_REF]. At least 70% of the additional cancer cases (120 at ZK and 42 at FA per million habitats based on LCR calculations) were caused by the exposure to high concentrations of benzene at both sites, might be highly emitted from traffic gasoline combustion. These numbers can be reduced by implementing strict vehicle emission control measures.

Health risk comparison between the classes of compounds and limitations of the study

As observed in Fig. 2, total HI values related to the non-cancer risk were significantly higher than the acceptable limit of 1 for NMVOCs for the different age categories at both sites (except for adults at FA), and for elements for adults. These compounds might pose non-carcinogenic health problems to humans like neurological effects, liver and kidney toxicities, lymphocyte count decrease, etc. [START_REF] Dhaini | Quantitative cancer risk assessment and local mortality burden for ambient air pollution in an eastern Mediterranean City[END_REF]. The major compounds contributing to the non-carcinogenic risk were mainly n-heptane, benzene and toluene for NMVOCs. While in the particulate phase, B[a]Peq, Mn, Pb, V and Ni were the major contributors despite their values of total HQi less than 1.Conversely, PAHs, dioxins, furans, dioxin-like polychlorobiphenyls, and phthalates have an acceptable non-cancer risk since their total HI values were lower than the USEPA limit. When comparing the different families of compounds, NMVOCs exhibited the highest values of total HI for the different age categories, followed by elements, PM2.5-bound PAHs, phthalates, and finally PCDD/Fs and DL-PCBs (Fig. 2).

For the cancer risk assessment, cumulative CR values for PAHs in the particulate phase, elements and NMVOCs exhibited values higher than the threshold limit of 10 -6 proposed by the USEPA. The major contributors to cancer risk were benzene, ethylbenzene and 1,3-butadiene (at ZK site) in the gas phase, while PAHs, Ni, Cr(VI), Co, and As were the main components in the particulate phase. Additionally, a similar order to the total hazard index was observed for the cumulative cancer risk of the different families of compounds except for PM2.5-bound PAHs that showed CCR values higher than elements (Fig. 2). Species that have CCR values higher than the threshold limit were mainly associated to combustion sources such as vehicular emissions, biomass burning, and HFO combustion leading to additional cancer cases for the different families of species.

This emphasizes on the relevance of reducing the concentrations of the species by adopting an effective air quality management plan, implementing a national transportation system in urban areas to reduce traffic emissions [START_REF] Abdallah | A first annual assessment of air quality modeling over Lebanon using WRF/Polyphemus[END_REF] and shifting to cleaner energy instead of traditional biomass and fuel combustion. This study used a comprehensive and well-defined calculation method for the carcinogenic and non-carcinogenic risk assessment due to exposure to different classes of compounds considered individually. However, the cancer and non-cancer risks for the classes of compounds were not summed since there were no available methods for the calculation of health risk hazards due to exposure to total air contaminants. These were considered as limitations of the health assessment studies which assume independence between toxic actions within and across compounds. Actually, the interactions between the different contaminants on health, defined as cocktail effect reflecting synergism or antagonism action is not well defined as it still remains unsolved. Additionally, uncertainties accompany risk assessment studies especially in the choice of exposure parameters and reference values.

Conclusions

This study provided for the first time an extensive health risk assessment considering different classes of compounds such as phthalates, dioxins, furans, dioxin-like polychlorobiphenyls, PAHs and elements in PM2.5, as well as NMVOCs according to age categories and different exposure pathways.

The non-carcinogenic risk estimated for the different components showed a risk from benzene and n-heptane exposure. Additionally, this was also observed for the sum of elements where Mn, Pb, V and Ni were the major contributors to the total hazard index.

PAHs, phthalates, PCDD/Fs, and DL-PCBs exhibited lower values and present acceptable non-carcinogenic health risks. As for the carcinogenic risk, CR for different species such as benzene, 1,3-butadiene (at Zouk site), ethylbenzene, PM2.5-B[a]Peq, As, Co, Cr(VI), Ni, and V showed values higher than the threshold limit of 10 -6 meaning that these compounds present a carcinogenic risk to different age categories. These compounds were mainly associated to different combustion sources such as vehicular emissions, biomass burning and HFO combustion. The results from this study are of major importance to assess the impact of the different contaminants on the human health.

Additionally, health risk assessment results should be combined to source apportionment studies in order to better relate health impact of the different sources of pollutants released in the atmosphere.

Acknowledgment:

  evaluate the cancer risk for a family of chemicals attributed to the combined three exposure pathways, the cumulative cancer risk was calculated according to (Eq.15): N NHG OPQ + = + = + (123435(61 + + (1=>?5(61 + + A>BC34( . 15)

  , low B[a]Peq concentrations can be estimated. This could be explained by the abundance of the PAHs with high contribution to the B[a]Peq value in the particulate phase. Consequently, only PM2.5-bound PAHs were studied. The B[a]Peq value for the 16 PAHs in the particulate phase was 2.58 and 0.69 ng/m 3 at ZK and FA, respectively. The 7 PAHs classified by the IARC as group 1, 2A or 2B (benz[a]anthracene, chrysene, benzo[b]fluoranthene, benzo[k]fluoranthene, benzo[a]pyrene, dibenz[a,h]anthracene, and indeno(1,2,3-c,d)pyrene) accounted for 98% of the B[a]Peq value at ZK and 99% at FA showing that these compounds were the main contributors to PM2.5-bound PAHs toxicity.

