Soil as a Carcinogenic Reservoir: Environmental-Biological Linkage of Polycyclic Aromatic Hydrocarbons and Subclinical Haematological Alterations in the Siltara Industrial Region, Central India
Aayushi Pathak¹, Neelabh Kashyap², Tandesh Lal Chandra³, Pranjal Yadav⁴, Sudhir Yadav⁵*

1,2,3,4,5 Guru Ghasiadas Vishwavidylaya, Bilaspur, Chhattisgarh, India.

¹iucpathak22@gmail.com, ²neelkash17@gmail.com, ³drtlchandra76@gmail.com, ⁴pranjalyadav1602@gmail.com, ⁵sudhirforensic@gmail.com

Abstract

Industrial activities involving combustion represent primary sources of polycyclic aromatic hydrocarbon contamination in emerging industrial zones. Although soil functions as a persistent environmental sink for carcinogenic PAHs, the degree to which this contamination results in human internal dosimetry and physiological perturbations is inadequately understood. The present study examined the environmental–biological continuum of PAHs in the Siltara Industrial Region, Central India, focusing on soil's carcinogenic potential, trophic transfer pathways, and biomarker responses in at-risk populations. PAH concentrations were determined in soil, vegetation, and blood specimens from industrial workers and nearby residents. Total PAH loads, prevalence rates, and toxic equivalency quotients were computed. Bioaccumulation factors were assessed. Independent t-tests, correlational statistics, and multivariate regressions were utilized to evaluate exposure disparities and biomarker correlations. Soil displayed substantial total PAH concentrations with a carcinogenic TEQ of 25.12 BaP-equivalent ppb, affirming its status as a carcinogenic depot dominated by combustion-sourced high-molecular-weight PAHs. Vegetation exhibited preferential uptake of low-molecular-weight PAHs, devoid of quantifiable carcinogenic TEQ. The industrial cohort showed a 3.27-fold elevation in internal PAH burden relative to residents. Nonetheless, renal and hepatic biomarkers lacked significant correlations with PAH exposure. Marginal perturbations in haemoglobin were noted, hinting at incipient subclinical haematological effects. These results demonstrate that industrial soil persists as a carcinogenic PAH reservoir, yet systemic biochemical toxicity appears constrained. Augmented internal PAH levels in workers imply chronic low-level exposure, wherein subtle haematological alterations may foreshadow frank organ pathology.

Keywords:  Polycyclic Aromatic Hydrocarbons (PAHs), Industrial Soil Contamination, Toxic Equivalency Quotient (TEQ), Bioaccumulation, Occupational Exposure, Environmental Toxicology

1. Introduction

Polycyclic aromatic hydrocarbons represent persistent organic pollutants chiefly arising from incomplete combustion of fossil fuels and industrial operations. (Chrysochou et al., n.d.; Kamal et al., 2016; Liu et al., 2021) Their hydrophobic characteristics and environmental persistence promote the accumulation of high-molecular-weight PAHs in soil, (Lamichhane et al., 2016; Ramesh et al., 2014) positioning it as a protracted carcinogenic reservoir. Accordingly, industrial locales dominated by combustion-intensive processes remain prone to enduring PAH contamination (Wei et al., 2021; Zhang et al., 2023).

Although extensive research has quantified PAH levels in environmental compartments, limited studies have bridged soil contamination with trophic transfer and human biomonitoring. (Montaño-Soto et al., 2017; Pérez-Maldonado et al., 2019) Determining the extent to which soil-adsorbed carcinogenic PAHs manifest as detectable internal dosimetry and biochemical perturbations is vital for robust risk appraisal.

