Pro-inflammatory cytokines, markers of oxidative stress, hepatic and renal functions in individuals occupationally exposed to fumes from burning tires

Abstract

AimBurning of tires releases a significant amount of toxic pollutants like polycyclic aromatic hydrocarbons (PAHs), heavy metals, and volatile organic compounds into the air. This study assessed the health implications of occupational exposure to fumes from burning tires.MethodsThis was a population-based cross-sectional study. Fifty exposed and 50 control male subjects were recruited for this study. Pro-inflammatory cytokines, markers of oxidative stress, and hepatic and renal functions were assayed for in the subjects using standard methods. Data were subjected to inferential statistics and analyzed using Student’s t-test.ResultsThe results revealed significantly higher levels of urea (8.67 ± 0.45 mg/dL) and lower levels of creatinine (73.99 ± 2.87 mg/dL) compared to the controls (7.55 ± 0.31 mg/dL and 81.44 ± 2.12 mg/dL respectively); significantly elevated levels of alanine aminotransferase (ALT) (31.61 ± 3.80 U/L), aspartate aminotransferase (AST) (51.12 ± 5.07 U/L) and alkaline phosphatase (ALP) (113.14 ± 7.83 U/L); alterations in the electrolyte panel, including higher potassium (4.63 ± 0.21 mmol/L) and bicarbonate (37.91 ± 4.60 mmol/L) and lower sodium (135.80 ± 2.26 mmol/L); significant increase in the level of interleukin-1 (IL-1β) and interleukin-6 (IL-6); significant increase in serum malondialdehyde and serum total antioxidant status (TAS) levels in subjects occupationally exposed to fumes from burning tires compared to the controls.ConclusionThe observed alterations in kidney and liver function biomarkers, along with pro-inflammatory cytokines and markers of oxidative stress, demonstrated that occupational exposure to fumes from burning tires could result in adverse health effects.

Keywords

Introduction

Burning of tires releases a range of harmful substances such as polycyclic aromatic hydrocarbons (PAHs), carbon monoxide, sulfur dioxide, nitrogen oxides, large quantities of soot, heavy metals like lead, cadmium, mercury, and many other substances into the atmosphere. Some of these pollutants are carcinogenic, and prolonged exposure to them has adverse effects on the renal, hepatic, respiratory, reproductive, cardiovascular, immunological, and inflammatory systems.^1-3 Occupational exposure to these pollutants, which gains entry into the body through inhalation, ingestion, and absorption through the skin, induces cellular oxidative stress by generating reactive oxygen species (ROS). Lipid peroxidation occurs when there is an imbalance in the generation and removal of these ROS, which leads to the breakdown of cellular components, especially phospholipids, which promotes DNA damage and cell necrosis. Studies have implicated lipid peroxidation in the underlying mechanisms of several diseases and disorders like renal, hepatic, cardiovascular, neurodegenerative diseases, and cancer.^4-6
Inflammation, which is the immune system's response to harmful stimuli such as toxic compounds, damaged cells, pathogens, and others, is one of the body’s defense/protective mechanisms that is crucial in maintaining normal health.^7,8 Inflammation protects the body by removing injurious stimuli, initiating the healing process, and restoring the physiological functions of affected tissues and organs ^9,10, but prolonged inflammation may contribute to chronic diseases.^11,12 Studies have shown that inflammation is linked to the genesis of many diseases in humans and that heavy metals exert toxicity in humans by interfering with immune homeostasis and promoting infection. ^13,14
After gaining entry into the body, these harmful substances accumulate in various organs or other parts of the body such as the liver, kidney, lung, heart, brain, and the muscles, making them more vulnerable to attacks. Studies have shown that detectable levels of polycyclic aromatic hydrocarbons occur in almost all internal organs, especially in those organs that are adipose tissue-rich, which can serve as storage depots from which the toxicants can be gradually released.¹⁵ Phases 1 and 2 pathways of xenobiotics biotransformation work together to help in the removal of xenobiotics from the body system. The hepatic cytochrome P450 mixed-function oxidase enzymes play a major role in the metabolism and the biotransformation of endogenous substrates as well as in the biotransformation of exogenous xenobiotics by converting lipophilic xenobiotics such as environmental pollutants, food additives, drugs, insecticides, and substances to hydrophilic compounds which are easier to excrete through the urine or feces. This process is catalyzed by a number of enzymes and generally involves oxidation, reduction, and hydrolysis reactions and is referred to as phase 1 xenobiotics metabolism reaction. Phase 2 conjugation reactions involve conjugation of lipophilic compounds with endogenous conjugation agents such as glucuronic acid, which increases the solubility of the xenobiotic compound.^16,17 In some cases, numerous xenobiotics yield toxic metabolites which are more toxic than the parent xenobiotic, a situation known as toxification.¹⁸
In Nigeria, flames from burning old tires are used in the processing of foods, including de-furring of slaughtered animals, because it is a cheap source of fuel. This is a common practice in most cities across Nigeria without considering the environmental effects and the impact on the health of abattoir workers and the general public who consume foods processed through such a method. De-furring of animals in abattoirs using flame from burning tires has resulted in elevated traces of heavy metals in meats.¹⁹ Despite the ban on the use of flame from burning tires in de-furring of meat, this practice is still ongoing. The purpose of this study was to investigate the adverse health effects that butchers may encounter as a result of occupational exposure to various degrees of emission from burning tires.

