# Comprehensive Health Risk Assessment of PM2.5 Chemical Composition in an Urban Megacity: A Case Study from Greater Cairo Area

Eliane Farah, Marc Fadel, Hassan R Dhaini, Nansi Fakhri, Minas Iakovides, Salwa K Hassan, Mohamed Boraiy, Mostafa El-Nazer, Ali Wheida, Magdy Abdelwahab, et al.

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## To cite this version:

Eliane Farah, Marc Fadel, Hassan R Dhaini, Nansi Fakhri, Minas Iakovides, et al. Comprehensive Health Risk Assessment of PM2.5 Chemical Composition in an Urban Megacity: A Case Study from Greater Cairo Area. Atmosphere, 2025, 16 (10), pp.1214. 10.3390/atmos16101214. hal-05535013

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Article

# Comprehensive Health Risk Assessment of PM<sub>2.5</sub> Chemical Composition in an Urban Megacity: A Case Study from Greater Cairo Area

Eliane Farah<sup>1,2</sup>, Marc Fadel<sup>2,* ID</sup>, Hassan R. Dhaini<sup>3</sup>, Nansi Fakhri<sup>1,4 ID</sup>, Minas Iakovides<sup>4 ID</sup>, Salwa K. Hassan<sup>5</sup>, Mohamed Boraiy<sup>6</sup>, Mostafa El-Nazer<sup>7 ID</sup>, Ali Wheida<sup>7</sup>, Magdy Abdelwahab<sup>8 ID</sup>, Stéphane Sauvage<sup>9,10 ID</sup>, Agnès Borbon<sup>11</sup>, Jean Sciare<sup>4 ID</sup>, Frédéric Ledoux<sup>2 ID</sup>, Charbel Afif<sup>1,4</sup> and Dominique Courcot<sup>2</sup>

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Received: 4 September 2025

Revised: 13 October 2025

Accepted: 17 October 2025

Published: 20 October 2025

**Citation:** Farah, E.; Fadel, M.; Dhaini, H.R.; Fakhri, N.; Iakovides, M.; Hassan, S.K.; Boraiy, M.; El-Nazer, M.; Wheida, A.; Abdelwahab, M.; et al. Comprehensive Health Risk Assessment of PM<sub>2.5</sub> Chemical Composition in an Urban Megacity: A Case Study from Greater Cairo Area. *Atmosphere* **2025**, *16*, 1214. https://doi.org/10.3390/atmos16101214

**Copyright:** © 2025 by the authors.
Licensee MDPI, Basel, Switzerland.
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(https://creativecommons.org/
licenses/by/4.0/).

Abstract

While many studies on the health effects of PM<sub>2.5</sub> exist, the risks of PM<sub>2.5</sub> species remain largely unexplored in Middle Eastern and North African countries. This study assesses, for the first time, the carcinogenic and non-carcinogenic health risks for elements, polycyclic aromatic hydrocarbons (PAHs), phthalates, polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and dioxin-like polychlorinated biphenyls (DL-PCBs) bound to PM<sub>2.5</sub> in the Greater Cairo Area. A total of 59 samples were collected from an urban site in Dokki (November 2019–January 2020). Chemical analysis showed higher concentrations of PCDFs (5418 fg/m<sup>3</sup>) than PCDDs (1469 fg/m<sup>3</sup>), with DL-PCBs being the most abundant (6577 fg/m<sup>3</sup>). Health risk assessment for inhalation showed non-carcinogenic risks for all age groups, especially for newborns. Manganese (Mn) and lead (Pb) posed the highest elemental non-carcinogenic risk, while the hazard quotient (HQ) for PAHs exceeded 1 across all ages. PCDDs, PCDFs, and DL-PCBs showed an estimated cancer risk reaching 10<sup>-6</sup> in adults, indicating a significant health concern. Key contributors to cancer risk included arsenic (As), chromium (Cr(VI)), and vanadium (V), which accounted for over 80% of the total elemental cancer risk. Major and trace elements posed the highest lifetime cancer risk, nearly 37 times the acceptable level.

<footnote n="1">¹ Emissions, Measurements, and Modelling of the Atmosphere (EMMA) Laboratory, CAR, Faculty of Science, Saint Joseph University, Beirut, Lebanon; eliane.farah@univ-littoral.fr (E.F.); nansi.fakhri1@usj.edu.lb (N.F.); charbel.afif@usj.edu.lb (C.A.)</footnote>

<footnote n="2">² Unité de Chimie Environnementale et Interactions sur le Vivant, (UCEIV) UR4492, University of Littoral Côte d'Opale (ULCO), 59140 Dunkirk, France; frederic.ledoux@univ-littoral.fr (F.L.); dominique.courcot@univ-littoral.fr (D.C.)</footnote>

<footnote n="3">³ Department of Environmental Health, Faculty of Health Sciences, American University of Beirut, Beirut, Lebanon; hd24@aub.edu.lb</footnote>

<footnote n="4">⁴ Climate and Atmosphere Research Center (CARE-C), the Cyprus Institute, Nicosia 2121, Cyprus; m.iakovides@cyi.ac.cy (M.I.); j.sciare@cyi.ac.cy (J.S.)</footnote>

<footnote n="5">5 Air Pollution Research Department, Environment and Climate Change Research Institute, National Research Centre, El Bohooth St., Dokki, Giza 12622, Egypt; sk.mohamed@nrc.sci.eg</footnote>

<footnote n="6">6 Physics and Mathematical Engineering Department, Faculty of Engineering, Port Said University, Port Said 42511, Egypt; mohmed.mahmoud@eng.psu.edu.eg</footnote>

<footnote n="7">7 Theoretical Physics Department, Physics Research Institute, National Research Centre, El Bohooth St., Dokki, Giza 12622, Egypt; mm.elnazer@nrc.sci.eg (M.E.-N.); aa.wheida@nrc.sci.eg (A.W.)</footnote>

<footnote n="8">⁸ Astronomy and Meteorology Department, Faculty of Science, Cairo University, Cairo 11511, Egypt; magdy@sci.cu.edu.eg</footnote>

<footnote n="9">⁹ IMT Nord Europe, Institut Mines-Télécom, Univ. Lille, Centre for Energy and Environment, 59000 Lille, France; stephane.sauvage@imt-nord-europe.fr</footnote>

<footnote n="10">¹⁰ Institut des Géosciences de l'Environnement (IGE), Centre National de la Recherche Scientifique, Institut de Recherche pour le Développement, INP, INRAE, Université Grenoble-Alpes, 38000 Grenoble, France</footnote>

<footnote n="11">¹¹ Laboratoire de Météorologie Physique, UMR6016, Université Clermont Auvergne, OPGC, CNRS, 63000 Clermont-Ferrand, France; agnes.borbon@uca.fr</footnote>

<footnote>* Correspondence: marc.fadel@univ-littoral.fr</footnote>
**Keywords:** PM<sub>2.5</sub>; Egypt; air pollution; cancer risk; persistent organic pollutants; elements

