1- Introduction

The biochemical activity of the body, represented by the functions of the

kidneys, liver, and heart, is the most important in the life of the organism, so
any external influence that leads to harm or malfunctions in these functions
will lead to great and serious damage to the vital activities of the entire body.
Several studies have been conducted on the effect of some chemical
compounds that are in direct contact with individuals in factories, stations and
refineries, and it was found that they have a significant impact on the
occurrence of such damages [1].
Study showed an increase in the rates of urea, creatine, uric acid and the
proportion of alprotin in the blood of gas station workers. As well as the
imbalance that occurred in the liver functions represented by an increase in
the effectiveness of each of the enzymes (ALT, AST, ALP) [1].
In a study it was shown that the increase in the concentration of lead in
the composition of gasoline has a strong relationship with the occurrence of a
deficiency in creatine [2]. It was noted an increase in the activity of
aminotransferase enzymes (ALT, AST) in the serum of experimental animals
when exposure to gasoline was increased and continued [3].
Also, study showed that exposure to a dose of 100 mg / kg of gasoline
leads to a defect in the concentrations of enzymes (ALT, AST, ALP) and
CPK enzyme in the liver and kidneys of laboratory rats [4]. It was shown that
a change occurred in the tissues of the kidneys and liver, but they noticed that
the increase in the concentration of the enzyme glutathione S-transferase
occurred [5].
Prolonged exposure to gasoline led to an increase in the concentration of
T4 hormone, while it led to a decrease in the concentration of T3 and TSH [6].

1
 Exposure to gasoline vapors leads to a defect in the manufacture of
hemoglobin, as a clear decrease in the concentration of hemoglobin was
observed in the blood of workers exposed to gasoline, as well as a decrease in
the number of red blood cells and the concentration of hemoglobin in male
guinea pigs when exposed to the same conditions of exposure to humans [7].
Study has shown that there is a significant correlation between exposure
to gasoline and leukocyte cancer, as the cells originate from the bone marrow
and, therefore, when the injury occurs, the cells will collect in the bone
marrow, causing the appearance of leukemia as it does not leave the places of
its maturity and thus It leads to a decrease in the number of red blood cells
and white blood cells in the body, in addition to the lack of blood platelets
and the occurrence of anemia [8].
In another study, they noticed that a significant decrease in hemoglobin
concentration was recorded as a result of exposure to leaded gasoline and
other compounds, as well as the case for red blood cells and the rate of
erythrocyte sedimentation, but they noticed that there was a noticeable
increase in the number of white blood cells and the number of platelets [9].
Exposure to gasoline also caused a decrease in the number of red blood cells,
hemoglobin and white blood cells after they obtained the data [10, 11].

2
Aim of the Work

This work aims to discuss the perceptions of gas station workers of the
risks they are exposed to in their work environment. The results can be
extrapolated to humans to assess potential risks to workers From exposure to
gasoline toxicity:

1. Determination of the effects of gasoline on liver and kidney injury,

hematological and biochemical parameters among gas station workers.
2. Diagnosing diseases of people who are highly exposed to gasoline.
3. Studying the side effects of inhaling gasoline and its effect on health.
4. Studying ways to prevent and reduce exposure to gasoline.

3
 2- Literatures Reviews
2.1- Gasoline definition
Automotive fuel, gasoline or petroleum is a clear, flammable, liquid
mixture derived from petroleum consisting primarily of hydrocarbons
[12,13]. It is mainly used as a fuel in most spark ignited internal combustion
engines. It consists mostly of organic compounds obtained by partial
distillation of petroleum, and is enhanced with a variety of (additives). On
average, a 160-liter (42 US gal) barrel of crude oil can produce up to about 72
liters (19 US gallons) of gasoline after processing in an oil refinery,
depending on the (crude oil assay) and on the refined products that are
processed. It is also extracted [14]. A particular gasoline blend has the
property of resisting early ignition (which causes knocking and reduces
efficiency in reciprocating engines) by its octane number, which is produced
in several grades. It was used extensively to increase octane ratings, tetraethyl
lead and other lead compounds, and is no longer used in most fields (but is
still used in aviation [15] and motor racing [16]). Oftentimes other chemicals
are added to gasoline to improve chemical stability and performance
properties, control corrosion and provide fuel system cleaning. Gasoline may
contain oxygen-containing chemicals such as ethanol, methyl tert-butyl ether
(MTBE) or ethyl tert-butyl ether (ETBE) to improve combustion.