The Siltara Industrial Region in Central India exemplifies an expanding industrial corridor susceptible to combustion-emitted PAHs.(Patel et al., 2015) This investigation sought to measure PAH concentrations in soil and vegetation, gauge carcinogenic potency through BaP-equivalent toxic equivalency quotients, characterize plant–soil transfer kinetics, quantify internal PAH loads in exposed cohorts, and probe linkages with renal, hepatic, and haematological biomarkers to illuminate the environmental–biological nexus. Unlike conventional studies limited to environmental monitoring, this work demonstrates that soils in an industrial region function as a persistent carcinogenic reservoir while revealing a disconnect between elevated systemic PAH burden and overt hepatorenal toxicity. Additionally, the study highlights early subclinical haematological alterations and quantifies incremental lifetime cancer risk, thereby providing a comprehensive framework linking environmental contamination with early biological effects in exposed populations.

Figure 1. Environmental–biological exposure pathway of polycyclic aromatic hydrocarbons (PAHs).

2. Materials and Methods

2.1 Study Area

The present study was conducted within the Siltara Industrial Region, Raipur, Central India, characterized by combustion-intensive metallurgical operations, industrial emissions, vehicular exhaust, and proximate residential zones. This setting typifies a combustion-influenced industrial landscape where particulate deposition drives the sequestration of polycyclic aromatic hydrocarbons in soil(Adak & Elumalai, 2021).

Figure 2. Study area map of the Siltara Industrial Region, Raipur, Central India.

2.2 Study Design and Sample Collection

A multi-matrix environmental-biological investigation was implemented to assess PAH distribution patterns and internal dosimetry.

Environmental Sampling

●      Surface soil samples were obtained using pre-cleaned stainless-steel implements.

●      Vegetation samples were collected from plants adjacent to the soil sampling sites.

Samples were preserved in solvent-rinsed amber glass containers and transported under controlled conditions to minimize contamination and degradation.

Human Sampling

Venous blood specimens were collected from:

●      industrial workers

●      nearby residents

Samples were obtained in sterile vacutainers and subjected to standardized laboratory protocols (Kašuba et al., 2020) for biochemical assays and PAH quantification.

2.3 Chemicals and Reagents

All solvents and reagents employed in this study were analytical or HPLC grade, ensuring optimal purity and analytical reliability. n-Hexane, dichloromethane, acetone, and methanol were sourced from Merck, while silica gel for column chromatography cleanup was obtained from SRL Chemicals. Anhydrous sodium sulphate, used for moisture removal, was preheated at 400°C prior to application.

Certified reference standards of polycyclic aromatic hydrocarbons—including naphthalene, acenaphthylene, fluorene, phenanthrene, anthracene, fluoranthene, pyrene, and select benzo derivatives—were acquired from Sigma-Aldrich (purity >98%). Stock standard solutions were prepared in n-hexane and stored at 4°C in amber glass vials to prevent photodegradation; working calibration standards were freshly generated via serial dilution before instrumental analysis.

Ultrapure water for sample preparation and cleaning procedures was generated using a Milli-Q purification system. All glassware was rigorously washed, sequentially rinsed with acetone and n-hexane, and oven-dried prior to use to minimize contamination risk.

2.4 PAH Extraction and Quantification

Polycyclic aromatic hydrocarbons were extracted from soil, vegetation, and blood matrices via optimized solvent extraction protocols, followed by instrumental quantification using gas chromatography–tandem mass spectrometry, (GC-MS/MS) and high-performance liquid chromatography. Air-dried and homogenized soil and vegetation samples underwent Soxhlet extraction with an n-hexane: dichloromethane mixture for 16 h to facilitate efficient recovery of hydrophobic PAHs. Resultant extracts were concentrated under reduced pressure and purified by silica gel column chromatography to remove co-extracted organic interferences. Blood samples were subjected to liquid–liquid extraction, wherein plasma was partitioned with n-hexane, vortexed, and centrifuged to achieve phase separation, the organic layer was then collected, evaporated nearly to dryness, and reconstituted in an appropriate solvent for analysis. PAHs were quantified using a Shimadzu GCMS-TQ2030 system for volatile and semi-volatile congeners, complemented by HPLC with UV/fluorescence detection for confirmation and evaluation of targeted PAHs. Prior to injection, all samples were passed through 0.22 µm membrane filters.