# 1. Introduction

Air pollution continues to be a critical environmental and public health threat [1]. Particulate matter (PM), especially PM<sub>2.5</sub>, comprising particles with an equivalent aerodynamic diameter less than 2.5 µm, represents the foremost environmental contributor to morbidity and leads to high premature mortality on a global scale [2]. In recent decades, a robust body of epidemiological evidence has established a significant association between exposure to PM<sub>2.5</sub> and all-cause mortality, particularly cardiopulmonary illnesses, including lung cancer and a range of non-communicable diseases and metabolic disorders [3]. However, the strength of such an association varies considerably across different studies. This variability can be partially attributed to the reliance on bulk PM mass concentration as a primary exposure metric. But such an approach does not take into consideration the differences in PM's physical and chemical properties, which are influenced by emission sources and the site's typology [4–6]. Consequently, considerable research has attempted to identify specific PM components that may serve as more sensitive predictors of its health impact [7]. For instance, polycyclic aromatic hydrocarbons (PAHs) have received considerable attention in recent years due to their persistent, bio-accumulative, carcinogenic, and mutagenic characteristics. Several papers have linked PAHs exposure to various health issues, including cataracts, renal damage, as well as cancers of the skin, liver, lungs, and gastrointestinal tract [8]. Polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs) constitute another class of persistent organic pollutants (POPs) of anthropogenic origins [9]. Due to their resistance to metabolic degradation, they accumulate in the fatty tissues of humans and animals [10]. Many of these compounds are associated with skin toxicity, immune system impairment, cancer, and adverse effects on reproduction, development, and endocrine functions [10]. Other components found in PM<sub>2.5</sub>, such as phthalates, were also recognized as endocrine-disrupting compounds [11]. Furthermore, trace elements in PM<sub>2.5</sub> have been demonstrated to elevate the incidence of respiratory infections and exacerbate asthma conditions [3].

Megacities, with populations exceeding 10 million, face considerable air quality challenges. Rapid urbanization and increasing energy demand from transport, industrial, and commercial activities have led to high pollution levels, raising urban residents' health risks and augmenting the socioeconomic burden [12]. Despite extensive research efforts, including air quality monitoring, field measurements, and modeling, the emission sources and processes driving high concentrations of key pollutants such as ozone and secondary particulate matter in these megacities remain insufficiently understood, limiting effective mitigation and accurate air quality forecasting [12]. The Greater Cairo Area (GCA), one of the world's most polluted megacities, encompassing three governorates (Cairo, Giza, and Qalyubia), had a population of nearly 25 million residents with 4.06 million vehicles on the streets in 2019–2020 [13,14]. In addition, the surrounding desert and predominantly semi-arid surface soils in GCA contribute to frequent exceedance levels of PM<sub>2.5</sub> concentrations in the atmosphere, surpassing the PM<sub>2.5</sub> World Health Organization's 24-h air quality standard (15 µg/m<sup>3</sup>), as well as its equivalent national Egyptian standard (80 µg/m<sup>3</sup>) [15,16].

Therefore, investigating the health risks associated with human exposure to various toxic components of PM<sub>2.5</sub> is of paramount importance; however, studies in this area remain limited, focusing on a limited family of pollutants. For instance, Hassan [17] found that inhabitants of El Giza and Ramsis Square areas in GCA were at a higher cancer risk due
to exposure to heavy metals. In addition, Khairy and Lohmann [8] assessed the lifetime
cancer risk posed by PAHs to both children and adults in Alexandria. Their analysis
revealed that the incremental lifetime cancer risk exceeded the acceptable threshold of 10⁻⁶
through dermal and ingestion pathways at all sampling locations, while the inhalation route
presented elevated risks specifically at industrial and traffic-affected sites. Furthermore,
Shetaya et al. [18] calculated the carcinogenic and non-carcinogenic risks linked to toxic
trace elements in PM₂.₅ for residents of the GCA, revealing markedly increased risks
attributable to 12 metal(loid)s. Notably, Pb emerged as the predominant contributor,
accounting for 56% of non-carcinogenic and 83% of carcinogenic risks. It is noteworthy
that Wheida et al. [19] conducted a health impact assessment in Greater Cairo, employing
concentration-response functions and the WHO methodology to estimate excess mortality
due to long-term exposure to PM₂.₅, NO₂, and O₃. Their findings indicated that PM₂.₅ and
NO₂ pose major health risks, with 11% and 8% of non-accidental mortality in individuals
over 30 years attributed to these pollutants, respectively. However, this assessment did not
consider the chemical composition of PM₂.₅, potentially underestimating the actual health
impacts associated with its toxic components.

Therefore, assessing the cumulative health risks posed by different families of PM<sub>2.5</sub> is crucial for public health policy and prevention strategies. However, existing studies in Egypt have primarily focused on either PM<sub>2.5</sub> mass or limited pollutant classes, often overlooking the cumulative effects and age-specific exposure pathways. To our knowledge, this is the first study in GCA that comprehensively assesses both carcinogenic and non-carcinogenic health risks associated with inhalation across multiple pollutant families, including PAHs, phthalates, PCDDs, PCDFs, DL-PCBs, and elements, bound to PM<sub>2.5</sub>. These findings are essential for guiding targeted air quality interventions and public health strategies in megacities like Cairo, where millions are chronically exposed to high pollution levels.

**2. Materials and Methods**

2.1. *Sampling Site*

The sampling site was previously described in Farah et al. [20] and is briefly pre-
sented in this section. The campaign was conducted between 26 November 2019, and
27 January 2020 (sampling was stopped at this date due to the COVID-19 pandemic-related
restrictions settled for at least one year), on the roof of the National Research Centre (NRC)
(30°02′11.0″ N 31°12′22.4″ E) in Giza (Dokki) (Figure 1). The NRC is situated approxi-
mately 3 km east-southeast of Cairo’s city center. The Dokki district is among GCA’s most
active and densely populated areas, known for its dynamic urban activities and consis-
tently heavy traffic throughout the year. The sampling equipment was installed on top of a
six-level building, which offered a clear, unobstructed 360° view for data collection.

## 2.2. *Sampling Strategy*

PM₂.₅ samples were collected continuously over 24 h, with filter replacements occur-
ring daily at 10 a.m. throughout the sampling period. A high-volume sampler operating at
a flow rate of 30 m³/h (CAV-A/mb, MCV S.A., Spain) was utilized, and 150 mm quartz mi-
crofiber filters were employed for particle collection. To ensure the removal of any organic
impurities, filters were pre-baked at 550 °C for 12 h before use [21]. A total of 59 samples
were collected, in addition to two blanks, and stored at -20 °C until further analysis.

2.3. *Chemical Analysis*

The analytical methodology for quantifying PAHs and phthalates was previously
described by Farah et al. [20]. Briefly, this approach involved the extraction of compounds
from quartz filters through sonication, using a mixture of acetone and dichloromethane solvents. The resulting extract was then concentrated to a volume of 300 µL under a gentle flow of nitrogen gas. Subsequent analysis was performed using gas chromatography coupled with mass spectrometry (ISQ 7000, Thermo Scientific, Waltham, MA USA). The detection limits ranged from 0.0002 to 2 ng/m³ (Table S1). Method accuracy was validated through recovery experiments, in which blank filters were spiked with known concentrations of standard solutions, resulting in recovery rates between 80% and 97%. Analytical precision was confirmed by assessing the repeatability of response factors across five successive injections of authentic standards, with relative standard deviations remaining below 10%. The analytical uncertainty is based on the compound quantification limit, repeatability, and concentration. The total uncertainty, which includes both analytical uncertainty and that associated with the mass flow measurement of the sampler, was found to be in the range of 9–30% at 2σ [22].

