INTRODUCTION:

Petrol (gasoline) is a complex mixture of low-molecular weightcompounds, mainly paraffins, naphthenes, olefins, aromatic and polycyclic hydrocarbon¹. Polycyclic aromatic hydrocarbons (PAHs) and their derivatives are associated with the incomplete combustion of organic material, arising partly from natural combustion, such as the burning of gasoline in engines and motor vehicles^2-3. Mahanty et al. (2006)⁴ reported that microorganisms isolated from soil sample in gasoline filling station (located in Guwahati) have pyrene- and anthracene-degrading potential, there was an indication that these compounds settle on the soil environment, showing that those that handle gasoline are daily exposed to these polycyclic compounds.

Investigations indicated that, engine roompersonnel on ships are exposed to polycyclic aromatic hydrocarbons(PAH) from oil and oil products⁵. The fact is obvious that refinery and especially petroleum workers are constantly exposed to gasoline and its combustion products.

The International Agency for Research on Cancer (IARC) has classified several PAH compounds into probable (2A) or possible (2B) human carcinogens⁶. Apart from PAH, the aromatics are also present in high concentrations. The major aromatic compounds of petrol are benzene, tolueneand xylene (BTX)¹. Benzene is the most hazardous component and has been classifiedas a human carcinogen by the International Agency for Researchand Cancer⁶ and the American Conference of GovernmentalIndustrial Hygienists⁷.

Human contact with these agents has been found to be deleterious. Keretetse et al. (2008)⁸ reported the genotoxic and carcinogenic effects of volatile organic compounds (VOCs) in African petrol attendants. A significant relationship was found between the volume of petrol sold during the shift and the average concentrations of benzene, toluene and the total VOCs measured. Significantly higher basal DNA damage was observed with the exposed group compared to the unexposed group. Several studies have shown that engine room personnel on shipshave an increased mortality from cancer of the lung and urinarybladder^9,10. Periago and Prado (2005)¹¹ reported significant relationship between years of exposure, the volume of gasoline handled and level of DNA damage in refinery workers . Report also shows that exposure of humans to toluene and xylene canlead to neurological effects such as anxiety, dizziness, fatigue,headache, tremors, impaired short-term memoryand inability to concentrate¹². In spite of these effects, humans are unavoidably exposed to hydrocarbons and its combustion products in refinery and its environment. We therefore, assessed the levels of polycyclic and aromatic hydrocarbons in the serum of oil zone plant workers in the refinery. The will enable us to know the rate of exposure and the likely disease effect. This will go a long way to help the workers.

MATERIALS AND METHODS:

Subjects:

Thirty (30) refinery workers (men) in oil zone plants were used in the study. The men were workers who had been exposed to refinery fumes for 8 hrs per day, 5 days per week for 10-13 years (Group A), 14-19 years (Group B) and 20-27 years (Group C). Group D comprised of 10 office workers (non-smokers) who had worked in the office for 10-27years. All subjects/volunteers involved willingly agreed because they wanted to know their health status. This study was conducted in accordance with the ethical principles that have their origins in the declaration of Helsinki. The institutional review board of the Department of Biochemistry, University of Port Harcourt, Port Harcourt, Rivers State, Nigeria, granted approval for this study. The research protocols were in collaboration with registered and specialized clinics and medical laboratories.

Collection and Preparation of Blood Samples:

The blood was transferred into sample bottles, centrifuged and the serum was digested. The digested sample was extracted with dichloromethane. The polycyclic aromatic hydrocarbon (PAH) was analyzed with Gas chromatography equipped with a flame ionization detector (FID) in Shell Petroleum Development Company (SPDC).

Statistical Analysis:

Statistical Analysis was done using a one way ANOVA with SPSS.

RESULTS:

Table 1: Levels of polycyclic aromatic hydrocarbon (PAH) in gasoline and blood samples of refinery workers in oil zone plants

Concentration In Gasoline

Workers Exposed for

10-13 yrs

(Group A)

Workers Exposed for 14-19 yrs Group B)

Workers Exposed for

20-27 yrs Group C)

Control Group D)

PAH (ppm)

66.75+ 0.03

BDL

The result represents mean + standard error of mean (n=10)

a = Represents significant difference (p<0.05) when groups A and B were compared to C, * BDL = below detention limit.

Polycyclic Aromatic Hydrocarbon (PAH) in Gasoline Sample Compared with Blood Samples of Refinery Workers in Oil Zone Plants:

Table 1 above shows that no polycyclic aromatic hydrocarbon was detected in the blood samples of workers when compared with that in gasoline sample. Figures 1-4 further explain the results; the levels of PAH in the blood of the refinery workers were not significantly (p<0.05) deposited in blood of human when compared with the concentration found in gasoline. The two PAHs detected within the limit of the experiment were acenaphthene and acenaphthylene. PAH was not detected in the control group.

Retention time (minutes)

Fig. 1: PAH in Gasoline sample showing the presence of acenaphthene and acenaphthylene.