Fig. 2 :

 2 Fig. 2: Cumulative Cancer Risk (CCR) and Total hazard index (THI) values for polycyclic aromatic hydrocarbons (PAHs) in particulate phase, total PCDD/Fs and DL-PCBs, phthalates (PAEs), elements, and non-methane volatile organic compounds (NMVOCs) for the different age categories (newborns, children, adolescents, and adults) at Zouk (ZK) and Fiaa (FA) (HI values and Cumulative CR below 1 means acceptable risk).

Table 1 :

 1 Exposure parameters for newborns, children, adolescents, and adults through inhalation, ingestion, and dermal contact considered in this study for the health risk

	assessment

Table 2 :

 2 Average atmospheric concentrations and standard deviations of total PAHs, phthalates, and elements in PM2.5 along with concentrations of non-methane volatile organic compounds (NMVOCs) during the entire sampling period

	Compounds (ng/m 3 )	ZK site	FA site	Reference
	Total PM2.5-bound PAHs	2.56 ± 2.5	0.95 ± 1.12	(Fadel et al., 2021)
	PM2.5-bound phthalates
	dibutyl phthalate	37 ± 29	12.4 ± 11.6	(Fadel et al., 2021)
	bis(2-ethylhexyl)phthalate	49 ± 17	66 ± 70
	Major and trace elements
	As	0.53 ± 0.28	0.49 ± 0.24
	Cd	0.13 ± 0.10	0.14 ± 0.10
	Co	1.22 ± 2.10	0.61 ± 0.76
	Cr	1.88 ± 1.50	1.97 ± 1.33
	Cu	4.63 ± 3.66	2.53 ± 1.75
	Mn	7.46 ± 8.78	5.61 ± 7.0
	Ni	11.7 ± 12.3	6.29 ± 4.50
	Pb	12.8 ± 20.1	17.5 ± 29.3
	Zn Ba	26.1 ± 16.3 14.2 ± 13.6	16.7 ± 11.1 9.1 ± 5.6	This study
	Al	593 ± 1000	492 ± 800
	V	25 ± 27	13 ± 9
	Fe	452 ± 615	298 ± 466
	Sr	5.4 ± 9.0	4.5 ± 5.7
	Sn	0.83 ± 0.60	0.57 ± 0.60
	Sb	1.11 ± 0.75	0.95 ± 0.92
	La	0.54 ± 0.63	0.33 ± 0.44
	Tl	0.03 ± 0.02	0.03 ± 0.03
	NMVOCs
	1,3-butadiene	77.7 ± 70	<D.L.
	hexane	419 ± 720	150 ± 137
	tetrachloroethene	291 ± 115	58 ± 9
	benzene	4318 ± 5393	1526 ± 3340
	cyclohexane heptane	398 ± 187 657 ± 170	94 ± 200 138 ± 84	This study
	methylcyclohexane	446 ± 93	88 ± 37
	toluene	16910 ± 3428	2740 ± 1280
	ethylbenzene	4210 ± 911	655 ± 354
	m+p-xylene	5730 ± 1293	743 ± 264

Table 3

 3

presents PCDD/Fs, and DL-PCBs congener concentrations observed in ZK and FA sites in the particulate phase. The total average concentrations of PCDDs and PCDFs were 164 and 124 fg/m 3 at ZK and FA, respectively. OCDD and 1,2,3,4,6,7,8-HpCDF were the two dominant congeners among PCDD/Fs contributing to 49% and 46% at ZK and FA, respectively, followed by 1,2,3,4,6,7,8-HpCDD and OCDF. DL-PCB congeners are dominated by PCB 105 and PCB 118 accounting for 86% and 83% of total DL-PCBs at ZK and FA, respectively. Elements' concentrations varied at ZK from 0.03 ng/m 3 for Tl to 593 ng/m 3 for Al, and from 0.03 ng/m 3 for Tl to 492 ng/m 3 for Al at FA (Table

2

).

