CHAPTER ONE

INTRODUCTION

1.1 Background of the study

The kidneys are vital excretory organs responsible for the elimination of metabolic waste

products such as urea and creatinine, regulation of electrolyte balance, blood pressure, acid–base

homeostasis, and production of erythropoietin and active vitamin D (NKUDIC, n.d.; Standring,

2021). The kidneys are particularly susceptible to chemically induced injury because of their

unique physiological features such as; a high renal blood flow rate, effective transport systems,

together with their bioconcentration and biotransformative functions (Gandzali-Ngabe et al.,

2020; Calderon et al., 2022). Renal function is commonly evaluated using biochemical markers

such as serum urea and creatinine, which reflect the kidney’s ability to excrete nitrogenous waste

products (Subramanyam, 2019).

Crude petroleum refining by fractional distillation results in a variety of complex organic

mixtures. They include several classes of liquid fuels like gasoline, diesel fuel, jet fuel, and

kerosene (Obodo et al., 2020; Diatta et al., 2020). These fuels are volatile liquid mixtures with

widespread usage in the internal combustion of engines. The vapor obtained may be considered

as petrol fumes. It consists of hydrocarbons (aromatic, saturated, and unsaturated) and non-

hydrocarbons (N, S, O₂, and various toxic heavy metals) (Diatta et al., 2019). The major routes

of petrol fume exposure are inhalational and dermal. The vapors of petroleum fuels are not safe

when inhaled, even for a few seconds (Obodo et al., 2020). Thus, there is a risk of occupational

exposure to petrol fumes and their constituent toxic compounds amongst affected workers. The

rate of absorption of petroleum hydrocarbons differs in the various organ systems (Obodo et al.,
2020). The lungs have a higher absorption capacity, with less absorption occurring in the

gastrointestinal tract and intact skin, although prolonged contact with gasoline can result in skin

burns (Diatta et al., 2020).

Occupational groups such as petrol station attendants and automobile mechanics are at risk of

chronic exposure to these petroleum products which have been demonstrated to produce

harmful effects, usually due to toxic accumulation of specific components of petroleum fuels in

the body (Obodo et al., 2020; Benson et al., 2021). Many of these effects can be attributed to

some specific hydrocarbon components of petrol, such as benzene, toluene, and xylenes (BTX),

otherwise known as volatile organic compounds (VOCs) (Rahimi Moghadam et al., 2020).

Kidney damage and toxicity caused by xylene and toluene have been reported in humans (Ismail

et al., 2021; Umicevic et al., 2022). Petrol station attendants are continuously exposed to petrol

vapors during fueling operations, (Obodo et al., 2020) while hazardous occupational practices of

automobile mechanics such as regular use of diesel and petrol to wash the hands and feet as

well as constant oral sucking of fuel may account for higher levels of some heavy metals in their

circulation (Oche et al., 2020). Although both groups are occupationally exposed, the pattern and

intensity of exposure may differ, which could influence renal function in different ways.

These hydrocarbon mixtures when in circulation, are oxidized particularly in the kidney and liver

cells of mammals and, in the process, are converted into free radicals or activated metabolites

(Diatta et al., 2020; Lawal, 2022). It is these activated metabolites that react with cellular

components such as membrane lipids to produce lipid peroxidation products, resulting in

structural changes to the plasma membrane and consequently eliciting their toxic effects.

Another possible mechanism of toxicant-mediated injury is via inactivation of enzymes through

protein oxidation and/or DNA strand breaks (Lawal, 2022). This toxicant-mediated cellular
injury results in tissue damage and consequently compromises the overall functionality of the

kidneys.

Several case-control studies in human and animal exposure to unleaded petrol has reported

nephrotoxicity (Diatta et al., 2019; Pontes-López et al., 2020). Renal dysfunction due to constant

exposure of these toxicants is reflected by elevation of certain biomarkers in the blood like urea,

creatinine, serum cystatin C, and serum β2-microglobulin (Sharma et al., 2022). They are used in

the evaluation of renal function. Urea and creatinine are nitrogenous end products of metabolism.

Urea is the primary metabolite derived from dietary protein and tissue protein turnover.

Creatinine is the product of muscle creatine catabolism. Both are relatively small molecules (60

and 113 daltons, respectively). They are excreted almost entirely by the kidneys. An increase in

BUN levels out of proportion to serum creatinine levels often reflects a critical condition

(Inaguma et al., 2018).

Thus, comparing serum urea and creatinine levels in petrol station attendants and automobile

mechanics is important for assessing the renal effects of differing occupational exposures to

petroleum products.