<figure><img src="image_4.png" /><figcaption>**Figure 1.** Location of the study area and the designated sampling site within Cairo (modified from Google Earth).</figcaption></figure>

Major and trace elements (Al, V, Cr, Mn, Co, Ni, Cu, Zn, As, Cd, Sb, and Pb) were analyzed in an Agilent 7500ce Inductively Coupled Plasma-Mass Spectrometer (ICP-MS) using the methodology described by Iakovides et al. [23]. Prior to analysis, punches of the quartz filters (2 × 1.5 cm²) were digested in a microwave oven (Speedwave Entry, Berghof) with 5 mL of 65% pure nitric acid (Suprasolv, Merck, Darmstadt, Germany), following a specific protocol [23]. Seven-level calibration curves (R² > 0.9999) were used to quantify each sample set (30 samples/batch) using certified standard solutions (CPA Chem). Ge, In, and Bi were used as internal standards to monitor the analytical response [23]. All concentrations reported herein were blank and recovery corrected. Method detection limits (MDLs) [23] ranged from 0.004 pg/m³ (Mn) to 7.65 (Al) ng/m³ (Table S1). Chemical analysis was routinely evaluated using predefined certified solutions, with absolute recoveries ranging between 90% and 105%. The validity of the entire protocol of analysis is assessed twice per year via proficiency testing organized by the International Atomic Energy Agency-IAEA (NSIL) and the European Monitoring and Evaluation Program (EMEP) (chemical coordinating center).

PCDDs, PCDFs, and DL-PCBs were analyzed using high-resolution gas chromatography coupled with high-resolution mass spectrometry. The analysis was conducted by MicroPolluants Technologie SA (Saint Julien Les Metz, France) following the methodologies established by the USEPA under methods 1613 and 1668 [4].
## 2.4. Health Risk Assessment Methodology

Health risk assessment methods and values used in the process integrated estimates of exposure intensity with appropriate toxicological values to determine the likelihood of adverse effects in potentially exposed populations in Cairo. In this study, we followed the United States Environmental Protection Agency (USEPA) approach [24–26], estimating both carcinogenic and non-carcinogenic risks through inhalation. Measured mean concentrations of chemical species were used to estimate exposure levels within the target population over a defined period. We also followed the Toxic Equivalent approach using toxic equivalent factors (TEFs) to determine the toxic potency of complex mixtures of PAHs, PCDDs, PCDFs, and DL-PCBs [27,28] (Tables S2 and S3). Specifically, B[a]P<sub>eq</sub>, the benzo[a]pyrene equivalent, expresses the toxicity of PAH mixtures relative to benzo[a]pyrene, while TEQ, the toxic equivalent, quantifies the overall toxicity of PCDDs, PCDFs, and DL-PCBs relative to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). B[a]P<sub>eq</sub> and TEQ were calculated as follows:

$$B[a]P_{eq} = \sum_{i=1}^{n} C_i \times TEF_i \quad (1)$$

$$TEQ = \sum_{j=1}^{n} C_j \times TEF_j \quad (2)$$

The concentration of hexavalent chromium (Cr(VI)) was estimated as one-seventh of the total chromium concentration [18,29–31].

Exposure estimation schemes are described elsewhere. Briefly, the assumed average daily dose (ADD) (mg/kg/day) and exposure concentration (EC<sub>inhalation</sub>) (mg/m³) for a specific toxicant were computed as follows:

$$ADD_{i-inhalation} = \frac{C_i \times IR_{inhalation} \times ED \times EF \times CF}{BW \times AT} \quad (3)$$

$$EC_{i-inhalation} = \frac{C_i \times ET \times ED \times EF \times CF}{AT \times 24} \quad (4)$$

where C<sub>i</sub> is the measured concentration expressed in ng/m³ for inhalation exposure. The definitions of the other parameters, along with their respective units and values, are summarized in Table 1 for the various age categories relevant to this study: newborns (0 to <1 years), children (1 to <12 years), adolescents (12 to <18 years), and adults (18 to 70 years). Due to the absence of specific exposure factor data for Egypt (body weight, inhalation rate, and exposure duration), generic values obtained from the USEPA reports have been employed (Table 1).

<table><caption>**Table 1.** Exposure factors utilized in the health risk assessment methodology.</caption><thead><tr><th>Exposure Parameters</th><th>Abbreviation</th><th>Unit</th><th>Newborn</th><th>Child</th><th>Adolescent</th><th>Adult</th><th>Reference</th></tr><tr><td></td><td></td><td></td><td>0 to &lt;1 Year</td><td>1 to &lt;12 Years</td><td>12 to &lt;18 Years</td><td>18–70 Years</td><td></td></tr></thead><tbody><tr><td>Inhalation intake rate</td><td>IR<sub>inhalation</sub></td><td>m³/day</td><td>5.4</td><td>11.2</td><td>15.6</td><td>15.5</td><td>USEPA [26]</td></tr><tr><td>Body weight</td><td>BW</td><td>kg</td><td>7.8</td><td>25</td><td>61</td><td>72</td><td>USEPA [32]</td></tr><tr><td>Exposure frequency</td><td>EF</td><td>Days/year</td><td>350</td><td>350</td><td>350</td><td>350</td><td>USEPA [33]</td></tr></tbody></table>
<table><caption>Table 1. *Cont.*</caption><thead><tr><th>Exposure Parameters</th><th>Abbreviation</th><th>Unit</th><th>Newborn</th><th>Child</th><th>Adolescent</th><th>Adult</th><th>Reference</th></tr><tr><td></td><td></td><td></td><td>0 to &lt;1 Year</td><td>1 to &lt;12 Years</td><td>12 to &lt;18 Years</td><td>18–70 Years</td><td></td></tr></thead><tbody><tr><td>Exposure time</td><td>ET</td><td>h/day</td><td>6</td><td>6</td><td>8</td><td>8</td><td>Dahmardeh Behrooz et al. [34]</td></tr><tr><td>Exposure duration</td><td>ED</td><td>Years</td><td>1</td><td>11</td><td>6</td><td>52</td><td>USEPA [26]</td></tr><tr><td>Average timing</td><td>AT</td><td>Days</td><td colspan="4">AT = ED × 365 days for non-carcinogens<br>AT = 70 years × 365 for carcinogens</td><td>USEPA [24]</td></tr><tr><td>Conversion factor</td><td>CF</td><td>kg/mg</td><td colspan="4">10<sup>-6</sup></td><td></td></tr></tbody></table>

### 2.4.1. Non-Cancer Risk Assessment

The estimation of non-cancer risks associated with inhalation for specific species was conducted using the hazard quotient (HQᵢ) as follows:

$$ HQ_i = \frac{ADD_i}{RfD_i} \quad \text{or} \quad HQ_i = \frac{EC_{i-\text{inhalation}}}{RfC_i} \qquad (5) $$

where ADDᵢ (in mg/kg/day) is the average daily dose, ECᵢ (in mg/m³) is the exposure concentration through inhalation, RfD (in mg/kg/day) and RfC (in mg/m³) are the USEPA reference dose and reference concentration, respectively. Values for RfD and RfC are presented in Table S4.

The Hazard Index (HI) for a specific chemical family was computed as follows:

$$ \text{HI(Inhalation)} = \sum_i HQ_i \qquad (6) $$

When HQᵢ and HI are equal to or less than 1, this indicates that adverse effects are not likely to occur. Conversely, when it exceeds 1, this indicates an exceedance of the non-cancer health guidelines [30,35].

### 2.4.2. Cancer Risk Assessment

The cancer risks (CRᵢ) associated with the inhalation exposure pathway were computed using the equations outlined below:

$$ CR_{i-\text{inhalation}} = LADD_{i-\text{inhalation}} \times CSF_i \qquad (7) $$

$$ CR_{i-\text{inhalation}} = EC_{i-\text{inhalation}} \times IUR_i \qquad (8) $$

where LADDᵢ is the lifetime average daily dose, which differs from ADDᵢ primarily in terms of average timing (AT). LADDᵢ considers a total exposure duration of 25,500 days, based on an average human lifespan of 70 years multiplied by 365 days per year. CSFᵢ represents the cancer slope factor (mg/kg/day), and IURᵢ is the inhalation unit risk (mg/m³). Values for CSF and IUR are presented in Table S5.