2.2- Physicochemical properties

Gasoline: It is a mixture derived from crude oil and it is of hydrocarbons
and its chemical formula is C6H6 and its molecular weight is (78.12 g / mmol)
according to its physical properties and under standard conditions it is a
colorless or pale yellow liquid and it is rapidly evaporating, quickly
flammable in the air and its solubility rate In water up to (1.8 g / liter at a
temperature of 25 °C), it has a slightly pungent smell, its boiling point is
4
(80.1 °C) and its vapor density is (2.77). Gasoline is used in many chemical
industries such as plastics, rubber and dyes [17-19]. The benzene ring was
discovered for the first time in 1825 by the English scientist Micheail Faradi,
who isolated it from gas oil, and in 1833 the German scientist Alhard
Metsherlitshis produced it by distilling benzoic acid and lime, then the
English chemist Sharolen Masphild in 1845 isolated benzene from Coal tar.
In 1948, gasoline was produced from the coal mine [20].

2.3- Adverse Health Symptoms Related to gasoline Toxicity

Adverse health symptoms experienced by workers were classified into
five levels [21] as follows; (1) non-symptomatic with smell recognition; (2)
mild or low level of symptoms, which were exhaustion, headache,
dizziness/fatigue, red eyes/burning eyes/itchy eyes, nasalms, which were
exhaustion, headache, dizziness/fatigue, red eyes/burning eyes/itchy eyes,
nasal congestion, sore throat/dry throat, suffocation, cough/hoarseness, runny
nose, skin itching/dry skin, cracked skin, itchy skin/red rash/blisters,
anorexia, and palpitations; (3) moderate level of symptoms, which were
numbness, depression, confusion, blurred vision, insufficient/abnormal
breathing, chest pain, nausea and vomiting, burning pain/swelling/muscle
weakness, tremor, cramp, scurvy/bleeding, epistaxis, and petechia; (4) high
level of symptoms, which were anaemia/epilepsy, convulsions, and
unconsciousness; and (5) very high-level symptom, which was leukaemia.
High and very high levels of symptoms must be diagnosed by a physician.
The severity levels of symptoms relating to gasoline toxicity that are
experienced by gasoline station workers depend on various factors. A
previous study found that the factors affecting gasoline exposure, identified
by tt-MA detection, include gasoline station workers standing close to the
fuel dispenser during their service period, receiving no relevant training, and
working in a location where the gasoline concentration is greater than 50 ppb
5
[22]. The health effects of gasoline exposure and their associated factors are
still unclear. Therefore, this study aimed to investigate the factors associated
with adverse health effects experienced by gasoline station workers in
Ajdabiya city.