1.2 Statement of the Problem

Petrol station attendants and automobile mechanics are chronically exposed to petroleum

products through inhalation of petrol vapors, dermal contact, and unsafe occupational practices

such as washing with or orally sucking fuel (Obodo et al., 2020; Oche et al., 2020). Such

exposures are known to introduce toxic hydrocarbons and heavy metals into circulation, which

can accumulate in target organs, particularly the kidney, leading to nephrotoxic effects (Rahimi

Moghadam et al., 2020; Ismail et al., 2021). Studies have shown that volatile organic compounds
like benzene, toluene, and xylene, as well as heavy metals in petroleum products, can generate

reactive metabolites and free radicals that cause lipid peroxidation, enzyme inactivation, and

DNA damage in renal cells (Diatta et al., 2020; Lawal, 2022).

Despite documented evidence of nephrotoxicity in experimental and human studies (Pontes-

López et al., 2020; Sharma et al., 2022), there is limited comparative data on how different

patterns and intensities of exposure between petrol station attendants (mainly via inhalation) and

automobile mechanics (primarily via dermal and oral routes) may differentially affect renal

function. This knowledge gap underscores the need to investigate variations in serum urea and

creatinine levels among these occupational groups to provide evidence of possible renal

impairment linked to exposure routes and practices.

1.3 Justification of the Study

The kidney plays a central role in waste excretion, electrolyte regulation, and maintenance of

homeostasis, making it highly vulnerable to toxic injury (Standring, 2021; Gandzali-Ngabe et al.,

2020). Occupational groups like petrol station attendants and automobile mechanics are often

overlooked in occupational health surveillance despite prolonged exposure to petroleum fumes

and fuels. If nephrotoxicity is not detected early, it can progress to chronic kidney disease, which

carries high morbidity, mortality, and economic burden (Inaguma et al., 2018).

Evaluating renal biomarkers such as serum urea and creatinine among these groups provides a

simple, cost-effective, and reliable means of monitoring renal health status (Subramanyam, 2019;

Sharma et al., 2022). This study is justified as it will generate baseline data that can help in

occupational health risk assessment, inform policy on workplace safety, and promote preventive

interventions to reduce renal complications among workers in petroleum-related occupations.

1.3 Aim and Objectives

Aim

To compare serum urea and creatinine levels as markers of renal function between petrol station

attendants and automobile mechanics occupationally exposed to petroleum products

Specific Objectives

1. To determine the serum urea levels of petrol station attendants and automobile mechanics.

2. To determine the serum creatinine levels of petrol station attendants and automobile

mechanics.

3. To compare the serum urea and creatinine levels between the two occupational groups.

4. To assess whether the route and intensity of exposure influence differences in renal function

between petrol station attendants and automobile mechanics.

1.4 Research Questions

1. What are the serum urea levels of petrol station attendants compared to automobile

mechanics?

2. What are the serum creatinine levels of petrol station attendants compared to automobile

mechanics?
3. Is there a significant difference in renal function markers (urea and creatinine) between the

two groups?

4. Could variations in exposure routes and practices account for differences in renal function

among these occupational groups?

1.5 Research Hypotheses

Null Hypotheses (H₀):

1. There is no significant difference in serum urea levels between petrol station attendants and

automobile mechanics.

2. There is no significant difference in serum creatinine levels between petrol station attendants

and automobile mechanics.

Alternative Hypotheses (H₁):

1. There is a significant difference in serum urea levels between petrol station attendants and

automobile mechanics.

2. There is a significant difference in serum creatinine levels between petrol station attendants

and automobile mechanics.

 CHAPTER TWO

LITERATURE REVIEW

2.1 Petroleum Exposure and Renal Risks in Fuel Attendants

2.1.1 Fuel Attendants

Fuel attendants, also known as gas station attendants or petrol pump workers, are individuals

employed at fueling stations to dispense gasoline, diesel, or other petroleum products into

vehicles, handle payments, and perform related tasks, often involving direct exposure to fuel

vapors and fumes through inhalation or skin contact.

They face several renal (kidney-related) risks due to chronic occupational exposure to

petrochemicals in gasoline, such as benzene, toluene, and other volatile organic compounds,

which can lead to nephrotoxicity (Awasthi et al., 2016). Studies have shown that prolonged

exposure is associated with elevated renal function parameters, including increased levels of

blood urea nitrogen (BUN), creatinine, and uric acid, indicating potential early renal dysfunction

or impairment (Asefaw et al., 2020; Moghadam et al., 2020). This exposure may also heighten

the risk of chronic kidney disease, with evidence suggesting alterations in renal electrolytes and

possible progression to more severe conditions over time. (Iyevhobu et al., 2024). Additionally,

there is an elevated risk of renal cell cancer linked to petroleum-related occupations, including

gasoline handling (Peters et al., 2018). These risks tend to correlate with the duration and

intensity of exposure, though some studies note that not all cases progress to full renal disease

(Emmanuel et al., 2025).