The cancer risk (CR) associated with multiple toxicants from a specific chemical family to which an individual may be exposed to is determined by summing the CRᵢ and can be calculated as follows:

$$ \text{CR(Inhalation)} = \sum_i CR_i \qquad (9) $$
The calculation of the individual lifetime cancer risk (ILCR) adjusting for the different age groups was performed as follows:

$$ILCR = CR_{\text{newborn}} \times \frac{1}{70} + CR_{\text{children}} \times \frac{11}{70} + CR_{\text{adolescent}} \times \frac{6}{70} + CR_{\text{adult}} \times \frac{52}{70} \quad (10)$$

# 3. Results

## 3.1. Atmospheric Concentrations

Table 2 presents the average, minimum, and maximum concentrations of the studied compounds, including major and trace elements, PAHs, and phthalates. Among the elements assessed, Al exhibited the highest concentration at 3861 ng/m³. Among PAHs, indeno [1,2,3-c,d]pyrene, benzo[g,h,i]perylene, and benzo[a]pyrene were identified as the most abundant compounds, contributing to 55% of the total PAHs concentration [20]. The PAHs concentration measured in this study was significantly lower than the value reported by Hassan and Khoder (2310 ng/m³) for the GCA during the winter of 2007. In contrast, the observed PAHs levels were higher than those obtained in Lebanon at the Zouk site in winter (4.35 ng/m³) [22], as well as in Bab Ezzouar City, Algeria, at an urban site (10.3 ng/m³) [36]. Among phthalates, bis(2-ethylhexyl)phthalate (DEHP) had the highest concentration, accounting for 94% of the total.

<table><caption>**Table 2.** Average, minimum, and maximum concentrations of compounds, reported in ng/m³, with values below the detection limit indicated as "<D.L." The concentrations of PAHs and phthalates were retrieved from Farah et al. [20]. The detection limits of these compounds can be found in Table S1.</caption><thead><tr><th>Pollutant</th><th>Mean (ng/m³)</th><th>Minimum (ng/m³)</th><th>Maximum (ng/m³)</th></tr></thead><tbody><tr><td colspan="4"><strong>Elements</strong></td></tr><tr><td>Al</td><td>3861</td><td>1041</td><td>21359</td></tr><tr><td>Zn</td><td>322</td><td>39</td><td>1366</td></tr><tr><td>Pb</td><td>182</td><td>9.1</td><td>1473</td></tr><tr><td>Mn</td><td>83</td><td>20</td><td>320</td></tr><tr><td>Cu</td><td>69</td><td>8.5</td><td>353</td></tr><tr><td>V</td><td>12.1</td><td>2.9</td><td>42</td></tr><tr><td>Cr</td><td>8.7</td><td>2.3</td><td>34.1</td></tr><tr><td>Ni</td><td>8.2</td><td>2.3</td><td>23</td></tr><tr><td>As</td><td>4</td><td>0.5</td><td>12.5</td></tr><tr><td>Sb</td><td>3.6</td><td>0.3</td><td>14</td></tr><tr><td>Co</td><td>1.7</td><td>0.3</td><td>6.9</td></tr><tr><td>Cd</td><td>1.1</td><td>0.2</td><td>3.4</td></tr><tr><td colspan="4"><strong>PAHs</strong></td></tr><tr><td>ΣPAHs</td><td>59</td><td>7.3</td><td>617</td></tr><tr><td>B[a]Peq</td><td>14</td><td>0.8</td><td>16</td></tr></tbody></table>
<table><caption>**Table 2.** *Cont.*</caption><thead><tr><th>Pollutant</th><th>Mean (ng/m³)</th><th>Minimum (ng/m³)</th><th>Maximum (ng/m³)</th></tr></thead><tbody><tr><td colspan="4" style="text-align: center; font-weight: bold;">Phthalates</td></tr><tr><td>Bis(2-ethylhexyl)phthalate (DEHP)</td><td>598</td><td>99</td><td>2201</td></tr><tr><td>Dibutylphthalate (DnBP)</td><td>36</td><td>&lt;D.L.</td><td>252</td></tr><tr><td>n-butylbenzylphthalate (BBP)</td><td>0.5</td><td>&lt;D.L.</td><td>2</td></tr></tbody></table>

Moreover, the total concentration of PCDDs was 1469.2 fg/m³, with octachlorinated dibenzo-p-dioxin (OCDD) emerging as the most abundant contributor at 645.6 fg/m³ (Table 3). Among this class of compounds, TCDD, recognized for its toxicity, exhibited a concentration of 10.7 fg/m³. The total concentration of PCDFs (5417.8 fg/m³) was significantly higher than that of PCDDs, with the heptachlorinated dibenzofuran (1,2,3,4,6,7,8 HpCDF) being the most prominent species, accounting for 26% of the total species examined. Furthermore, DL-PCBs reached 6577.3 fg/m³, with PCB 118 representing the major contributor at 3335.8 fg/m³. The observed concentrations in this study were higher by almost three orders of magnitude than those reported for an urban site in Lebanon, where the levels of PCDDs, PCDFs, and DL-PCBs in PM₂.₅ were measured at 26.6 fg/m³, 4.2 fg/m³, and 648 fg/m³, respectively [4]. Moreover, these values surpassed those reported at two urban sites under industrial influence in Lebanon; the Zouk site (PCDDs: 81.1 fg/m³, PCDFs: 82.5 fg/m³, and DL-PCBs: 454.8 fg/m³), and the Fiaa site (PCDDs: 52.0 fg/m³, PCDFs: 71.8 fg/m³, and DL-PCBs: 586.3 fg/m³) [31], and also higher than the values recorded at an urban site in Dalian, China during winter (PCDD/Fs: 1.46 pg/m³ and DL-PCBs: 0.20 pg/m³) [37].