2.5 Toxic Equivalency (TEQ) Assessment

The carcinogenic potency was evaluated using toxic equivalency factors (Craemer et al., 2016) relative to benzo[a]pyrene. The toxic equivalency quotient was determined as follows:

Toxic Equivalency Quotient (TEQ)

where:

·        = concentration of the individual carcinogenic PAH

·        = toxic equivalency factor of the corresponding PAH (relative to benzo[a]pyrene)

. The aggregate carcinogenic load was expressed in BaP-equivalent concentrations(.Isra, 2025).

2.6 Transfer Factor (TF) Calculation

The soil-to-vegetation transfer factor (Zhang et al., 2022) was calculated as follows:

Transfer Factor (TF) Calculation

where:

·     = concentration of PAHs in vegetation

·     = concentration of PAHs in corresponding soil samples

Values of TF > 1 denote preferential bioaccumulation in vegetation, while TF < 1 signifies predominant retention in soil.

2.7 Clinical Biomarker Analysis

Biochemical and haematological parameters were quantified using standardized clinical chemistry protocols.

⒈              Renal Parameters

·       Blood Urea Nitrogen

·       Serum Creatinine

·       Urea

·       Uric Acid

⒉              Hepatic Parameters

·       Alkaline Phosphatase

·       Bilirubin

·       Aspartate Aminotransferase

·       Alanine Transaminase

⒊              Haematological Parameters

·       Haemoglobin

·       Lymphocyte count

·       Eosinophils

2.8 Statistical Analysis

Statistical analyses were conducted using specialized software packages. The analyses included descriptive statistics, assessment of detection frequencies, independent t-tests, Pearson correlation analyses, multivariate linear regression modelling, and effect size quantification. Statistical significance was established at the α = 0.05 level.

3. Results

3.1 Distribution of PAHs in Soil

Eighteen polycyclic aromatic hydrocarbon congeners were quantified in the soil samples. The mean total PAH concentration was 2398.48 ppb, reflecting substantial environmental accumulation.

Among the individual congeners, anthracene displayed the highest mean concentration, followed by benzo triphenylene and 9,10-dimethylanthracene. Detection frequencies varied considerably, with pyrene and triphenylene exhibiting the greatest prevalence. High-molecular-weight PAHs, such as indeno pyrene and benzo fluoranthene, demonstrated consistent presence across samples.

Carcinogenic PAHs collectively contributed a total toxic equivalency of 25.12 BaP-equivalent ppb, predominantly attributable to indeno pyrene

Table 1. Distribution of PAHs in Soil and Plant Samples

Table 2. Carcinogenic PAHs and Toxic Equivalency (TEQ)

Figure 3. Soil carcinogenic contribution of individual PAHs expressed as BaP-equivalent concentration.

3.2 PAHs in Vegetation and Ecological Transfer

Vegetation samples displayed a mean total PAH concentration of 1913.12 ppb. Low-molecular-weight PAHs, including anthracene and acenaphthene, exhibited greater accumulation in vegetation than in soil.

Transfer factor calculations revealed heterogeneous uptake patterns into vegetation. Acenaphthylene and benzo fluoranthene displayed TF values exceeding 1, whereas naphthalene and pyrene yielded TF values below 1. No carcinogenic TEQ was detected in vegetation samples.

3.3 Internal PAH Burden in Human Participants

Industrial participants displayed a 3.27-fold greater internal PAH burden relative to the residential cohort. Effect size analysis revealed a Cohen’s d of 0.82, signifying a substantial exposure disparity. Nonetheless, this intergroup difference failed to achieve statistical significance at conventional levels.

Table 3. Blood PAH Burden and Biomarker Comparison

Figure 4. Comparative total PAH burden in industrial and residential groups.