2.1.2 Petroleum Exposure and Renal Risks

1. Exposure-Related Factors

The core predisposing element is the nature, duration, and intensity of exposure to gasoline

vapors and related petrochemicals, which act as nephrotoxins by inducing oxidative stress,

inflammation, and tubular damage in the kidneys.

Duration of Exposure: Prolonged occupational exposure significantly increases renal risk. For

instance, Neghab et al. (2015) found that workers with an average exposure duration of about

6.75 years showed higher blood urea and plasma creatinine levels, indicating subclinical renal

dysfunction. Similarly, Olmedo-Buenrostro et al. (2017) reported that the risk of early renal

dysfunction (measured by microalbuminuria) rose notably after 6 or more years of exposure,

with an odds ratio of 2.46 after adjustments. Asefaw et al. (2020) observed more pronounced

increases in urea, creatinine, and uric acid among workers exposed for over 6 years compared to

shorter durations. Emmanuel et al. (2025) noted significant positive correlations between

exposure duration (1-5 years in their cohort) and elevated urea levels, as well as negative

correlations with estimated creatinine clearance. Okoye et al. (2022) linked exposures exceeding

10 years to a 5.9-fold increased CKD risk in petrochemical workers, suggesting cumulative toxin

buildup leads to progressive impairment.

Intensity and Frequency of Exposure: Higher exposure levels, even below threshold limits,

amplify risks. Neghab et al. (2015) documented associations between BTEX concentrations and

altered renal markers like decreased serum sodium and calcium, despite sub-TLV exposure.

Moghadam et al. (2020) , in a meta-analysis, confirmed higher creatinine and BUN in exposed

workers, indicating dose-dependent effects from frequent fuel handling. Roles involving daily 8-

hour shifts with direct vapor inhalation or skin contact further heighten vulnerability.

Route of Exposure: Inhalation is primary, but dermal and incidental ingestion contribute. Studies

like those by Neghab et al. (2015) and Emmanuel et al. (2025) imply that unchecked vapor

exposure without recovery systems leads to systemic absorption, affecting electrolyte balance

(e.g., lower sodium and chloride).

2. Personal and Demographic Factors

Individual characteristics can modulate susceptibility to renal damage from gasoline exposure,

often interacting with occupational hazards.

Age: Older workers may be more predisposed due to natural declines in renal function. Okoye et

al. (2022) found significantly higher mean ages among exposed CKD(Chronic kidney disease)

patients, suggesting age exacerbates petrochemical related risks. Studies like Neghab et al.

(2015) and Olmedo-Buenrostro et al. (2017) adjusted for age (averages around 33-35 years),

noting it as a confounder in biochemical alterations.

Sex: While not always a strong predictor, some studies matched groups by sex to control for

potential differences in toxin metabolism. Olmedo-Buenrostro et al. (2017) and Asefaw et al.

(2020) found no significant sex-based disparities but included it in adjustments.

Genetic and Physiological Variability: Inherent differences in detoxification pathways may play

a role, though specific data in these studies is limited. Moghadam et al. (2020) suggest

variability in responses to BTEX could influence outcomes like lower albumin levels.

3. Environmental and Occupational Factors

The work setting plays a critical role in amplifying exposure and thus renal risks.

Lack of Protective Measures: Absence of personal protective equipment (PPE) like gloves or

vapor recovery systems heightens risks. Neghab et al. (2015)071aa7 and Emmanuel et al. (2025)

highlight poor ventilation and unregulated environments in regions like Iran and Nigeria as

contributors to subclinical effects.

Work Environment Conditions: High-traffic stations or integration with repair shops increase

intensity. Okoye et al. (2022) noted proximity to petrochemical sources (e.g., refineries) as a

factor, with 45.9% of exposed cases residing nearby, compounding occupational exposure.

Job-Specific Roles: Attendants and mechanics face varying intensities; Olmedo-Buenrostro et al.

(2017) focused on repair shop workers, linking their roles to 2.5-fold higher microalbuminuria

risk.

4. Lifestyle Factors

Behavioral habits can synergize with occupational exposure to heighten renal predisposition.