<table><caption>**Table 3.** Averaged concentrations and TEQ of PCDDs, PCDFs, and DL-PCBs, expressed in fg/m³.</caption><thead><tr><th>Compounds</th><th>Abbreviation</th><th>Mean (fg/m³)</th></tr></thead><tbody><tr><td colspan="3" style="text-align: center; font-weight: bold;">PCDDs</td></tr><tr><td>2,3,7,8-tetrachlorinated dibenzo-p-dioxin</td><td>2,3,7,8 TCDD</td><td>11</td></tr><tr><td>1,2,3,7,8-pentachlorinated dibenzo-p-dioxin</td><td>1,2,3,7,8 PeCDD</td><td>60</td></tr><tr><td>1,2,3,4,7,8-hexachlorinated dibenzo-p-dioxin</td><td>1,2,3,4,7,8 HxCDD</td><td>52</td></tr><tr><td>1,2,3,6,7,8-hexachlorinated dibenzo-p-dioxin</td><td>1,2,3,6,7,8 HxCDD</td><td>110</td></tr><tr><td>1,2,3,7,8,9-hexachlorinated dibenzo-p-dioxin</td><td>1,2,3,7,8,9 HxCDD</td><td>72</td></tr><tr><td>1,2,3,4,6,7,8-heptachlorinated dibenzo-p-dioxin</td><td>1,2,3,4,6,7,8 HpCDD</td><td>519</td></tr><tr><td>octachlorinated dibenzo-p-dioxin</td><td>OCDD</td><td>646</td></tr><tr><td style="font-weight: bold;">Sum PCDDs</td><td></td><td style="font-weight: bold;">1469</td></tr><tr><td style="font-weight: bold;">TEQ PCDDs</td><td></td><td style="font-weight: bold;">99.5</td></tr><tr><td colspan="3" style="text-align: center; font-weight: bold;">PCDFs</td></tr><tr><td>2,3,7,8 tetrachlorinated dibenzofuran</td><td>2,3,7,8 TCDF</td><td>419</td></tr><tr><td>1,2,3,7,8 pentachlorinated dibenzofuran</td><td>1,2,3,7,8 PeCDF</td><td>348</td></tr><tr><td>2,3,4,7,8 pentachlorinated dibenzofuran</td><td>2,3,4,7,8 PeCDF</td><td>536</td></tr><tr><td>1,2,3,4,7,8 hexachlorinated dibenzofuran</td><td>1,2,3,4,7,8 HxCDF</td><td>612</td></tr></tbody></table>
<table><caption>**Table 3.** *Cont.*</caption><thead><tr><th>Compounds</th><th>Abbreviation</th><th>Mean (fg/m³)</th></tr></thead><tbody><tr><td>1,2,3,6,7,8 hexachlorinated dibenzofuran</td><td>1,2,3,6,7,8 HxCDF</td><td>575</td></tr><tr><td>2,3,4,6,7,8 hexachlorinated dibenzofuran</td><td>2,3,4,6,7,8 HxCDF</td><td>521</td></tr><tr><td>1,2,3,7,8,9 hexachlorinated dibenzofuran</td><td>1,2,3,7,8,9 HxCDF</td><td>176</td></tr><tr><td>1,2,3,4,6,7,8-heptachlorinated dibenzofuran</td><td>1,2,3,4,6,7,8 HpCDF</td><td>1398</td></tr><tr><td>1,2,3,4,7,8,9-heptachlorinated dibenzofuran</td><td>1,2,3,4,7,8,9 HpCDF</td><td>213</td></tr><tr><td>octachlorinated dibenzofuran</td><td>OCDF</td><td>620</td></tr><tr><td><strong>Sum PCDFs</strong></td><td></td><td><strong>5418</strong></td></tr><tr><td><strong>TEQ PCDFs</strong></td><td></td><td><strong>417.9</strong></td></tr><tr><td colspan="3"><strong>DL-PCBs</strong></td></tr><tr><td>3,4,4',5-tetrachlorobiphenyl</td><td>PCB 81</td><td>57</td></tr><tr><td>3,3',4,4'-tetrachlorobiphenyl</td><td>PCB 77</td><td>157</td></tr><tr><td>2,3',4,4',5'-pentachlorobiphenyl</td><td>PCB 123</td><td>176</td></tr><tr><td>2,3',4,4',5-pentachlorobiphenyl</td><td>PCB 118</td><td>3336</td></tr><tr><td>2,3,4,4',5-pentachlorobiphenyl</td><td>PCB 114</td><td>&lt;D.L.</td></tr><tr><td>2,3,3',4,4'-pentachlorobiphenyl</td><td>PCB 105</td><td>1485</td></tr><tr><td>3,3',4,4',5-pentachlorobiphenyl</td><td>PCB 126</td><td>&lt;D.L.</td></tr><tr><td>2,3',4,4',5,5'-hexachlorobiphenyl</td><td>PCB 167</td><td>414</td></tr><tr><td>2,3,3',4,4',5-hexachlorobiphenyl</td><td>PCB 156</td><td>492</td></tr><tr><td>2,3,3',4,4',5'-hexachlorobiphenyl</td><td>PCB 157</td><td>131</td></tr><tr><td>3,3',4,4',5,5'-hexachlorobiphenyl</td><td>PCB 169</td><td>&lt;D.L.</td></tr><tr><td>2,3,3',4,4',5,5'-heptachlorobiphenyl</td><td>PCB 189</td><td>220</td></tr><tr><td><strong>Sum DL-PCBs</strong></td><td></td><td><strong>6577</strong></td></tr><tr><td><strong>TEQ DL-PCBs</strong></td><td></td><td><strong>4.5</strong></td></tr><tr><td><strong>Average Total TEQ for PCDDs, PCDFs, and DL-PCBs</strong></td><td></td><td><strong>521.9</strong></td></tr></tbody></table>

## 3.2. Health Risk Assessment

Computed hazard quotients (HQᵢ) and cancer risks (CRᵢ) for various compounds across the inhalation exposure pathway and the different age groups are summarized in Tables S6 and S7.

### 3.2.1. Non-Carcinogenic Risk Assessment

The total hazard index for the various examined families of compounds (ΣHI) was 9.7 for newborns, 6.9 for children, 5.4 for adolescents, and 4.9 for adults (Table 4). These values indicate that, for each age group, a significant health risk exists, with the ΣHI surpassing the safety threshold of 1 by up to nearly an order of magnitude. These variations highlight the differing levels of risk exposure across the lifespan.

In this assessment of non-carcinogenic health risks, the families of compounds evaluated included major and trace elements, PAHs, PCDD/Fs, and DL-PCBs. In contrast, phthalates were not considered in this assessment, owing to the absence of established reference values for the non-carcinogenic risk calculation.
<table><caption>**Table 4.** Hazard Index (HI) values for various classes of compounds, along with total Hazard Index (ΣHI) values for these compound classes, categorized by age groups. Values are not reported for phthalates due to the absence of reference values (RfD and RfC).</caption><thead><tr><th>Age Category</th><th>Class of Compounds</th><th>Inhalation</th></tr></thead><tbody><tr><td rowspan="5">Newborns</td><td>PAHs</td><td>1.7</td></tr><tr><td>Phthalates</td><td>-</td></tr><tr><td>Major and trace elements</td><td>8.0</td></tr><tr><td>PCDDs, PCDFs, and DL-PCBs</td><td>0.003</td></tr><tr><td>ΣHI</td><td>9.7</td></tr><tr><td rowspan="5">Children</td><td>PAHs</td><td>1.7</td></tr><tr><td>Phthalates</td><td>-</td></tr><tr><td>Major and trace elements</td><td>5.2</td></tr><tr><td>PCDDs, PCDFs, and DL-PCBs</td><td>0.003</td></tr><tr><td>ΣHI</td><td>6.9</td></tr><tr><td rowspan="5">Adolescents</td><td>PAHs</td><td>2.2</td></tr><tr><td>Phthalates</td><td>-</td></tr><tr><td>Major and trace elements</td><td>3.2</td></tr><tr><td>PCDDs, PCDFs, and DL-PCBs</td><td>0.004</td></tr><tr><td>ΣHI</td><td>5.4</td></tr><tr><td rowspan="5">Adults</td><td>PAHs</td><td>2.2</td></tr><tr><td>Phthalates</td><td>-</td></tr><tr><td>Major and trace elements</td><td>2.7</td></tr><tr><td>PCDDs, PCDFs, and DL-PCBs</td><td>0.004</td></tr><tr><td>ΣHI</td><td>4.9</td></tr></tbody></table>

1. Major and trace elements

Among the evaluated major and trace elements via the inhalation pathway, HQᵢ values of Pb and Mn consistently exceeded the threshold in all age groups, indicating potential health concerns (Table S6). Specifically, Mn posed the greatest risk, with HQᵢ values of 3.9 for newborns, 2.5 for children, 1.4 for adolescents, and 1.2 for adults. Pb also exhibited elevated HQᵢ values, with newborns showing the highest value (3.4), followed by children (2.2), adolescents (1.3), and adults (1.1). The remaining elements, such as Al, V, Cr(IV), Co, Ni, Cu, Zn, As, Cd, and Sb, had HQᵢ values below 1, suggesting a negligible probability of non-carcinogenic risk. Moreover, together Mn and Pb were the primary contributors to HI values, accounting for over 84% across all age groups. Prolonged exposure to Pb results in its accumulation within the bone matrix, leading to neurotoxicity, anemia, renal toxicity, and reproductive health effects, particularly in children and infants [38], while excessive Mn inhalation is linked to neurotoxic effects [39]. The findings of this study are consistent with those reported by Shetaya et al. [18] at an urban site in Dokki, GCA, indicating that Pb represents the highest non-carcinogenic risks for adults and children, while other elements, such as Cr(VI) and Cu, showed negligible risk.