Materials and Methods

This was a population-based cross-sectional study in which the renal and hepatic functions, pro-inflammatory cytokines, markers of oxidative stress, and electrolyte panel were investigated in butchers who use flame from burning tires in de-furring animals. This study was conducted between April and September 2025.Study LocationThis study was conducted at the old and new Artisan markets in Enugu metropolis. The old Artisan market, located along Ogui Road adjacent to the Ebeano tunnel driveway, stands as one of the oldest markets in Enugu, specializing in livestock trade such as cows, goats, and sheep. The new Artisan market is situated along the Enugu-Port Harcourt expressway. Butchers at these markets utilize mud blocks or old metal water/oil drums to construct fire mounds with a round base and tapering top covered with metal gauze, where animal and animal parts for de-furring are placed. Old tires are placed inside the fire mound through a side hole and ignited (Figure 1).
Figure 1: De-furring mound used by butchers in meat processing (Image created by the first author)SubjectsUsing a purposive sampling method targeted at selecting subjects occupationally exposed to fumes from burning tires, fifty (50) male butchers were selected for this study. The subjects were recruited for this study if they: were aged 18 years and above, expressed willingness to participate and gave their informed consent, had worked as a butcher and had been exposed to fumes of burning tires through inhalation, dermal absorption, or ingestion for at least 3 years, had no pre-existing liver or kidney disease and no pre-existing inflammatory conditions.
Subjects were excluded if they were below 18 years of age, were unwilling to participate or unable to give informed consent, had worked as a butcher for less than 3 years, or had pre-existing liver or kidney or inflammatory disease or conditions. Those with any form of cancerous condition and those who smoked cigarettes were also excluded from the study. The control subjects involved 50 males who were not occupationally exposed to fumes from burning tires and who did not meet any of the exclusion criteria listed above. Details of the study design and sample size determination were as described by Leidel et al. 1977.²⁰Sample CollectionAfter fulfilling the above inclusion criteria, blood samples (6 mL) were collected from each subject into a container for biochemical assays.Biochemical AssaysLiver FunctionSerum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were measured for the evaluation of liver function. The method described by Reitman and Frankel 1957 ²¹ was used in the determination of the levels of alanine aminotransferase and aspartate aminotransferase with slight modification, while alkaline phosphatase was determined according to the method described by Kind and King 1954.²²Kidney FunctionUsing a colorimetric method, creatinine in the serum was determined by the Jaffe reaction, where creatinine combines with alkaline picrate to form a red‐colored chromophore. The absorbance was measured in the 490–510 nm range, and the absorbance is directly proportional to the serum creatinine concentration.²³ Blood urea was determined using the direct colorimetric method as described by Barker 1944.²⁴Pro-Inflamatory CytokinesSerum concentrations of interleukin-1β (IL-1β) and interleukin-6 (IL-6) were measured using Melsin human enzyme-linked immunosorbent assay (ELISA) kits (EKHU-0147, EKHU-0140; Melsin Medical Co. Ltd, Changchun, China).Markers of Oxidative StressMalondialdehyde (MDA), a marker of lipid peroxidation, was analyzed using the method of Ohkawa et al., 1979 ²⁵, while the method described by Koracevic et al., 2001 ²⁶ was employed to assay total antioxidant status (TAS).Electrolyte PanelSerum electrolyte levels were determined using the ion-selective electrode module of the COBAS 6000 (c501) analyzer manufactured by Roche Diagnostics, Germany.Ethical ApprovalBefore the commencement of this study, the protocol and ethical approval were sought and obtained from the University of Nigeria College of Medicine Ethics Committee on 3rd April 2025, with approval number COMHREC/2025/04/029.Statistical AnalysisData analysis was performed using the Statistical Package for the Social Sciences (SPSS) version 22 and subjected to inferential statistics, including Student’s t-test (independent two-sample t-test). A probability value less than 0.05 was considered statistically significant.Reporting GuidelinesThis study was reported in accordance with the STROBE guideline.