Tobacco use amplifies benzene toxicity. Neghab et al. (2015) reported higher smoking rates

(24.5%) among exposed workers, adjusting for it as a confounder in renal marker changes.

Olmedo-Buenrostro et al. (2017) also controlled for smoking, noting its potential to interact with

exposure.

Diet, Hydration, and Physical Activity: Inadequate hydration in hot climates may concentrate

toxins, though not directly quantified. Studies imply overall health behaviors influence

outcomes.

5. Comorbid Conditions

Pre-existing health issues interact with gasoline exposure to dramatically elevate renal risks.

Overweight/Obesity: Olmedo-Buenrostro et al. (2017) found that exposed workers with obesity

and high cardiovascular risk had an 11.8-fold increased odds of early renal damage.
High Cardiovascular Risk: Combined with exposure and obesity, this factor significantly boosts

risk, as per Olmedo-Buenrostro et al. (2017)8ad3c3. Okoye et al. (2022)274aa8 noted non-

significant trends with hypertension and diabetes.

Other Comorbidities: Conditions like hypertension or diabetes were excluded in some studies

(e.g., Olmedo-Buenrostro et al., 2017) to isolate exposure effects, but they likely amplify risks in

real-world scenarios.

2.2 Automobile Mechanics: Work Practices and Occupational Hazards

Automobile mechanics (also called automotive service technicians or service technicians)

inspect, maintain, diagnose, and repair motor vehicles and their systems, including engines,

transmissions, brakes, electrical systems, heating, ventilation and air conditioning (HVAC), and

bodywork. They work in a variety of settings such as authorized dealerships, private garages,

repair shops, and informal roadside workshops, which are very common in Nigeria. In the course

of their work, mechanics are frequently exposed to fuels, lubricants, solvents, and metal

particulates through tasks such as handling petrol and diesel, changing engine oil, welding, spray

painting, battery servicing, and brake repairs (Oche et al., 2020).

Due to the largely informal and unregulated nature of many mechanic workshops in Nigeria,

personal protective equipment (PPE) is often underutilized, and workplace hygiene standards are

poor, which increases occupational exposure risks (Ozomata et al., 2021). Studies among

Nigerian automobile mechanics have documented significant exposure to heavy metals such as

lead and cadmium (from batteries, paints, and brake linings), volatile organic compounds from

paints and solvents, and hydrocarbons from fuels and exhaust fumes (Iwegbue et al., 2024;

Ogbodo et al., 2024). These exposures have been linked to adverse health outcomes, particularly
affecting the respiratory, hepatic, and renal systems. Long-term occupational exposure has been

shown to predispose mechanics to chronic kidney disease (CKD), liver dysfunction, and other

systemic complications (Adejumo et al., 2023). Furthermore, because many mechanics operate

in hot, poorly ventilated environments, they are also at risk of dehydration and heat stress, which

can aggravate renal injury (Afolabi, 2021).

2.2.1 Occupational Hazards across Automobile Mechanic Subgroups

1. Engine and Brake Specialists

Mechanics who service batteries, brake linings, clutches, and soldered engine parts are

frequently exposed to lead and cadmium. Elevated serum levels of these metals have been

repeatedly associated with impaired renal biomarkers such as increased serum creatinine and

reduced estimated glomerular filtration rate (eGFR). In a cross-sectional study in Southwest

Nigeria, Adejumo et al. (2023) found significantly higher serum lead and cadmium levels among

automobile mechanics compared to controls, with strong correlations to renal dysfunction

indicators, suggesting early chronic kidney disease (CKD). Systematic reviews further confirm

that even low-level chronic exposure to cadmium and lead is nephrotoxic (Yin, 2024).

2. Bodywork Technicians and Spray Painters

Bodywork specialists and spray painters are at risk from volatile organic compounds (VOCs)

such as benzene, toluene, and xylene contained in paints, solvents, and thinners. Diesel

mechanics and technicians are also exposed to petrol and diesel exhaust fumes. Studies among

Nigerian spray painters reported significant associations between solvent exposure and altered
renal biochemical parameters, suggesting subclinical kidney injury (Ogbodo et al., 2024). A

meta-analysis on hydrocarbon exposure also linked chronic exposure in occupational groups

(including petrol station workers) with increased odds of renal dysfunction (Moghadam et al.,

2020).

3. Roadside Mechanics

Mechanics working in informal roadside workshops often operate in hot, poorly ventilated

environments, with little access to hydration. Prolonged exposure to high temperatures combined

with heavy physical activity predisposes them to heat stress and recurrent dehydration.