The HI values via inhalation were 8.0 for newborns, 5.2 for children, 3.2 for adolescents, and 2.7 for adults (Table 4). In fact, children are particularly vulnerable due to mouth breathing and higher physical activity levels, which increase the penetration of airborne particles into the lungs [34]. In contrast, Motesaddi Zarandi et al. [40] reported in an urban area of Tehran, Iran, that the non-carcinogenic risk via the inhalation pathway was below unity. The observed differences can be primarily attributed to exposure parameters. Notably, the exposure frequency and the exposure duration employed in this study (350 days/year and 52 years, respectively) are considerably higher than the values reported in the latter study (180 days/year and 24 years, respectively). Furthermore, HI values in this study were higher than those reported by Shetaya et al. [18] and by Hu et al. [41] in Nanjing,
China. These findings highlight ongoing risks from elemental contaminants, particularly for newborns and children, as vulnerable subgroups within the general population [40,42], emphasizing the need for targeted interventions to reduce exposure.

## 2. PAHs

The total concentration of the 16 PM<sub>2.5</sub>-bound PAHs in this study was 58.9 ng/m<sup>3</sup>, yielding a B[a]P<sub>eq</sub> value of 14.0 ng/m<sup>3</sup> [20]. Chronic exposure to PAHs has been associated with the development of respiratory diseases, cardiovascular disorders, and suppression of immune system function [43]. The HQ values for B[a]P<sub>eq</sub> via inhalation were equal for newborns and children, with a value of 1.7, while adolescents and adults had a slightly higher HQ of 2.2 (Figure S1), all exceeding the threshold value of 1. This indicates potential non-carcinogenic risks across all age groups.

## 3. PCDD/Fs and DL-PCBs

The total TEQ for PCDDs, PCDFs, and DL-PCBs yielded a total toxic equivalent concentration (TEQ) of 521.9 fg/m<sup>3</sup> (Table 3). This value was 127 and 61 times higher than the values reported for sites in northern (4.1 fg/m<sup>3</sup>) and central Taiwan (8.5 fg/m<sup>3</sup>) [44], indicating significantly higher PCDDs, PCDFs, and DL-PCBs contamination in Cairo. Among these classes, PCDFs emerged as the predominant contributor to total TEQ (80%), followed by PCDDs (19%), and DL-PCBs (1%). The HQ for inhalation exposure was lower than 1 across all demographic groups, with values of 0.003 for newborns and children, and slightly higher at 0.004 for adolescents and adults (Table 4), indicating the absence of significant non-carcinogenic health risks in any age group.

### 3.2.2. Carcinogenic Risk Assessment

The total cancer risk (ΣCR) for the various families of compounds across different age groups exhibited distinct trends. ΣCR values for each age group were as follows: 2.4 × 10<sup>-6</sup> for newborns, 1.9 × 10<sup>-5</sup> for children, 7.7 × 10<sup>-6</sup> for adolescents, and 6.0 × 10<sup>-5</sup> for adults (Figure 2). These values indicate that, for each age group, exposure to the various carcinogenic species highly exceeded the acceptable risk of 10<sup>-6</sup>. Notably, regulatory agencies have adopted *de minimus* and *de manifestis* risk limits of 10<sup>-6</sup> and 10<sup>-4</sup>, respectively; risk values exceeding 10<sup>-4</sup> are considered unacceptable [6,34].

In this context, and in our assessment in Cairo, none of the calculated ΣCR values surpassed the *de manifestis* limit of 10<sup>-4</sup>, and all age groups exhibited risks well above the *de minimis* threshold of 10<sup>-6</sup>. This places the estimated risks within the intermediate range between 10<sup>-6</sup> and 10<sup>-4</sup>, which regulatory agencies typically interpret as indicative of potential concern and requiring further evaluation or risk management. Among the studied populations, adults and children showed the highest ΣCR values (6.0 × 10<sup>-5</sup> and 1.9 × 10<sup>-5</sup>, respectively), reflecting a particularly elevated level of concern compared to newborns and adolescents. These findings suggest that, although the risks do not yet reach the level considered unequivocally unacceptable, they remain significantly above the level regarded as negligible, warranting careful attention and preventive action. To date, only a limited number of studies have assessed the cancer risk associated with various families of compounds.
<figure><img src="image_5.png" /><figcaption>**Figure 2.** Cancer risk (CR) values for various chemical families, including PAHs, phthalates, major and trace elements, PCDDs, PCDFs, and DL-PCBs, assessed across different age categories: newborns, children, adolescents, and adults, as well as for all the population (ILCR). The red dashed line denotes the acceptable threshold value of $10^{-6}$.</figcaption></figure>

## 1. Major and trace elements

The $CR_i$ was assessed for 7 key elements with available IUR and CSF across the different age groups (Table S7). When evaluating cancer risk associated with species via the inhalation pathway, results revealed that $Cr(VI)$, As, and V exhibited noteworthy $CR_i$ values, surpassing the safety limits of $10^{-6}$ for adults, children, and adolescents (Table S7), and highlighting a potential cancer risk. Specifically, As posed the greatest risk, with $CR_i$ values above the threshold for all age groups, except for newborns, which exhibited a value of $5.7 \times 10^{-7}$. The corresponding $CR_i$ values were $4.1 \times 10^{-6}$ for children, $1.3 \times 10^{-6}$ for adolescents, and $9.3 \times 10^{-6}$ for adults. $Cr(VI)$ also demonstrated elevated $CR_i$ values, with newborns showing the lowest risk at $4.8 \times 10^{-7}$, followed by children ($3.4 \times 10^{-6}$), adolescents ($1.1 \times 10^{-6}$), and adults ($7.8 \times 10^{-6}$). V exhibited $CR_i$ values of $3.4 \times 10^{-7}$ for newborns, $3.8 \times 10^{-6}$ for children, $2.7 \times 10^{-6}$ for adolescents, and $2.4 \times 10^{-5}$ for adults. The highest values were observed in children and adults (Table S7), highlighting the need for targeted interventions and regulatory measures to mitigate exposure to these carcinogenic substances. According to IARC, As and $Cr(VI)$ are classified as Group 1 carcinogens to humans, while V is categorized as Group 2B, possibly carcinogenic to humans. Collectively, these elements represented 80% of the $CR_i$ value in newborns, 82% in children, 87% in adolescents, and 88% in adults. Other elements, such as Co, Ni, Cd, and Pb, had $CR_i$ values below the threshold, except for adults (and children, in the case of Co), suggesting minimal risk through inhalation for newborns and adolescents. For inhalation exposure, $CR$ values were $1.8 \times 10^{-6}$ for newborns, $1.4 \times 10^{-5}$ for children, $5.9 \times 10^{-6}$ for adolescents, and $4.7 \times 10^{-5}$ for adults, exceeding the acceptable risk threshold (Table S8). Newborns have a marginally elevated risk, while children and adults face an approximately 8 and 26-fold increase, respectively. Shetaya et al. [18] reported significantly higher $CR$ values in comparison to our study: $1.7 \times 10^{-5}$ for children and $5.6 \times 10^{-5}$ for adults. The observed discrepancies between the two studies can be primarily attributed to potential variations in
the parameters employed in the methodology, such as variations in the exposure durations, exposure time, and body weight of different age categories.

