Akinfolarin, O.M., Joe-Omusuku, C.N., and Konne, J.L.
References
Concentration (mg/m3) Inhalation Unit Risk (mg/m3) ?1 Health Effect Source Benzo[a]pyrene 2.0 × 10?6 1.1 × 10?3 Carcinogenic (lung cancer) USEPA IRIS (2017) Table 5: Acceptable Risk Levels Risk Type Acceptable Limit Interpretation Carcinogenic Risk (CR) 1 × 10?6 – 1 × 10?4 Acceptable lifetime cancer risk range Hazard Quotient (HQ) HQ < 1 No significant non-cancer health risk Hazard Index (HI) HI < 1 Combined non-carcinogenic effects acceptable These standard values were adopted in this study for calculating exposure concentrations and estimating potential health risks for both adults (abattoir workers) and children (residents near abattoirs). Data Analysis Descriptive statistics were used to summarize pollutant concentrations. Analysis of Variance was applied to determine significant differences among sampling sites. Pearson correlation analysis was used to examine relationships between PAHs and heavy metal concentrations. The statistical analyses were conducted using SPSS version 26 and Microsoft Excel. Graphical representations of results were generated using Origin Pro software. Quality Assurance and Quality Control (QA/QC) Strict QA/QC procedures were followed throughout the study. All reagents used were of analytical grade, and instruments were calibrated prior to each analysis. Field and laboratory blanks were included to monitor contamination. Results and Discussion Polycyclic Aromatic Hydrocarbons and Heavy Metal Levels The Statistical Summary for PAHs at different Locations is presented in Table 6 while the analysis of variance is in Table 7. The mean concentrations of PAHs at the three sampling locations were as follows: Rumuokoro, RM (38.50 ± 21.20 mg/m3), Mile 3, M3 (21.65 ± 19.43 mg/m3), and Government Reserved Area, GR (2. 68 ± 2. 63 mg/m3). The trend is in the order RM > M3 > GR (Fig.2). Table 6: Statistical Summary for PAHs at different Locations PAHs (mg/m3) Locations Mean Std Min Max CV RM 38.50 21.20 8.90 69.80 -28.54 M3 21.65 19.43 4.49 56.20 -12.48 GR 2.68 2.63 1.23 6.62 RM – Rumuokoro, M3 – Mile 3 & GR – Government reserved area (Control) , Fig.2: Comparison of PAHs concentrations at different locations Table 7: ANOVA Results for PAHs Source of Variation Sum of Squares (SS) df Mean Square (MS) F-value p-value Decision Between Groups 2184.53 2 1092.27 17.83 0.001 Significant Within Groups 550.80 9 61.20 Total 2735.33 11 Post-hoc (Tukey’s HSD) Results: RM vs. GR: (p < 0.01); M3 vs. GR: (p < 0.05); RM vs. M3: (p > 0.05) Health Risk Assessment of Polycyclic Aromatic Hydrocarbons The health risk assessment was conducted to evaluate the potential non-carcinogenic and carcinogenic risks to adults and children exposed to PAHs in abattoir air. Benzo[a]pyrene was used as the representative PAH compound due to its high toxicity and carcinogenic potency [12]. Calculations were based on the mean PAH concentrations from the three sites, Rumuokoro (38.50 mg/m3), Mile 3 (21.65 mg/m3), and GRA (2.68 mg/m3) applying standard USEPA equations and toxicity parameters [11]. Carcinogenic risk (CR) was calculated using the inhalation unit risk of BaP, 1.1 × 10?3 (mg/m3) ?1 [12]. The results are presented in Tables 8 and 9. Table 8: Non-Carcinogenic Risk (HQ and HI) of PAHs in Abattoir Air Location Mean PAH (mg/m3) RfC (mg/m3) HQ HQ (Children) HI HI (Children) RM 38.50 2.0×10?6 1.93×107 1.93×107 1.93×107 1.93×107 M3 21.65 2.0×10?6 1.08×107 1.08×107 1.08×107 1.08×107 G 2.68 2.0×10?6 1.34×106 1.34×106 1.34×106 1.34×106 -20.00 -10.00 0.00 10.00 20.00 30.00 40.00 50.00 60.00 RM M3 G PAHs (mg/m3) Locations , Table 9: Carcinogenic Risk (CR) of PAHs in Abattoir Air Location Mean PAH (mg/m3) IUR (mg/m3)?1 CR CR (Children) Acceptable Range (10?6 –10?4) RM 38.50 1.1×10?3 4.24×10?2 4.24×10?2 Exceeds M3 21.65 1.1×10?3 2.38×10?2 2.38×10?2 Exceeds G 2.68 1.1×10?3 2.95×10?3 2.95×10?3 Exceeds Polycyclic Aromatic Hydrocarbons The concentrations of total PAHs (?PAHs) across the three sampling locations showed significant spatial variation. As