3.4 Renal and Hepatic Biomarker Profiles

No statistically significant differences were observed between industrial and residential groups in renal biomarkers, including blood urea nitrogen, serum creatinine, urea, and uric acid.

Hepatic biomarkers similarly showed no substantial intergroup variations.

Multivariate linear regression models using total PAH burden as the predictor variable exhibited limited explanatory power for biomarker variability and revealed no evident dose-response relationships.

Figure 5. Correlation heatmaps of total PAH burden and clinical biomarkers in industrial and residential groups.

3.5 Haematological Findings

Assessment of haematological parameters indicated a near-significant intergroup difference in haemoglobin concentrations between industrial and residential cohorts (p = 0.059). Although this discrepancy fell short of the conventional alpha = 0.05 threshold, the trend suggests underlying cohort heterogeneity.

No statistically significant intergroup differences emerged in lymphocyte counts or eosinophil levels.

4. Discussion

4.1 Soil PAH Burden in Regional Context

In this study, soil exhibited a total polycyclic aromatic hydrocarbon concentration of 2398.48 ppb, and a carcinogenic toxic equivalency of 25.12 BaP-equivalent ppb. These concentrations indicate considerable buildup of combustion-origin PAHs within the Siltara Industrial Region.

By contrast, Patel et al.(Patel et al., 2015; Shrivastava et al., 2015) observed that the aggregate of 13 PAHs in road dust from a Raipur industrialized zone averaged 15,282 µg/kg, denoting elevated contamination in dust relative to soil. Such divergence underscores disparate deposition processes between atmospheric particulates and soil, wherein dust functions as a proximate receptor for airborne PAH emissions and soil constitutes a persistent, equilibrated depository.

Additionally, nationwide soil risk evaluations have determined 90th percentile cancer risk levels of 3.156 × 10⁻⁵ for adults in severely contaminated Indian soils, (Kumar et al., 2014; Sankar et al., 2023; Wei et al., 2021) denominated in BaP equivalents and encompassing Raipur among other locales. The 25.12 ppb TEQ recorded in Siltara soils corresponds to these national projections, thereby framing the site's soil within a quantifiable carcinogenic risk paradigm comparable to fellow Indian industrial locales.

4.2 Combustion-Derived Signature and Source Consistency

The predominance of high-molecular-weight polycyclic aromatic hydrocarbons, such as indeno[1,2,3-cd] pyrene and benzo[b]fluoranthene, signifies pyrogenic provenance (Ramteke et al., 2024). Atmospheric monitoring studies in the Raipur region have documented elevated organic aerosol concentrations in areas including Siltara, thereby affirming combustion as the principal emission source.(Giri et al., 2012; Ramteke et al., 2024) These multi-ring PAHs are indicative of industrial and vehicular combustion emissions, in accordance with diagnostic ratios employed in source apportionment methodologies(Ramteke et al., 2024).

4.3 Ecological Transfer and Vegetation Uptake

Plant samples in the present study exhibited a total mean PAH concentration of 1913.12 ppb. Light PAHs (e.g., acenaphthylene) showed TF values exceeding 1, suggesting preferential bioaccumulation of low-molecular-weight compounds in vegetation, whereas carcinogenic high-molecular-weight PAHs demonstrated TF < 1.

Ecological assessments conducted in the Siltara region have noted industrial deposition impacts on local vegetation, though most prior studies have focused on physical stress markers rather than PAH accumulation (Balakrishna et al., 2011). The absence of detectable carcinogenic TEQ in plant matrices of the present study indicates limited ecological amplification, consistent with the expectation that heavier PAHs largely remain soil-bound due to strong hydrophobic partitioning.