The estimated ILCR associated with exposure to certain elements has been quantified at $3.7 \times 10^{-5}$, markedly higher than the acceptable threshold of $10^{-6}$. This value exceeded those reported in various cities worldwide, including Milan, Thessaloniki, and Los Angeles (Figure 3). This finding indicates a considerable potential risk for cancer development linked to exposure to these elements, particularly As, Cr(VI), and V, which have the highest contribution to cancer risk among examined elements, and account for the majority of the $CR_i$ across all age groups.

## 2. PAHs

B[a]P and DiB[a,h] classified by the IARC as carcinogenic to humans (Group 1) and probably carcinogenic to humans (Group 2A), respectively, contributed the most significantly to the $B[a]P_{eq}$, accounting together for 82% of its value [45]. Among CR values for inhalation, all age groups except newborns ($5.1 \times 10^{-7}$) exceed the threshold value (Table S8), with adults having the highest risk ($8.2 \times 10^{-6}$), followed by children ($3.6 \times 10^{-6}$) and adolescents ($1.1 \times 10^{-6}$). The results of our study were higher than those reported in Khairy and Lohmann [8] for the inhalation pathway, where PAH-related cancer risks in residential/traffic sites in Alexandria, Egypt, ranged from $4.5 \times 10^{-7}$ to $2.0 \times 10^{-6}$.

The estimated individual lifetime cancer risk (ILCR) associated with exposure to PAHs is calculated to be $6.8 \times 10^{-6}$, significantly surpassing the acceptable limits of $10^{-6}$. This value was higher than those reported in several other cities worldwide, such as Milan, Thessaloniki, and Los Angeles, but lower than those reported in Zouk, Peshawar, Xia-men, Changzhou, Karaj, and Nicosia (Figure 3). This finding indicates that individuals exposed to PAHs face a lifetime cancer risk that is approximately 7 times greater than the regulatory benchmark for acceptable risk. Such a deviation from the threshold suggests a pressing concern regarding public health and the need for mitigation measures. B[a]P and DiB[a,h]An are identified as the predominant contributors to the $B[a]P_{eq}$, as previously discussed. Therefore, it is imperative to prioritize managing these compounds by thoroughly investigating their respective sources and implementing stringent regulatory measures in GCA.

## 3. Phthalates

At the cancer risk level from phthalates, DEHP was the sole compound among those examined for which a reference value was established for the inhalation route (Table S7). The CR values were below the threshold across all age groups. These results indicate that inhalation exposure to DEHP does not pose a significant cancer risk. The $CR_i$ values for DEHP in this study were significantly higher than those reported in Dongying, China, where the values were $5.92 \times 10^{-11}$ for adults and $5.78 \times 10^{-11}$ for children [46]. Additionally, the $CR_i$ values for DEHP exceeded those recorded at the Fiaa site in Lebanon ($5.2 \times 10^{-9}$ for newborns, $3.7 \times 10^{-8}$ for children, $1.2 \times 10^{-8}$ for adolescents, and $8.6 \times 10^{-8}$ for adults) [31]. These results suggest a potential long-term carcinogenic concern associated with DEHP exposure, aggravated in children and adults, who exhibited the highest $CR_i$ values.

The estimated ILCR associated with phthalate exposure was $6.4 \times 10^{-7}$, which falls below the commonly accepted threshold of $10^{-6}$. This indicates that the lifetime cancer risk from phthalate exposure in this study can be considered negligible or within the range regarded as acceptable by regulatory standards. This value exceeded those reported for two sites in Lebanon (Zouk and Fiaa) [31] (Table S9). Notably, the primary contributor to this risk is DEHP, accounting for the CR values observed across all age demographics, due to its widespread use as a plasticizer [47]. A previous study by Farah et al. [20] has suggested a possible correlation between DEHP exposure and local environmental
practices, particularly the open burning of municipal waste, since this practice is prevalent throughout Cairo. These results underline the need for public health interventions and regulatory measures to mitigate DEHP exposure, particularly in regions where such waste management practices are common.

## 4. PCDD/Fs and DL-PCBs

Inhalation CR associated with TEQ varied across different age groups (Table S7), reflecting differences in exposure and vulnerability. CR values were above the threshold of $10^{-6}$ in adults (4.7 $\times$ $10^{-6}$), while lower values (below $10^{-6}$) were observed in children, adolescents, and newborns (Figure 2), suggesting that adults are more susceptible to potential carcinogenic risks compared to other age groups. This heightened risk could be attributed to cumulative lifetime exposure. Furthermore, newborns (6.8 $\times$ $10^{-8}$) and adolescents (5.4 $\times$ $10^{-7}$) have lower CR values compared to children and adults. Studies reporting CR values for TEQ are limited, making direct comparisons with other studies conducted in different regions challenging.

The estimated ILCR for inhalation linked to exposure to PCDDs, PCDFs, and DL-PCBs was $3.7 \times 10^{-6}$, which was higher than the threshold of $10^{-6}$, indicating a considerable health risk. This value exceeded those reported for measurement sites such as Taipei, Zouk, and Fiaa (Table S9). Based on this estimate, approximately 4 excess cancer cases per 1 million exposed individuals might occur over a lifetime. PCDDs, PCDFs, and DL-PCBs are generated and released into the environment from various sources, including solid waste incineration and the combustion of agricultural residues such as rice straw [9]. The emissions raise considerable concerns for nearby populations in GCA, particularly due to the prevalent practice of waste burning [48]. This is particularly revealed by the significant difference between the estimated ILCR and the acceptable limit, which indicates that current exposure levels could be harmful to public health, necessitating interventions to reduce exposure to PCDDs, PCDFs, and DL-PCBs, thus safeguarding public health and the environment.

## 3.3. Limitations

Risk assessment is often associated with significant uncertainty, especially in ecological risk assessment, where single-point short-term estimates are used to assess population-level chronic risk. In addition, given the complexities of assessing risks from combined chemical exposure, we followed the USEPA default method in applying the additivity principle to quantify cancer risks within and between different examined families of pollutants, particularly when site-specific toxicity data for the combined exposures are lacking. This method is limited by assuming toxicological independence between and within the fractions, meaning it does not account for interactions. Although synergistic or potentiating effects could theoretically occur, such interactions are unlikely at the concentrations observed in our study. Moreover, with respect to toxicological reference values, uncertainties primarily arise from the reliance on animal data to predict human responses. Many substances identified as carcinogens in animal models may not necessarily pose the same risk to humans, and vice versa. To address this uncertainty, regulatory agencies generally adopt conservative assumptions, such as treating humans as at least as sensitive as the most sensitive animal species [49]. Additionally, uncertainty exists in estimating cancer risk from some compounds due to inconclusive evidence regarding their carcinogenicity to humans, such as those classified in IARC Groups 2A and 2B. In addition, the use of a no-threshold assumption for carcinogens introduces further uncertainty, as the hypothesis that any exposure above zero carries some cancer risk has not been conclusively proven, particularly for substances with non-genotoxic modes of action [49].
<figure><img src="image_6.png" /><figcaption>**Figure 3.** Carcinogenic risk examples for children (C), adults (A), and the whole population (P) across selected countries worldwide. a This study; b [18]; c [29]; d [31]; e [50]; f [51]; g [52]; h [53]; i [41]; j [54]; k [55]; l [56]; m [6]; n [23].</figcaption></figure>

Furthermore, a key limitation lies in the use of concentration data averaged over a defined period, which may not capture temporal variability in pollutant levels over a longer period. Risk estimates are calculated for different age groups, including newborns, children, adolescents, and adults, with extrapolation to lifetime exposure. However, as ambient pollutant concentrations evolve, the associated risk estimates also change. Consequently, health risk assessments must be recalculated whenever updated concentration data become available to maintain accuracy and relevance. Because this data was unavailable, we instead used a concentration-based model combined with potency indicators, such as cancer slope factor or inhalation unit risk value, to estimate health risks [57]. Future studies in Cairo could benefit from cohort-based designs to better assess short- and long-term health effects associated with PM<sub>2.5</sub> components and to compare exposure and health outcomes across various geographic areas.