2.4- Metabolism of gasoline

Effects of gasoline exposure are time dependent. If unprotected
individuals are exposed for long periods, it may lead to permanent
suppression of bone marrow functioning, accompanied by reduction in the
formation of new blood cells causing aplastic anemia [23-25]. Such disorders
are believed to be caused by toxic Benzene metabolites. gasoline is
metabolized in the liver to its primary metabolite phenol by cytochrome
P4502E1 (CYP2E1) through the benzene oxide intermediate. It is
subsequently metabolized by CYP2E1 to hydroquinone (HQ) [26,27]. HQ is
transported to the bone marrow and oxidized to benzoquinones, which
eventually release reactive oxygen species (ROS) damaging hematopoietic
cells [29,30]. Therefore, chronic exposure to gasoline is believed to be
associated with many bone marrow failures and hematological malignancies
like acute myeloid leukemia (AML), aplastic anemia myelodysplastic
syndrome, acute lymphoblastic leukemia and chronic myeloid leukemia
[28,31].
Gasoline is metabolized in the liver by cytochrome P450 (CYP) 2E1 to
benzene oxide. The metabolites undergo further metabolism through
oxidation, dehydrogenation or conjugation with sulfate or glucuronic acid
[32,33]. “Activation of gasoline and its reactive metabolites leads to
continuous production of reactive oxygen species (ROS), which leads to lipid
peroxidation and damages DNA, RNA, leading to genetic modification and
alterations in the functions of important enzymes (i.e. liver) and proteins”
[34].
6
2.5- Production and use
Gasoline is a volatile and inflammable liquid mixture derived from
petroleum that is mainly used for internal machine combustion. It is
commonly used as a fuel for vehicles, synthetic solvents, pesticides and
cleaners. It comprises many organic compounds, aromatic and inorganic. Any
of its products are particularly human carcinogenic [35,36]. Gasoline is a
complex mixture of aliphatic and aromatic hydrocarbons, some of which are
key components of gasoline, toluene, ethylbenzene, xylene, and are
considered among the most harmful compounds for human health [37].
Gasoline is also used in the manufacture of some types of rubber
materials, lubricants, dyes, detergents, medicines, and pesticides. Natural
sources of gasoline include volcanic emissions and forest fires [38].

2.6- Physiological effects of gasoline

Awide range of harmful health conditions, including respiratory
disorders, liver diseases, kidney diseases, hematotoxicity and cancer are
associated with gasoline [39]. High gasoline exposure is usually found to
cause hematotoxicity, such as anaemia, thrombocytopenia, leukopenia and
lymphoma. But the consequences of low levels exposure appear to be
obscure. In addition, the possible effects in hemopoietic components may
lead later in life to harmful effects in various parts of the body [40]. Studies
have shown that in gasoline-exposed individuals, bilirubin, alanine
aminotransferase (ALT), aspartate aminotransferase (AST), blood urea, and
serum creatinine were significantly increased relative to unexposed
individuals. While total protein, albumin, sodium and calcium serum
concentrations have been significantly reduced [41,36]. Fuel stations are
known sources for occupational gasoline exposures. Labor disease caused by
gasoline exposure is recognized as a global health concern and the fatal or
non-fatal incident in both developing and developed countries is continuously
7
increasing in gas station workers [42].
Study [43] showed that lead acetate affected the biochemical
components of the body, including AST, ACP, TSB, LDH, and Albumin.
Study [44] showed the phenotypic and biochemical changes associated with
lead poisoning in gasoline in kidney and liver functions.
Several authors have reported that toxicity of gasoline comes mainly
from gasoline metabolites [45–49]. According to existing evidence,
petroleum hydrocarbons have the potential to cause deoxyribo nucleic acid
(DNA) damage in gasoline-exposed individuals and exposure to petrol vapor
induces genotoxic effects, confirming that the gas station workers have a high
risk of cancer due to their daily occupational exposure [50,53,54]. Once
gasoline is inhaled, gasoline, as the main ingredient of gasoline, enters the
lungs then is passed to the blood stream from which it goes to the liver, where
three main phenolic metabolites of gasoline are released, transient phenol and
accumulated hydroquinone and catechol, in relatively high concentrations
[51,52]. gasoline is a lipophilic agent, so its metabolites go directly to fatty
tissues such as bone marrow where actual toxic species are generated
[49,52,55].
It has been shown that genetic polymorphisms of xenobiotic
metabolizing enzymes may modulate the susceptibility of individuals to toxic
compounds like the glutathione S-transferase (GST) superfamily, which plays
an important role in detoxification of various toxicants [56]. It is reported that
these enzymes are involved in detoxification of several toxins, including
some of the compounds present in gasoline [57]. Evidence is provided also
for wide toxic effects of benzene metabolites with prolonged exposure
including: pancytopenia and leucopenia [57–59] and other blood disorders
such as leukemia [59]. The gasoline component has a known carcinogen
primarily affecting the hematopoietic system.