Occupational reviews highlight this as an emerging non-chemical risk factor for kidney injury,

causing repeated subclinical acute kidney injury (AKI) that can progress to CKD (Chapman et

al., 2021). The risk is further compounded in Nigerian contexts where roadside mechanics lack

adequate workplace safety regulation (Oche et al., 2020).

2.3 Renal Biomarkers

2.3.1 Urea

Urea is an organic compound with the chemical formula CO(NH₂)₂. It is produced in the liver

and serves as the metabolic by-product of protein and nitrogen metabolism (Adeyomoye &

Adewoye, 2018). It helps in the excretion of most nitrogen-containing compounds and is highly

soluble in water; it has a molecular weight of 60 g/mol. It is colorless, odorless, and neutral in

solution. Exogenous urea is usually taken up by specific urea transporters (UT-A and UT-B)

(Anderson et al., 2012).

Urea is the primary metabolite of dietary protein and turnover of tissues. To determine its blood

concentration, the whole urea is assayed and in some cases, only the nitrogen components of

urea are measured. The normal range of urea nitrogen is between 5 and 20 mg/dL. This range

varies due to several factors which include protein content of the diet, protein catabolism, water

content of the body, liver urea biosynthesis, and urea excretion in the kidney (Duranton et al.,

2012). Several methods exist for analyzing urea. The recent techniques are automated, and they

produce reproducible and reliable results. Urea nitrogen can be measured using a diacetyl or

Fearon reaction, which produces a yellow chromogen product when added to urea (Hosten,

1990). The quantification occurs through photometry procedure. Urea concentration can also be

assayed using the enzymatic procedure which involves the breakdown of urea to ammonia and

carbonic acid by the enzyme urease. The absorbance is then measured at a specific wavelength.

Blood urea nitrogen (BUN) test measures the amount of nitrogen in the blood that is derived

from the waste product urea; however, the assay could be performed using serum and not whole

blood (Gounden et al., 2020).

2.3.2 Biosynthesis of Urea (Urea Cycle)

The urea cycle is a series of reactions that result in the production of urea from ammonia. It was

discovered in 1932 by Hans Krebs and Henseleit. Protein catabolism produces ammonia, which

is highly toxic to the body organs. Most organisms eliminate ammonia directly to the external

environment. However, in some animals including humans, ammonia is converted to urea before

its clearance (Keshet et al., 2018). The production of urea is controlled by a series of enzymes

within the cytosol and the mitochondria of cells (Wild et al., 2019; Barmore et al., 2020). In the
mitochondria, ammonia combines with CO₂ using energy from adenosine triphosphate (ATP) to

form carbamoyl phosphate. This combines with ornithine to form citrulline. Citrulline diffuses

out of the mitochondria into the cytosol, where it combines with aspartate to form arginine

succinate, which breaks down to form arginine and fumarate. Arginine receives water to form

ornithine and urea. Ornithine re-enters the mitochondria to initiate another cycle, while urea is

excreted in urine.

2.3.3 Serum Creatinine

Creatinine (Cr), chemically known as α-methyl guanidinoacetic acid, is a substance that appears

as white crystalline particles in its pure state. It has a molecular weight of 113.1 Daltons and

behaves as a cation in aqueous solutions.

It is consistently produced as part of normal muscle cell metabolism, serving as the final product

of creatine (Crn) and phosphocreatine (PCrn) metabolism, and dietary protein intake, and is

eliminated by extrarenal degradation and urinary excretion (Rosner, & Ostermann, 2020).

Serum creatinine (SCr) concentration is the most widely used clinical indicator for assessing the

glomerular filtration rate (GFR). Its widespread use is based on the correlation of its

concentration with the precise measurement of the GFR using the clearance of substances like

inulin, which is considered the gold standard (Levey & Inker, 2017). The broad availability,

technical simplicity, and low cost of Cr measurement contribute to its use in routine renal

function assessment.

Despite these practical advantages, creatinine has limitations as a GFR marker. These include the

imprecision of conventional quantification methods, which rely on chemical reactions (Jaffé)

prone to interference from other molecules. Certain medications, such as cimetidine,

trimethoprim, and abemaciclib, inhibit the tubular secretion of creatinine by competing for

secretion pathways, thereby increasing SCr levels and leading to erroneous estimates of the GFR

(Andreev, Koopman, & Arisz, 1999).

Additionally, Cr levels vary with muscle mass, dietary protein intake, and creatine

supplementation. Levels tend to decrease with aging, in females, and in individuals of White

ethnicity (National Kidney Foundation, 2000).