**4. Conclusions**

This study offers a thorough assessment of the health risks associated with PM<sub>2.5</sub>-bound species, including major and trace elements, PAHs, phthalates, PCDDs, PCDFs, and DL-PCBs, collected in an urban location in the Greater Cairo Area. It is the first study to measure PCDDs, PCDFs, and DL-PCBs in Egypt. Moreover, it represents the first ecological risk assessment linked to exposure to these families of air pollutants in Cairo, Egypt.

Findings reveal significantly high atmospheric concentrations of various hazardous pollutants, with Al being among the most prevalent elements, DEHP being the predominant phthalate, and PCDFs making up the majority of the total toxic equivalent concentration of PCDDs, PCDFs, and DL-PCBs. Moreover, this risk assessment raises important concerns regarding both non-carcinogenic and carcinogenic risks. For all age categories, the total hazard index (ΣHI) values exceeded the safety threshold of 1, with newborns and children being the most vulnerable. Pb, and Mn were linked to the most significant non-carcinogenic hazards. Similarly, carcinogenic risk assessments indicated that the total cancer risk (ΣCR) surpassed the acceptable limit (10<sup>-6</sup>) across all demographics. The main contributions comprised As, Cr(VI), V, PAHs, and PCDDs/PCDFs/DL-PCBs. Notably, the highest
individual lifetime cancer risk was found for major and trace elements, and PAHs, followed by PCDDs/PCDFs/DL-PCBs. These findings highlight the need for more stringent air pollution management measures in Cairo, with a particular focus on protecting at-risk populations. Effective mitigation strategies should prioritize key pollution sources by establishing a clear linkage between health risks and specific pollutant origins, enabling the reduction in exposure to the most hazardous air contaminants, and thereby minimizing the associated health burden. Ultimately, this study can serve as a baseline for policymakers in developing targeted interventions and implementing stricter regulatory measures to safeguard public health and the environment, thereby mitigating exposure.

**Supplementary Materials:** The following supporting information can be downloaded at: https://www.mdpi.com/article/10.3390/atmos16101214/s1, Table S1: Detection limits of major and trace elements, PAHs, and phthalates expressed in ng/m3; Table S2: Proposed Toxicity Equivalency Factors (TEF) for individual Polycyclic Aromatic Hydrocarbons (PAHs) [28]; Table S3: TEF for polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and dioxin-like polychlorinated biphenyls (DL-PCBs) according to WHO 2005 guidelines [27]; Table S4: Reference dose (RfD) values for the inhalation pathway, for the different compounds assessed, as well as reference concentration (RfC) values, as reported by Fadel et al. [31]; Table S5: Cancer slope factor (CSF) values for the inhalation exposure pathway, for the different compounds assessed, as well as inhalation unit risk (IUR) values, as reported by Fadel et al. [31]; Table S6: Hazard quotients (HQi) for different compounds across the inhalation exposure pathways by age group, including newborns, children, adolescents, and adults; Table S7: Cancer risk (CRi) for different compounds across the inhalation exposure pathways by age group, including newborns, children, adolescents, and adults; Table S8: Cancer risk (CR) values for different classes of compounds, along with total cancer risk (ΣCR) values for these compound classes, stratified by age categories; Table S9: Carcinogenic risk examples for newborns (N), children (C), adolescents (Ado), adults (A), and the whole population (P) across various countries worldwide [58–60]; Figure S1: Hazard Index (HI) values assessed for various chemical families, including PAHs, phthalates, major and trace elements, and PCDDs, PCDFs, and DL-PCBs, across different age categories: newborns, children, adolescents, and adults, as well as for all the population. The red dashed line indicates the acceptable threshold value of 1.

**Author Contributions:** Conceptualization, A.B., J.S. and C.A.; methodology, C.A.; validation, C.A.; formal analysis, E.F., M.F. and M.I.; investigation, E.F., H.R.D., N.F., F.L. and D.C.; resources, J.S.; writing—original draft preparation, E.F.; writing—review and editing, M.F., H.R.D., N.F., S.K.H., M.B., M.E.-N. A.W., M.A., M.I., S.S., A.B., J.S., F.L., C.A. and D.C.; supervision, M.F., J.S., F.L., C.A. and D.C.; project administration, A.B. and C.A.; funding acquisition, A.W., A.B., J.S. and C.A. All authors have read and agreed to the published version of the manuscript.

**Funding:** This study has been supported by the European Union's Horizon 2020 research and innovation programme under grant agreement no. 856612 (EMME-CARE) and by the STDF-AUF-IRD launched in 2016 (POLCAIR 'Air Pollution in Cairo: sources and impact).

**Institutional Review Board Statement:** Not applicable.

**Informed Consent Statement:** Not applicable.

**Data Availability Statement:** The data presented in this study are available on request from the corresponding author. The data are not publicly available as it is a part of a thesis study of a student.

**Acknowledgments:** The authors would like to acknowledge Saint Joseph University of Beirut, Lebanon, and Université du Littoral Côte d'Opale (ULCO), France, for granting a doctoral fellowship to Eliane Farah. This project was also funded by the Research Council and the Faculty of Sciences of Saint Joseph University of Beirut, Lebanon. The "Unité de Chimie Environnementale et Interactions sur le Vivant" (UCEIV-UR4492) participates in the ECRIN project, which is financially supported by the Hauts-de-France Region Council, the French Ministry of Higher Education and Research, and the European Regional Development Funds.
**Conflicts of Interest:** The authors declare no conflicts of interest.

**Abbreviations**

The following abbreviations are used in this manuscript:

<table><tr><td>ADD</td><td>Average Daily Dose</td></tr><tr><td>EC</td><td>Exposure Concentration</td></tr><tr><td>RfD</td><td>Reference Dose</td></tr><tr><td>RfC</td><td>Reference Concentration</td></tr><tr><td>HQi</td><td>Hazard Quotient</td></tr><tr><td>HI</td><td>Hazard Index</td></tr><tr><td>LADD</td><td>Lifetime Average Daily Dose</td></tr><tr><td>CSF</td><td>Cancer Slope Factor</td></tr><tr><td>IUR</td><td>Inhalation Unit Risk</td></tr><tr><td>ILCR</td><td>Individual Lifetime Cancer Risk</td></tr><tr><td>PAHs</td><td>Polycyclic Aromatic Hydrocarbons</td></tr><tr><td>PCDDs</td><td>Polychlorinated Dibenzo-p-dioxins</td></tr><tr><td>PCDFs</td><td>Polychlorinated Dibenzofurans</td></tr><tr><td>DL-PCBs</td><td>Dioxin-like Polychlorinated Biphenyls</td></tr><tr><td>B[a]P</td><td>Benzo[a]pyrene</td></tr><tr><td>B[a]P<sub>eq</sub></td><td>Benzo[a]pyrene equivalent</td></tr><tr><td>DEHP</td><td>Bis(2-ethylhexyl)phthalate</td></tr></table>

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