8
 The effects of systemic gasoline exposure can cause acute and chronic
clinical disorders of the cardiovascular, respiratory, neurological,
gastrointestinal, liver, renal and dermatological local effects, and
immunological, metabolic and allergic reactions. While several studies
pointed to the risk of occupational exposure to gasoline on hematological
profiles and other tests of the above disorders, there are no published studies
in this regard in the country, so this study tries to address only the
hematological profile of exposed attendants.
A recent study showed that exposure, even to permanently low levels of
gasoline, leads to a change in blood properties, including a sharp decrease in
white blood cells that perform the function of fighting diseases [60].
The study, which was published in the journal Science, showed that
workers in the factory Chinese shoe producers, who are exposed to inhaled
gasoline in quantities of less than one part per million, are prone to
developing blood diseases, and have reduced ability to fight Diseases [61].
The US Department of Health and Human Services (DHHS) classifies
gasoline as It is carcinogenic, and prolonged exposure to gasoline in the air
can cause leukemia [62].
Inhaling very high levels of gasoline can cause death, while only high
levels may cause dizziness, drowsiness, rapid heartbeat, headache, tremors,
confusion, and unconsciousness. Eating or drinking foods that contain high
levels of gasoline can also cause vomiting, stomach irritation, dizziness,
drowsiness, violent convulsions, rapid heartbeat, and ultimately death [38].
The main effect of long-term exposure to gasoline is limited to the
blood. gasoline causes harmful effects on the bone marrow and can cause a
decrease in red blood cells, leading to anemia. It can also cause severe
bleeding and affect the immune system, increasing the chance of infection.

9
Some women who inhaled high levels of gasoline for several months
experienced [38].

2.7- Gasoline Vapors under Various Conditions

Studies [63,64-66] have indicated that the exposure risk of petrol station
attendants is likely higher due to elevated ambient temperatures and the
increased volatilization of the gasoline, especially in tropical countries. In
such countries, filling station workers are likely to inhale more gasoline
vapours than in other countries with average ambient temperatures below
30°C. This is applicable for increasing the risk of exposure to fuel vapours at
petrol stations in Saudi Arabia, particularly during the hot weather conditions.
The location of the petrol stations is also an important factor in
determining exposure risks, particularly for those petrol stations close to
highways or busy traffic. A gasoline vapour exposure study of petrol station
attendants compared exposure levels to gasoline at two stations located near
high traffic roads and in suburban areas with low traffic roads in the cities of
Torino and Biella in northwestern Italy. The study concluded that stations
near high traffic roads had 22% higher exposure concentrations [67].
Brief exposure (5-10 minutes) to very high levels of gasoline in the air
(20,000-10,000 ppm) can lead to death, lower levels (3,000-700 ppm) can
cause drowsiness, dizziness, rapid heart rate, headache, tremors, confusion,
loss of consciousness, in most cases, people will You stop feeling these
effects when you are no longer exposed and start breathing Clean Air [68].
The current levels of benzene in the air in the workplace are much lower
than in the past, and due to this decline and the availability of protective
equipment such as respirators, fewer workers have symptoms of benzene
poisoning [69].

10
 3- Materials and Methods
3.1- Methodology
A cross-sectional case control study was done on 8 males working in
fuel stations (study group) and 8 males didn’t work in fuel stations (control
group) in the city of Ajdabiya, eastern Libya.

3.2- Patients’ Selection Criteria:

The study included 8 workers who were randomly selected from gas
stations in Ajdabiya city working for at least 6 months in gas stations and 8
males of the same age group working in different jobs in Ajdabiya city and
not exposed to gasoline. All groups were males in the age group 20-40 years.

3.3- Exclusion Criteria:

Known cases of liver, renal, blood disease or anemia. Each case under
study was interviewed with a detailed questionnaire to collect information
regarding their

3.3.1- Sociodemographic data:

• Age
• Residence

3.3.2- History including

• Duration of the work in the fuel station.
• Smoking

3.4- Collection of samples:

5 ml of venous blood was collected by a single prick from studied and
control groups under complete sterile conditions, from peripheral vein
without tying any tourniquet at the end of the interview.
Blood samples were sent to the laboratory for analysis of complete
blood count (CBC), Liver (serum alanine transaminase, serum aspartate

11
transaminase, serum alkaline phosphatise, gamma glutamyl transferase and
bilirubin), kidney functions (urea and creatinine levels) of studied and control
groups, thyroid hormones (plasma triiodothyronine and thyroxine hormone),
minerals concentration (Sodium, potassium, calcium, magnesium and
chlorine).