2.3.4 Production

Creatinine is the end product of creatine and creatine phosphate metabolism (Shahbaz et al.,

2024; Kashani et al., 2020). Creatine, a nitrogenous organic acid, is generated predominantly in

the kidney and liver, and to a lesser extent in the pancreas, using three amino acids: glycine,

arginine, and methionine. This biosynthetic process consumes up to 10% of daily glycine intake,

22% of arginine, and 42% of methionine (Kashani et al., 2020). Formation of creatine begins

with an aminotransferase reaction between L arginine and glycine, producing ornithine and

guanidinoacetate in the liver, pancreas, and kidney. Guanidinoacetate then travels to the liver,

where guanidinoacetate methyltransferase converts it using S adenosylmethionine (SAM) into

creatine and S adenosylhomocysteine (Kashani et al., 2020).

The synthesized creatine is transported to tissues, especially skeletal and cardiac muscle, where

creatine kinase (CK) phosphorylates it to form creatine phosphate (PCr). This high energy

compound acts as a rapid ATP reservoir, particularly during early stages of intense muscular

activity. Within skeletal muscle, creatine and creatine phosphate exist in equilibrium:

approximately 25% is free creatine, and the remainder is creatine phosphate.

Serum creatinine (molecular weight ~113 Da) is produced by the spontaneous, non enzymatic

anhydration (cyclization) of creatine within muscle cells. This process is influenced by pH and

temperature; higher rates occur in acidic environments and elevated temperatures, and it is

irreversible in vivo, occurring at a constant rate: about 1% of total body creatine and ~2.6% of

creatine phosphate are converted to creatinine per day (Ávila et al., 2025; Kashani et al., 2020).

Because this conversion happens continuously, the body’s creatine stores necessitate daily

replenishment via dietary intake of essential amino acids. For example, in a 70 kg man, this may

equate to approximately 500 g of raw meat or the equivalent in protein.