shown in Table 6 and Fig, 2 the highest mean concentration (38.50 ± 21.20 mg/m3) was recorded in Rumuokoro, followed by Mile 3 (21.65 ± 19.43 mg/m3) while the control site had the lowest concentration (2.68 ± 2.63 mg/m3). The elevated levels observed in Rumuokoro and Mile 3 may be attributed to open burning of animal waste and tyres used in processing hides, coupled with vehicular emissions and limited ventilation typical of abattoir environments [8, 17]. The one-way ANOVA for PAHs revealed a significant difference (p = 0.001 < 0.05) in mean PAH concentrations among the three locations. This indicates that abattoir activities significantly influence PAHs levels in the ambient air. Post hoc comparisons (using Tukey’s HSD) showed that the mean PAHs concentration in Mile 3 and Rumuokoro was significantly higher than in GRA, while the difference between Rumuokoro and Mile 3 was not statistically significant. These results confirm that abattoir operations, such as open burning of animal waste, roasting of hides, and vehicular movement, are the main sources of PAHs in the abattoir environments [17, 18]. The lower PAHs levels in GRA demonstrate the absence of such combustion-based activities, consistent with findings from similar studies in low-emission zones [19]. Health Risk Assessment of Polycyclic Aromatic Hydrocarbons The HQ and HI values for both adults and children far exceed the threshold value of 1, indicating a significant potential for non-carcinogenic health effects among individuals exposed to PAHs in the abattoir environments. The Rumuokoro site recorded the highest HQ/HI, consistent with its higher PAHs concentration, followed by Mile 3 and GRA (control). These values suggest that chronic inhalation exposure could lead to respiratory irritation, oxidative stress, and other toxic effects linked to PAHs [20]. The calculated carcinogenic risks for all sites are significantly higher than the acceptable lifetime cancer risk range (10?6 – 10?4) recommended by USEPA, implying that exposure to PAHs in abattoir air may pose serious long-term carcinogenic risks. Rumuokoro again recorded the highest risk value (4.24 ×10?2), followed by Mile 3 (2.38 ×10?2) and GR (2.95 ×10?3). Although children generally have higher sensitivity to environmental toxins due to their lower body weights and developing systems, in this model both groups exhibited similar CR values because exposure concentration (EC) dominated the calculation. Nonetheless, in real-world conditions, children near abattoirs would experience greater effective risk per body weight due to their physiological vulnerability [9, 21]. Comparatively, the overall health risk pattern (Rumuokoro > Mile 3 > GRA) aligns with the spatial distribution of PAHs concentrations. Elevated HQ and CR values in the abattoir zones reflect intense combustion of animal wastes, burning of tyres and wood for singeing hides, and poor ventilation [22, 23]. The results underscore the need for urgent emission control measures, , enforcement of environmental regulations, and public health awareness among abattoir workers and residents. Conclusion Analytical results revealed that PAHs concentrations were significantly higher in abattoir environments compared to the control area. Analysis of variance results confirmed significant spatial differences (p < 0.05) in PAHs concentrations across the three locations. The order of PAHs concentrations recorded is RM > M3 > G. The HQ and HI values of PAHs for both adults and children far exceeded the threshold value of 1, indicating a significant potential for non-carcinogenic health effects among individuals exposed to PAHs in the abattoir environments. The calculated carcinogenic risks for all sites are significantly higher than the acceptable lifetime cancer risk range (10?6 – 10?4) recommended by USEPA, implying that exposure to PAHs in abattoir air may pose serious long-term carcinogenic risks. , References 1. Amaibi, P., Iyor, E., & Akinfolarin, O. (2025). Assessm
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