Results

Subjects exposed to fumes from burning tires showed a significant increase (P < .05) in ALT (31.61 ± 3.80 U/L), AST (51.12 ± 5.07 U/L), ALP (113.14 ± 7.83 U/L), interleukin-1 (22.17 ± 4.09 pg/mL), and interleukin-6 (13.63 ± 7.11 pg/mL) when compared with their respective controls (Table 1).
Renal function results showed higher urea levels (8.67 ± 0.45 mg/dL) and lower creatinine levels (73.99 ± 2.87 mg/dL) in individuals exposed to fumes from burning tires than in controls (7.55 ± 0.31 mg/dL and 81.44 ± 2.12 mg/dL, respectively) (Table 2).
Malondialdehyde (MDA) of subjects exposed to fumes from burning tires was elevated (10.60 ± 58 µmol/L) compared with the control (7.42 ± 0.31 µmol/L). The P value < .05 showed a statistically significant difference between the test group and the control group (Table 3). The mean TAS of 8.11 ± 0.22 mmol/L of the subjects exposed to polycyclic aromatic hydrocarbon was statistically significantly higher (P < .05) than the mean TAS of 5.16 ± 0.27 mmol/L of the control (Table 3).
Subjects exposed to fumes from burning tires showed statistically significant increases (P < .05) in potassium (4.63 ± 0.21 mmol/L) and bicarbonate (37.91 ± 4.60 mmol/L), and statistically significant decreases in sodium (135.80 ± 2.26 mmol/L) when compared with their respective controls. There was no statistically significant difference in chloride levels between the test group (102.06 ± 2.34 mmol/L) and the control group (101.19 ± 0.32 mmol/L) (Table 4).