3.5- Blood Specimens

3.5.1- Hematology assays

All CBC tests were performed by automatic blood cell analyzer (XP-
300 Automated Hematology Analyzer, Sysmex American, Inc [70]. CBC
were performed on EDTA as anti-coagulated samples. Differential cell counts
were performed manually using Dif-Quik-stained blood smears. Data were
recorded according to the following categories: white blood cell (WBC); red
blood cell (RBC); hemoglobin (HB) and platelet.

3.5.2- Biochemical assay

The other part of heparted blood samples were placed immediately on
ice. Plasma was obtained by centrifugation of samples at 860 xg for 20 min,
and was stored at -20°C until used for analyses. Stored plasma samples were
analyzed for total protein (TP) by the Biuret method according to [61].
Albumin (A) concentration was determined by the method of [72]. Plasma
urea and creatinine concentrations were measured by the method of [73] and
[74], respectively. Plasma total bilirubin was measured using the method of
[75].
The activities of plasma aspartate transaminase (AST; EC 2.6.1.1) and
alanine transaminase (ALT; EC 2.6.1.2) were assayed by the method of [76].
Alkaline phosphatase (AlP; EC 3.1.3.1) activity was determined in plasma
according to the method of [77]. Serum minerals was determined br
photometric test with cresolphthalein complexone [78] using DiaSys reagent

12
kit. Thyroxine (T4) and Triiodothyronine (T3) hormone concentrations were
assayed by using commercial kit that was supplied by Coat - A - Count, from
Los Angeles, USA.

3.6- Statistical analysis

Where applicable, statistical analysis was carried out in Minitab
software (version17).

13
 4- Results
A total of 16 study participants comprising of 8 gasoline station
workers and 8 not worker. Their average age was 18 to 35 years (min–max:
18–35). Most of them were younger than 35 years. The control group was
working in different jobs, aged also between 18 and 35 years’ old. Regarding
comparison of the parameters of CBC, liver and kidney function tests, table
(1 and 2) and Figures of (1) to (20) shows that the mean value of red blood
cells count for the studied group was no significant as compared to the
control group. There were no statistically significant differences in the
hemoglobin level, WBCs count, the platelet count, serum concentrations of
albumin level, total bilirubin level, direct bilirubin level , creatinine level and
minirals.

14
Table 1. statistical analysis to compare the parameters of CBC, liver and kidney function
among controla and worker.

Parameter Groups P-value

Control Worker
Mean±SD Mean±SD
RBCs (109/μl) 5.039± 0.405 5.180± 0.685 0.625

Hb (gm/dL) 15.74± 1.05 15.78± 1.37 0.952

WBCs (109/μl) 6.93± 1.36 5.92± 1.78 0.226

PLT(109/μl) 230.0±59.9 226.5±44.0 0.896

AST (IU/L) 15.51± 4.88 19.08± 5.12 0.178

ALT (IU/L) 14.15± 6.23 17.5± 12.1 0.506

AlP (U/L) 79.7±23.7 82.9±20.0 0.776

ɣ-GT (U/L) 22.46± 9.33 27.8± 23.2 0.564

Creatinine 0.4700± 0.0701 0.575± 0.134 0.079

(mg/dl)

Urea 23.00±4.24 26.25±7.63 0.317

(mg/dl)

T.Bili 0.564± 0.362 0.439± 0.275 0.450

(mg/dl)

Dir.Bili 0.2162± 0.0932 0.195± 0.104 0.674

(mg/dl)

Ind.Bili 0.271±0.175 0.266±0.158 0.953

(mg/dl)

15
Figure 1. comparative between worker and control on red blood cells.

Figure 2. comparative between worker and control on haemoglobin.