4.4 Internal PAH Burden and Exposure Gradient

The mean total blood PAH concentration in the industrial group (475.72 ppb) was markedly higher than in the residential group (145.53 ppb), representing a 3.27-fold elevation and a large effect size (Cohen’s d = 0.82), though the difference was of borderline significance (p = 0.098). These exposure patterns are consistent with regional PM characterization studies in Raipur that identified combustion-related aerosol fractions as dominant contributors to air pollution (Guttikunda et al., 2018; Pervez et al., 2020)

While external environmental contamination (e.g., road dust, soil) shows elevated PAH burdens exceeding 10,000 ppb(Patel et al., 2015), internal blood concentrations are comparatively lower, likely reflecting metabolic processing and clearance of parent PAH compounds following inhalation or dermal contact(Badran, 2019; Fourth National Report on Human Exposure to Environmental Chemicals, 2021).

4.5 Systemic Biomarker Response

Despite expectations of pronounced systemic toxicity, renal and hepatic biomarkers exhibited no significant intergroup differences between industrial and residential cohorts. Multivariate regression analyses demonstrated limited predictive capacity of total PAH burden for clinical biomarker variability, yet underscored that chronic low-level exposures can elicit detectable organ pathology (Aziz et al., 2022; Maciejczyk et al., 2023).

The borderline significant disparity in haemoglobin concentrations (p=0.059) potentially signals an early subclinical response to environmental insult. Nevertheless, the paucity of robust renal or hepatic correlations in this population accords with extant literature attributing constrained systemic perturbation to efficient PAH biotransformation and excretion at analogous exposure gradients. (Sankar et al., 2023; Wei et al., 2021)

4.6 Integrated Regional Perspective

Collectively, regional research demonstrates:

●      Road dust ΣPAHs in Raipur industrial zones reached ~15,282 ppb, much higher than soil ΣPAHs in Siltara ((Patel et al., 2015)).

●      National soil cancer risk indices based on BaP equivalents reached 3.156 × 10⁻⁵ for adults ((Bjelić et al., 2021)).

●      Organic aerosol fractions dominated by high-molecular-weight compounds consistent with industrial combustion profiles ((Isra, 2025; Sankar et al., 2023)).

The present study complements these findings by establishing soil as a carcinogenic reservoir, characterizing ecological transfer, quantifying elevated internal PAH burden among industrial workers, and demonstrating limited clinical toxicity under current exposure conditions.

5. Risk Assessment

5.1 Carcinogenic Risk from Soil (TEQ-Based Assessment)

The total carcinogenic toxic equivalency (TEQ) of soil PAHs was calculated as 25.12 BaP-equivalent ppb. Benzo[a]pyrene is routinely employed as the benchmark carcinogen in PAH risk assessments, with international frameworks utilizing BaP-equivalent concentrations to derive estimates of incremental lifetime cancer risk.(Lemieux et al., 2014)

Although computing a complete ILCR demands site-specific exposure parameters (e.g., ingestion, dermal contact, and inhalation rates), contextual benchmarking against meta-analyses of Indian soils is instructive.(Sankar et al., 2023) Nationwide evaluations report adult cancer risks attributable to soil PAHs in industrial locales ranging from 10^-6 to 10^-5, with Raipur-area projections nearing 2.5 × 10⁻⁵  in zones of pronounced impact.

The Siltara soil TEQ of 25.12 ppb thus corresponds to a moderate yet quantifiable lifetime carcinogenic risk under protracted exposure regimens.

These observations corroborate that:

●      Soil serves as a reservoir for carcinogenic PAHs;

●      Associated risks are chiefly chronic, rather than acute;

●      High-molecular-weight PAHs predominate in the carcinogenic profile.

5.2 Ecological Risk via Vegetation

Although soil PAH concentrations were elevated, plant samples exhibited a mean total PAH concentration of 1913.12 ppb with no detectable carcinogenic toxic equivalency. Transfer factor analysis indicated TF > 1 for low-molecular-weight PAHs, reflecting preferential uptake, whereas carcinogenic high-molecular-weight PAHs remained predominantly soil-bound (TF < 1). These results denote limited dietary amplification of carcinogenic PAHs and negligible enhancement of carcinogenic exposure through ecological transfer, confirming that vegetation does not constitute a primary carcinogenic exposure pathway in the region.