REFERECES
Awasthi, G., Joshi, D., Swarup, A., Mandal, T. K., & Awasthi, D. K. (2016). Nephrotoxicity in
petrol pump attendants of Dehradun region. World Journal of Pharmaceutical Research, 5(7).
Asefaw, T., Wolde, M., Edao, A., Tsegaye, A., Teklu, G., Tesfay, F., & Gebremariam, G.
(2020). Assessment of liver and renal function tests among gasoline exposed gas station workers
in Mekelle city, Tigray region, Northern Ethiopia. PloS one, 15(10), e0239716.
Moghadam, S. R., Afshari, M., Ganjali, A., & Moosazadeh, M. (2020). Effect of occupational
exposure to petrol and gasoline components on liver and renal biochemical parameters among
gas station attendants, a review and meta-analysis. Reviews on environmental health, 35(4), 517–
530.
Iyevhobu, K. O., Usiobeigbe, O. S., Adebanjo, H. A., Kehinde, A., Airhomwanbor, K. O.,
Oweifa, J. T., Obohwemu, K. O., Goodness, O. B., Asibor, E., & Aliche, P. C. (2024). Effect of
petrochemicals to the renal electrolytes of fuel attendants (a case study of Oluyole area in Ibadan,
Nigeria). Acta Scientific Medical Sciences, 8(10), 53–61.
Peters, C. E., Parent, M.-É., Harris, S. A., Bogaert, L., Latifovic, L., Kachuri, L., Villeneuve, P.
J., & The Canadian Cancer Registries Epidemiology Group. (2018). Occupational exposure to
diesel and gasoline engine exhausts and the risk of kidney cancer in Canadian men. Annals of
Work Exposures and Health, 62(8), 978–989
Emmanuel, O. O., Stanley, U. O., Eromosele, O. L., Kingsley, A., Osemu, E. L., Sunday, Y.
B., ... & Oshiokhayamhe13, I. K. (2025). Effects of Petrol Fumes on Renal Function Parameters
of Petrol Station Attendants in Sagamu, Nigeria.
Neghab, M., Hosseinzadeh, K., & Hassanzadeh, J. (2015). Early liver and kidney dysfunction
associated with occupational exposure to sub-threshold limit value levels of benzene, toluene,
and xylenes in unleaded petrol. Safety and Health at Work, 6(4), 312-316.
Okoye, O. C., & Awunor, N. (2022). Is exposure to hydrocarbons associated with chronic kidney
disease in young Nigerians? A case–control study. Frontiers in Nephrology, 2, 1010080.
Olmedo-Buenrostro, B. A., Ortega-Ortiz, J. G., Guzman-Esquivel, J., Delgado-Enciso, O. G.,
Ceja-Espiritu, G., Paz-Michel, B. A., Rodriguez-Sanchez, I. P., Martinez-Fierro, M. L., Baltazar-
Rodriguez, L. M., Melnikov, V., Rodriguez-Hernandez, A., & Delgado-Enciso, I. (2017).
Workplace gasoline exposure increases the risk for early renal dysfunction: A case-control study
in Mexico. Biomedical Research, 28(22), 9859-9863.
Afolabi, F. J., de Beer, P., & Haafkens, J. A. (2021). Occupational risk perception and the use of
personal protective equipment (PPE): a study among informal automobile artisans in Osun state,
Nigeria. Sage Open, 11(1), 2158244021994585.
Iwegbue, C. M., Nnanna, C. A., Ogwu, I. F., Odali, E. W., & Martincigh, B. S. (2024).
Concentrations, sources and exposure to metals in dust from automobile mechanic workshops in
Nigeria. Journal of Trace Elements and Minerals, 10, 100186.
Oche, O. M., Nneka, O. C., Abiola, O. R., Raji, I., Jessica, A. T., Bala, H. A., & Adamu, I.
(2020). Determinants of occupational health hazards among roadside automobile mechanics in
Sokoto Metropolis, Nigeria. Annals of African medicine, 19(2), 80-88.
Ogbodo, J. O., Egba, S. I., Ogbodo, C. G., Onwurah, I. E., & Njoku, O. U. (2024). Effects of
exposure to volatile organic compounds (VOCs) content from paint on automobile paint workers
in Nsukka, South Eastern Nigeria. Heliyon, 10(17).
Ozomata, E. A., Odugbemi, T. O., & Osagiede, E. F. (2021). A study of knowledge of
Occupational Health Hazards and Safety practices among Automobile Mechanics in an urban
area of South-western Nigeria. Nigerian Medical Journal, 62(3), 104-112.
Chapman, C. L., Johnson, B. D., Parker, M. D., Hostler, D., Pryor, R. R., & Schlader, Z. (2021).
Kidney physiology and pathophysiology during heat stress and the modification by exercise,
dehydration, heat acclimation and aging. Temperature, 8(2), 108-159.
Adeyomoye, O. I., & Adewoye, E. O. (2018). Preliminary assessment and antioxidative
properties of methanol extract of Parquetina nigrescens in alloxan-induced diabetic rats. Asian
Journal of Research in Medical and Pharmaceutical Sciences, 3(1), 1–10.
Anderson, M. O., Zhang, J., Liu, Y., Yao, C., Phuan, P. W., & Verkman, A. S. (2012).
Nanomolar potency and metabolically stable inhibitors of kidney urea transporter UT-B. Journal
of Medicinal Chemistry, 55(13), 5942–5950.
Barmore, W., Azad, F., & Stone, W. L. (2020). Physiology, urea cycle. In StatPearls. StatPearls
Publishing.
Duranton, F., Cohen, G., De Smet, R., Rodriguez, M., Jankowski, J., Vanholder, R., … &
European Uremic Toxin Work Group. (2012). Normal and pathologic concentrations of uremic
toxins. Journal of the American Society of Nephrology, 23(7), 1258–1270.
Gounden, V., Bhatt, H., & Jialal, I. (2020). Renal function tests. In StatPearls. StatPearls
Publishing.
Hosten, A. O. (1990). BUN and creatinine. In H. K. Walker, W. D. Hall, & J. W. Hurst (Eds.),
Clinical methods: The history, physical, and laboratory examinations (3rd ed., Chap. 193).
Butterworths.
Keshet, R., Szlosarek, P., Carracedo, A., & Erez, A. (2018). Rewiring urea cycle metabolism in
cancer to support anabolism. Nature Reviews Cancer, 18(10), 634–645.
Wild, K. T., Ganetzky, R. D., Yudkoff, M., & Ierardi-Curto, L. (2019). Hyperornithinemia,
hyperammonemia, and homocitrullinuria syndrome causing severe neonatal hyperammonemia.
JIMD Reports, 44, 103–107.
National Kidney Foundation. (2000). K/DOQI clinical practice guidelines for nutrition in chronic
renal failure. American Journal of Kidney Diseases, 35(6 Suppl. 2), S17–S104.
Kashani, K., Rosner, M. H., & Ostermann, M. (2020). Creatinine: From physiology to clinical
application. European Journal of Internal Medicine, 72, 9–14.
Subramanyam, L. (2019). AMAZING INTERACTION OF VITALS–ORGAN CROSS TALK.
Indian Journal of Practical Pediatrics, 21(2), 111.
Awadalla, A. H., Ahmed, N. A., & Yagoob, A. Y. (2017). The effects of Petroleum Products on
Renal Function among Petroleum Filling Workers Stations in EL-Obied City. European Journal
of Pharmaceutical and Medical Research (ejpmr), 4(10), 395-399
Standring S. Gray's Anatomy: The Anatomical Basis of Clinical Practice. 42nd ed. 2021. Chapter
70-73:Page:1239-1291. 22: 341-364.
The Kidneys and How They Work. National Kidney and Urologic Diseases Information
Clearinghouse (NKUDIC).