Retention time (minutes)

Fig. 2: PAH in Samples A (BDL)

Retention time (minutes)

Fig. 3: PAH in Samples B (BDL)

Retention time (minutes)

Fig. 4: PAH in Samples C (BDL)

DISCUSSION:

Polycyclic aromatic hydrocarbon (PAH) is naturally found in crude oil and in gasoline samples. In the present study, the concentration of PAH found in the gasoline was 66.74701+0.03355 ppm/ ml of gasoline. The fact stands that a relationship exists between the nature of gasoline sold, year of occupational exposure, nature of combustion products and health effects of these products in the body. Three gasoline fuels (i.e., PLG, 92-LFG, and 95-LFG) analyzed for their total PAH concentration showed that the concentrations of PAH in most gasoline samples are comparable¹⁴. The PAH for these gasoline were 13.8, 16.9, and 15.0 mg/L. Total PAHs obtained for PLG, 92-LFG, and 95-LFG were contributed mostly by naphthalene, which accounted for 83%, 76%, and 77% of PAHs respectively¹³. The PAHs detected in gasoline sample in the current study were acenaphthene and acenaphthylene as compared with naphthalene found above.

Several PAHs are known carcinogens and mutagens¹⁴. The two major PAHs found in the present study were acenaphthene and acenaphthylene. Earlier studies showed that these two compounds were not toxic except at a very high concentration. Reshetyuk et al. (1970)¹⁵ examined the comparative toxicity of acenaphthene and acenaphthylene with naphthalene. They reported a range of LD₅₀ of 0.6 - 1.7 g/kg for the three compounds. On intraperitoneal administration in rats, they reported that naphthalene was more toxic than acenaphthene and acenaphthylene. The International Agency for Research on Cancer (IARC) classified naphthalene as possibly carcinogenic to humans (group 2B) based on the evidence of carcinogenicity in animals¹⁶. The EU system classifies naphthalene as a category 3 carcinogen, meaning that it has limited evidence of a carcinogenic effect and so naphthalene is not mutagenic in animals. There is insufficient data available regarding the carcinogenicity of acenaphthene and acenaphthylene in humans and thus, comparatively with naphthalene, the compounds are not carcinogenic.

Gershbein, (1975)¹⁷ exposed partially hepatectomized rats to 15 mg/kg acenaphthene in the diet for 7 days and reported increased liver regeneration. Knobloch et al. (1969),¹⁹ administered 2 g/kg acenaphthene orally to rats and mice for 32 days and found weight loss and mild histopathological alterations in the liver and kidney. Also four groups of CD-1 mice (20/sex/group) were gavaged daily with 0, 175, 350, or 700 mg/kg/day acenaphthene for 90 days, liver weight changes accompanied by microscopic alterations (cellular hypertrophy) were noted in both mid- and high-dose animals and seemed to be dose-dependent. Although increased liver weights, without accompanying microscopic alterations or increased cholesterol levels, were also observed at the low dose, this change was considered to be adaptive and was not considered adverse. The no observed adverse effect level (NOAEL) is 350 mg/kg/day based on hepatotoxicity; the lowest observed adverse effect level (LOAEL) for this effect on health.LOAEL is 175 mg/kg/day¹⁸. The above reports show that the concentrations of acenaphthene and acenaphthylene reported in the current study cannot cause the hepatoxic effects observed in the studies above, this implies that before the reported toxic effects could be found in the refinery workers under study, they must have worked for more than 50 years.

The fact that much hazardous PAHs were not found in gasoline was similarly reported by Hsiao-Hsuan et al., 1998¹⁹. They found that major emissions of PAHs were not contributed by the gasoline but by the additives. Investigations with PAH emission from the powered engines fueled by a 95 lead free gasoline (95-LFG), a 92 lead free gasoline (92-LFG) and a Premium leaded gasoline (PLG) with two gasoline additives, showed that the gasoline additives contain more amounts of carcinogenic PAHs than gasolines. Blending these additives rose the PAH content in the gasolines, and simultaneously, greater amount of PAHs from the tailpipe of engine exhaust were emitted.

Rui et al., 2004²⁰, characterized the unregulated Polycyclic Aromatic Hydrocarbons (PAHs) emissions that create health hazards. Total PAH values ranged from 1.133 to 5.801 mg km⁻¹. Naphthalene, phenanthrene, fluoranthene, pyrene and chrysene were detected in all tests. In addition, PAH emission was observed to be inversely related to emission of CO₂. In the present study, only acenaphthene and acenaphthylene were found and the total concentration of PAH was 66.74701 + 0.03355 ppm. This is highly recommended since the level of PAH in the present study is very small compared with the reports of other studies.

Pyrenes which are more dangerous PAHs were not detected in the present study unlike the report of Mahanty et al. (2006)⁴, who detected pyrene- and anthracene in gasoline filling station.

There were no significant depositions of PAH in the blood of men in groups A, B, C and D (control). The concentrations were below the detection limit in these four groups. This is highly recommendable since the Health guidelines National Occupational Health and Safety Commission (NOHSC) recommended that TWA (eight-hour time weighted average) exposure limit for naphthalene in the workplace: should be 10 ppm (52 mg/m³) while the STEL (short-term exposure limit) should be (15 minutes): 15 ppm (79 mg/m³)²¹ (DEH, 2001). These findings suggest that the current threshold limit value of 200µg/m³of benzene –soluble matter, which indicates PAH exposure, may be too high after 40 years of exposure, gives a relative risk of 1.2 – 1.4 for lung cancer and 2.2. for bladder cancer²².

CONCLUSION:

The current study proved that the level of these dangerous substances are kept at minimum and thus may take up to 50 years before such compounds might be detected at high concentrations in the workers or cause cancer, however, the workers are advised to go for a regular checkup.

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Received on 08.04.2010 Modified on 20.05.2010

Asian J. Research Chem. 3(3): July- Sept. 2010; Page 801-804