Figure 3. comparative between worker and control on whit blood cells.

16
Figure 4. comparative between worker and control on platelet count.

Figure 5. comparative between worker and control on aspartate transaminase.

Figure 6. comparative between worker and control on alanine transaminase.

17
Figure 7. comparative between worker and control on alkaline phosphatise.

Figure8. comparative between worker and control on gamma glutamyl transferase.

18
Figure 9. comparative between worker and control on creatinine.

Figure 10. comparative between worker and control on urea.

19
Figure 11. comparative between worker and control on total bilirubin.

Figure 12. comparative between worker and control on direct bilirubin.

Figure 13. comparative between worker and control on indirect bilirubin.

20
Table 2. statistical analysis to compare the parameters of Tryodothyronine (T3), thyroxine
(T4) and some minerals among controla and worker.

Parameter Groups P-value

Control Worker
Mean±SD Mean±SD
T3 1.178± 0.243 1.168± 0.197 0.929

T4 8.61±3.05 9.06±2.52 0.753

Ca (mg/dl) 9.662± 0.414 9.813± 0.485 0.518

Na (mg/dl) 142.56± 3.49 142.63± 3.73 0.973

Mg (mg/dl) 2.2612±0.0656 .206±20.146 0.357

K (mg/dl) 4.299± 0.522 4.219± 0.338 0.722

Cl (mg/dl) 99.64±1.58 100.09±2.04 0.629

Figure 14. comparative between worker and control on tryodothyronine.

21
Figure 15. comparative between worker and control on thyroxine.

Figure 16. comparative between worker and control on calcium.

Figure 17. comparative between worker and control on sodium.

22
Figure 18. comparative between worker and control on magnesium.

Figure 19. comparative between worker and control on potassium.

Figure 20. comparative between worker and control on chlorine.

23
 5- Discussion
A wide variety of adverse effects; either acute or chronic and may be
fatal could occur after gasoline exposure. Gasoline has the ability to cause
hematotoxicity, hepatotoxicity and nephrotoxicity. The aim of this study was
to assess the effects of gasoline on haematological parameters, the liver,
kidney functions, some minerals and some hormones in Libya. No statistical
significant difference between the studied group and the control group was
found. The possible metabolic mechanisms for the underlying alterations in
the liver enzymes as proposed by the various investigators worldwide are that
following inhalation, benzene and the other hydrocarbons present in gasoline
are readily absorbed from the lungs and get metabolized in the liver by
CYP450 2E1 oxidative pathways which contribute to the production of free
radicals and quinine metabolites such as phenol, hydroquinone,
benzoquinone; 1,2,4 benzenetriol [79]. count and [80] found that, there was a
significant positive correlation between the urea levels and the duration of
exposure in (years). Theabsence of such correlations could be explained by
the idea that the workers with different exposure periods are still having an
effective compensatory system to cope with possible changes that might be
found during the exposed levels and thus ending up with good hemostasis
[81]. Such differences in the findings of various research works are quite
possible, might be due to the variations in the duration and concentrations to
which the fuel filling attendants are exposed, methodology adopted,
differences in handling of the potential confounding factors such as age, sex,
BMI, personal habits (smoking and alcohol intake), and use or neglect of
personal protective devices in the workplace [82].

24
 Conclusion
The exposure to petroleum products at gasoline stations workers
showed that No significant in all parameters increase the probability of liver
and kidney function tests among gasoline stations workers with increased
exposure time.

25
 Recommendations
From the obtained results, the present study suggests that:

1. Attention of safety precautions should be taken during usage and

exposure to gasoline to avoid its harmful effect.
2. our study recommends gas station owners should provide basic
personal protective equipment like face masks and protective wears for
workers
3. Further research is recommended on other biological samples of gas
station workers. In other parts of the country.
4. Gas station workers with chronic exposure to gasoline products should
have periodic medical examinations including the evaluation of their
hematological profile and measurement of blood benzene and blood
lead levels.

26
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