Khalaf, E. M., Taherian, M., Almalki, S. G., Asban, P., Kareem, A. K., Alhachami, F. R., ... &
Mohammadi, M. J. (2024). Relationship between exposure to heavy metals on the increased
health risk and carcinogenicity of urinary tract (kidney and bladder). Reviews on Environmental
Health, 39(3), 539-549.
Lafta, M. H., Afra, A., Patra, I., Jalil, A. T., Mohammadi, M. J., Baqir Al-Dhalimy, A. M., ... &
Asban, P. (2024). Toxic effects due to exposure heavy metals and increased health risk
assessment (leukemia). Reviews on Environmental Health, 39(2), 351-362.

Inaguma, D., Koide, S., Ito, E., Takahashi, K., Hayashi, H., Hasegawa, M., Yuzawa, Y., &
AICOPP group (2018). Ratio of blood urea nitrogen to serum creatinine at initiation of dialysis is
associated with mortality: a multicenter prospective cohort study. Clinical and experimental
nephrology, 22(2), 353–364.

Benson, N. U., Anake, W. U., Etesin, U. M., Fred-Ahmadu, O. H., Adedapo, A. E., Ayejuyo, O.
O., & Olajire, A. A. (2021). Chemical fingerprinting and risk evaluation of polycyclic aromatic
hydrocarbons in sediments of coastal ecosystems from the Bight of Bonny, Gulf of Guinea.
Marine Pollution Bulletin, 162, 111–912.

Calderon, J., Martinez, L. M., Gonzalez, C. M., & Perez, A. R. (2022). Petroleum-derived
hydrocarbons: Mechanisms of toxicity and renal implications. Journal of Environmental
Toxicology, 36(4), 421–433.

Diatta, J. B., Konan, K. S., & Okafor, C. (2019). Environmental and health implications of
petroleum fume exposure in urban settings. International Journal of Environmental Health
Research, 29(2), 187–198.

Diatta, J. B., Konan, K. S., & Okafor, C. (2020). Occupational exposure to petrol vapors:
Toxicological perspectives. Toxicology Reports, 7, 56–64.

Gandzali-Ngabe, G., Okeke, A. O., & Eze, C. (2020). Renal oxidative stress in hydrocarbon-
exposed populations: An emerging concern. African Journal of Nephrology, 23(1), 44–52.

Ismail, A. O., Mohammed, K. I., & Suleiman, Y. (2021). Nephrotoxicity associated with toluene
and xylene exposure: Evidence from human case studies. Human & Experimental Toxicology,
40(8), 1290–1298.
Lawal, A. O. (2022). Free radical generation and renal toxicity of petroleum hydrocarbons: A
mechanistic review. Environmental Science and Pollution Research, 29(12), 18145–18158.

Obodo, N. C., Chukwu, O. S., & Ede, C. O. (2020). Health hazards of petroleum fume exposure
among filling station workers. Nigerian Journal of Toxicology, 14(2), 33–41.

Rahimi Moghadam, S., Karimi, A., & Fathi, M. (2020). Volatile organic compounds (VOCs) and
their nephrotoxic effects: A review. Toxicology and Industrial Health, 36(5), 321–330.

Umicevic, M., Petrovic, N., & Markovic, D. (2022). Occupational exposure to xylene: Renal and
systemic effects in workers. International Archives of Occupational and Environmental Health,
95(7), 1453–1462.

Pontes-López, S., Moreno, J., Esteve-Turrillas, F. A., & Armenta, S. (2020). Development of a
simulation chamber for the evaluation of dermal absorption of volatile organic compounds.
Atmospheric Pollution Research, 11(5), 1009–1017.

Sharma, R., Sinha, R., Kaur, R., & Rani, S. (2022). Drug-induced nephrotoxicity and use of
biomarkers. In Biomarkers in toxicology (pp. 1-33). Cham: Springer International Publishing.