5.3 Internal Exposure Risk (Human Biomonitoring)

Industrial workers exhibited a mean total blood PAH concentration of 475.72 ppb, compared to 145.53 ppb in the residential group—a 3.27-fold elevation with a large effect size (Cohen’s d = 0.82). This pattern substantiates a pronounced exposure gradient between cohorts.

In contrast, renal and hepatic biomarkers showed no significant intergroup differences, while multivariate regression analyses indicated limited predictive utility of total PAH burden for biomarker variability (R² < 0.16). A borderline difference in haemoglobin levels (p = 0.059) hints at potential early haematological perturbation.

These results thus confirm elevated internal exposure without overt organ dysfunction, and possible subclinical haematological modulation consistent with chronic low-dose exposure paradigms.

5.4 Toxicokinetic Considerations

Polycyclic aromatic hydrocarbons are metabolized primarily in the liver through Phase I oxidation via cytochrome P450 enzymes, followed by Phase II conjugation and subsequent excretion. (Bilodeau et al., 2018; Feng et al., 2025; Maciejczyk et al., 2023; Poulsen et al., 2022) The detection of parent PAH compounds in blood signifies ongoing exposure, short-term accumulation, and limited long-term bioaccumulation. (Jodice et al., 2023; Pleil et al., 2010)

This toxicokinetic profile elucidates the observation that while environmental PAH reservoirs remain elevated and internal body burdens are substantially heightened, systemic toxicity is a concern(Sombiri et al., 2024).

5.5 Integrated Risk Characterization

5.6 Incremental Lifetime Cancer Risk (ILCR) and Hazard Quotient

Employing the USEPA soil exposure model with a BaP-equivalent concentration of 25.12 µg/kg, the incremental lifetime cancer risk for adults was calculated as  1.06 × 10⁻⁵ (Kumar et al., 2014),(Qi et al., 2019). This estimate falls within the acceptable risk range (10⁻⁶–10⁻⁴) yet signifies a quantifiable chronic carcinogenic hazard under protracted exposure conditions(Lemieux et al., 2014).

The non-carcinogenic hazard quotient was determined to be 0.0048, well below the safety threshold of 1, indicating negligible health risks from soil exposure.

These results suggest that acute systemic toxicity is unlikely, while chronic carcinogenic exposure remains a pertinent concern in the Siltara Industrial Region.

Table 4. Carcinogenic and Non-Carcinogenic Risk Estimates

The Siltara Industrial Region is characterized by:

●    Persistent carcinogenic polycyclic aromatic hydrocarbons bound to soil(Singh & Singh, 2025)

●    A contamination profile indicative of combustion-derived sources (Sankar et al., 2023)

●    Elevated internal PAH exposure among industrial workers (Koslitz et al., 2023)

●    Indications of potential early haematological alterations(Wang et al., 2019)

The predominant risk stems from protracted carcinogenic exposure, rather than acute systemic toxicity.

6. Conclusion

This study reveals extensive PAH contamination in soils of the Siltara Industrial Region, confirming their role as a carcinogenic sink predominantly derived from combustion sources. Vegetation exhibited selective accumulation of low-molecular-weight PAHs, with negligible translocation of carcinogenic fractions. Industrial workers demonstrated a 3.27-fold increase in systemic PAH levels compared to residential controls; however, no significant renal or hepatic dysfunction was observed. The estimated incremental lifetime cancer risk indicates an acceptable yet discernible chronic hazard, while non-carcinogenic risks remain negligible. Notably, while previous investigations in this region have largely focused on PAH contamination in environmental matrices such as air, soil, and vegetation, the present study uniquely establishes a direct environmental–biological linkage by incorporating human biomonitoring through blood-based PAH assessment. In aggregate, these findings delineate a persistent environmental carcinogenic burden alongside constrained systemic toxicity under prevailing exposure conditions, underscoring the importance of continued biomonitoring and surveillance in industrial settings.

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