No abstract

There is current great international concern about the contribution of environmental pollution to the global burden of disease particularly in the developing, low- and medium-income countries. Industrial activities, urbanization, developmental projects as well as various increased anthropogenic activities involving the improper generation, management and disposal of pollutants have rendered today’s environment highly polluted with various pollutants. These pollutants include toxic metals (lead, cadmium, mercury, arsenic), polycyclic aromatic hydrocarbons, polychlorinated biphenyls, pesticides and diesel exhaust particles most of which appear to be ubiquitous as well as have long-term environmental persistence with a wide range of toxicities such as oxidative stress among others. Oxidative stress, which may arise from increased production of damaging free radicals emanating from increased pollutant burden and depressed bioavailability of antioxidant defenses causes altered biochemical and physiological mechanisms and has been implicated in all known human pathologies most of which are chronic. Oxidative stress also affects both flora and fauna and plants are very important components of the terrestrial environment and significant contributors of nutrients for both man and animals. It is also remarkable that the aquatic environment in which sea animals and creatures are resident is also highly polluted, leading to aquatic stress that may affect the survival of the aquatic animals, sharing in the oxidative stress. These altered terrestrial and aquatic environments have an overarching effect on human health. Antioxidants neutralize the damaging free radicals thus, they play important protective roles in the onset, progression and severity of the unmitigated generation of pollutants that ultimately manifest as oxidative stress. Consequently, human health as well as that of aquatic and terrestrial organisms may be protected from environmental pollution by mitigating oxidative stress and employing the principles of nutritional medicine, essentially based on antioxidants derived mainly from plants, which serve as the panacea of the vicious state of environmental pollutants consequently, the health of the population. Understanding the total picture of oxidative stress and integrating the terrestrial and aquatic effects of environmental pollutants are central to sustainable health of the population and appear to require multi-sectoral collaborations from diverse disciplinary perspectives; basically the environmental, agricultural and health sectors.

Objectives: There is increasing exposure to petrochemicals, including benzene, particularly in the low and medium-income countries. Benzene is a component of many petrochemicals and a ubiquitous environmental pollutant. Phenol is one of its principal metabolites and serves as a biomarker of exposure to benzene. The mechanism of its toxicity is incompletely elucidated. Benzene’s interaction with key micronutrients; copper (Cu), iron (Fe), and zinc (Zn) in the haemopoietic system has only been poorly explored, particularly in the developing countries where their status is variable and uncertain, with attendant intense exposure to petrochemicals. Material and Methods: Two groups of 50 gasoline dispensers (GDs) and 50 non-occupationally exposed participants were selected from Oye Local Government Area, Nigeria. The duration of occupational exposure was 2–10 years. Serum levels of Cu, Fe, and Zn were determined using flame atomic absorption spectrophotometry while heme and phenol were determined by standard spectrophotometry. Results: Phenol was significantly higher in GDs (P = 0.000), compared to controls (P < 0.05). The micronutrients, Cu, Fe, and Zn were all significantly decreased in GDs compared to controls (P = 0.000 in all cases). Phenol and Fe demonstrated significant inverse correlation (r = −0.557, P = 0.00), while heme and Zn also exhibited inverse correlation respectively to phenol (r = −0.38, P = 0.01; r = −0.37, P = 0.01). Conclusion: These data suggest intense perturbation of the haemopoietic system in GDs; likely from altered xenobiotic metabolism requiring heme in cytochrome P450; cell cycle dysregulation, where Zn is pivotal, p53 suppression also dependent on Zn and oxidative stress all converging in haemopoietic dysregulation. Importantly, depression of these micronutrients implies potentiation of myelotoxicity and risk of myeloproliferation, probably arising from alterations in transcription, differentiation errors, genome instability, and derangement in cell signal transduction moderated by Zn; accentuating risk of myeloproliferation; suggesting a role for these micronutrients in chemoprevention. Understanding these events may be important in risk assessment, policy formulation, regulatory measures and chemoprevention in GDs and the general population.