Table 3 :

 3 Dioxins (PCDD), furans (PCDF) and dioxin-like polychlorobiphenyls (DL-PCBs) average concentrations (fg/m 3 ) in PM2.5 samples at Zouk (ZK) and Fiaa (FA)

	Compounds (fg/m 3 )	Abbreviation	ZK site	FA site
	PCDDs		81.1 ± 38.7	52.0 ± 21.7
	2,3,7,8-tetrachlorinated dibenzo-p-dioxin	2,3,7,8 TCDD	<D.L.	<D.L.
	1,2,3,7,8-pentachlorinated dibenzo-p-dioxin	1,2,3,7,8 PeCDD	0.43 ± 0.20	<D.L.
	1,2,3,4,7,8-hexachlorinated dibenzo-p-dioxin	1,2,3,4,7,8 HxCDD	0.51 ± 0.30	<D.L.
	1,2,3,6,7,8-hexachlorinated dibenzo-p-dioxin	1,2,3,6,7,8 HxCDD	1.77 ± 0.93	1.69 ± 0.06
	1,2,3,7,8,9-hexachlorinated dibenzo-p-dioxin	1,2,3,7,8,9 HxCDD	1.26 ± 0.95	<D.L.
	1,2,3,4,6,7,8-heptachlorinated dibenzo-p-dioxin 1,2,3,4,6,7,8 HpCDD	23.18 ± 7.50	16.13 ± 3.07
	octachlorinated dibenzo-p-dioxin	OCDD	53.98 ± 28.81 34.20 ± 18.6
		TEQ for PCDD	1.03	0.34
	PCDFs		82.5 ± 35.1	71.8 ± 36.7
	2,3,7,8 tetrachlorinated dibenzofuran	2,3,7,8 TCDF	1.31 ± 1.20	1.57 ± 0.96
	1,2,3,7,8 pentachlorinated dibenzofuran	1,2,3,7,8 PeCDF	2.43 ± 2.28	1.95 ± 0.75
	2,3,4,7,8 pentachlorinated dibenzofuran	2,3,4,7,8 PeCDF	4.49 ± 3.32	7.35 ± 7.13
	1,2,3,4,7,8 hexachlorinated dibenzofuran	1,2,3,4,7,8 HxCDF	7.76 ± 3.99	6.51 ± 4.52
	1,2,3,6,7,8 hexachlorinated dibenzofuran	1,2,3,6,7,8 HxCDF	6.61 ± 3.29	5.37 ± 3.13
	2,3,4,6,7,8 hexachlorinated dibenzofuran	2,3,4,6,7,8 HxCDF	8.79 ± 1.52	8.30 ± 3.0
	1,2,3,7,8,9 hexachlorinated dibenzofuran	1,2,3,7,8,9 HxCDF	2.79 ± 0.77	2.60 ± 1.02
	1,2,3,4,6,7,8-heptachlorinated dibenzofuran	1,2,3,4,6,7,8 HpCDF	26.43 ± 8.62	23.04 ± 9.7
	1,2,3,4,7,8,9-heptachlorinated dibenzofuran	1,2,3,4,7,8,9 HpCDF	3.16 ± 0.35	2.63 ± 2.4
	octachlorinated dibenzofuran	OCDF	18.75 ± 9.76	12.46 ± 4.11
		TEQ for PCDF	4.45	4.96
	DL-PCBs		454.8 ± 202	586.3 ± 128
	3,4,4',5-tetrachlorobiphenyl	PCB 81	<D.L.	<D.L.
	3,3′,4,4′-tetrachlorobiphenyl	PCB 77	21.66 ± 6.64	8.39± 8.0
	2,3',4,4',5'-pentachlorobiphenyl	PCB 123	20.20 ± 23.52	55.51± 7.67
	2,3',4,4',5-pentachlorobiphenyl	PCB 118	278.2 ± 112.6	325.2 ±50.7
	2,3,4,4',5-pentachlorobiphenyl	PCB 114	<D.L.	4.59 ± 5.0
	2,3,3',4,4'-pentachlorobiphenyl	PCB 105	111.4 ± 45.0	158.6 ± 37.1
	3,3',4,4',5-pentachlorobiphenyl	PCB 126	<D.L.	<D.L.
	2,3',4,4',5,5'-hexachlorobiphenyl	PCB 167	8.37 ± 8.0	<D.L.
	2,3,3',4,4',5-hexachlorobiphenyl	PCB 156	15.08 ± 6.33	13.40 ± 6.0
	2,3,3',4,4',5'-hexachlorobiphenyl	PCB 157	<D.L.	<D.L.
	3,3',4,4',5,5'-hexachlorobiphenyl	PCB 169	<D.L.	11.66 ± 6.2
	2,3,3',4,4',5,5'-heptachlorobiphenyl	PCB 189	<D.L.	8.95 ± 7.0
		TEQ for PCB	0.02	0.37
		Total TEQ	5.49	5.67

Table 4 :

 4 Hazard Index (HI) and cancer risk values (CR) for dermal, ingestion and inhalation pathways for the different age categories and

	547
	548	family of compounds at Zouk site

Table 5 :

 5 Hazard Index (HI) and cancer risk values (CR) for dermal, ingestion, and inhalation pathways for the different age categories

	550
	551	and family of compounds at Fiaa site
	552	Age category	Class of compounds		Hazard index (HI)		Cancer risk (CR)
				Dermal	Ingestion	Inhalation	Dermal	Ingestion	Inhalation
			PAHs	-	1.7 x 10 -2	8.3 x 10 -2
		Newborns