Discussion

The liver plays a vital role in almost every metabolic process in the body, including maintenance of homeostasis, and is involved in the metabolism of drugs and xenobiotics.²⁷ The findings of this study showed significant alterations in liver function biomarkers. The result revealed significantly elevated levels of alanine aminotransferase (ALT) (31.61 ± 3.80), aspartate aminotransferase (AST) (51.12 ± 5.07) and alkaline phosphatase (ALP) (113.14 ± 7.83) in individuals occupationally exposed to fumes from burning tires compared to the controls (20.30 ± 0.81, 21.61 ± 1.05 and 84.19 ± 3.23) respectively (Table 1); which is suggestive of liver damage. The observed increase in ALT and AST levels may indicate liver cell damage or inflammation due to PAH-induced hepatotoxicity. Additionally, the elevated ALP levels suggest cholestasis, which can occur secondary to liver injury caused by PAH exposure. This is in accordance with the study carried out by Ufelle et al. (2020), Zhang et al. 2019 and Chen et al. 2006 with elevations in liver enzymes among workers exposed to PAHs and other xenobiotics in various occupational settings.^28-30
Xenobiotic detoxification involves multiple organs working together to remove harmful substances from the body. The kidney filters waste and toxins from the blood, which are excreted through the urine. Individuals exposed to fumes from burning tires had higher urea levels (8.67 ± 0.45 mg/dL) and lower creatinine levels (73.99 ± 2.87 mg/dL) than controls (7.55 ± 0.31 mg/dL and 81.44 ± 2.12 mg/dL, respectively), indicating possible kidney injury or dysfunction (Table 2).When the kidneys are injured as a result of polycyclic aromatic hydrocarbons, toxins, medications, and other harmful substances, their ability to filter and remove waste products like urea and creatinine is impaired, resulting in increased blood levels of the metabolites. Studies have suggested that polycyclic aromatic hydrocarbons and other environmental toxicants may play a role in the development of chronic health conditions including renal dysfunction.³¹
Oxidative stress, which is a state of imbalance between the production of reactive oxygen species and the ability of the body to detoxify these harmful substances, is caused by environmental factors such as exposure to fumes from burning tires and other air pollutants, among other factors.³² There was a significant increase in both the serum malondialdehyde (MDA) and serum total antioxidant status (TAS) levels (Table 3), which are markers of lipid peroxidation due to oxidative stress in subjects occupationally exposed to fumes from burning tires compared to the control. Studies on the mechanism of damage caused by polycyclic aromatic hydrocarbons have shown that polycyclic aromatic hydrocarbons and heavy metals can enhance the body’s oxidative stress and increase the body’s reactive oxygen species.^33,34 Polycyclic aromatic hydrocarbons are known potent oxidant stressors which can contribute to inflammation and pathogenesis of chronic disease.³⁵ The potent oxidant stressor of PAHs has been observed in various studies, including studies on occupationally exposed adults in which higher levels of oxidative stress biomarkers and lipid peroxidation were found.³⁶
The kidney is largely thought of as the organ responsible for elimination of drugs, toxins, and waste products from the body, but it performs many other important functions like maintenance of plasma osmolarity, water, and electrolyte balance.^37,38 In this study, subjects exposed to fumes from burning tires showed statistically significant increases (P < .05) in potassium (4.63 ± 0.21 mmol/L) and bicarbonate (37.91 ± 4.60 mmol/L), and a statistically significant decrease in sodium (135.80 ± 2.26 mmol/L) when compared with their respective controls (Table 4). Exposure to PAH has been linked to kidney injury, which can impair the ability of the kidneys to filter and balance electrolytes, leading to imbalances such as hyperkalemia (high potassium) and hyponatremia (low sodium), as was observed in this study.
The immune system is continually exposed to various environmental xenobiotics, including polycyclic aromatic hydrocarbons and heavy metals. As a result of this, various inflammatory signaling pathways are activated, along with reduced disease resistance and inflammation.³⁹ This study showed that fumes from burning tires had a deleterious impact on the immune system. It impacts several pro-inflammatory cytokines, such as interleukins (IL-1β and IL-6), which were significantly increased when compared with their respective controls (Table 1), contributing to inflammatory disorders. Occupational exposure to heavy metals has consistently increased the levels of the pro-inflammatory cytokines.⁴⁰

Limitations

This study was limited by difficulty in isolating tire smoke exposure from lifestyle factors and general ambient urban air pollution.

Conclusion

The observed alterations in kidney and liver function biomarkers, along with pro-inflammatory cytokines and markers of oxidative stress, indicated that occupational exposure to fumes from burning tires could lead to adverse health effects. Burning tires releases a range of harmful substances, including polycyclic aromatic hydrocarbons (PAHs), heavy metals such as lead, cadmium, and mercury, and other compounds, into the atmosphere, which can have adverse effects on the renal, hepatic, and inflammatory systems after prolonged exposure.

Declarations

Abbreviations

References

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