Introduction

The effects of airborne pollutants on the immune system have been most widely studied [₁]. Entry may occur as a volatile gas (ozone, benzene), as liquid droplets (sulfuric acid, nitrogen dioxide), or as particulate matter (diesel exhaust, aromatic hydrocarbons) [₁]. The subsequent interaction with the immune system may result in local and systemic responses, and studies have shown examples of disease occurring from both overactive immune responses and immunosuppression [₁].

Benzene is a colorless poisonous air pollutant [₂]. Breathing extremely high level of benzene can result in death while chronic benzene exposure brief many adverse systemic reactions. Recently, a study was performed to assess the correlation between average daily pollution and acute asthma admissions in Northern Ireland [₃]. In this study, they concluded that benzene level was the only variable associated independently with asthma emergency-department admissions in children.

Although the mechanisms underlying benzene-induced allergy are not yet fully understood, they are likely to be complicated by various pathways, especially those of metabolism and cytokine pathway [₄]. Obstructive bronchitis was observed more frequently in children exposed to increased concentrations of benzene, as well as toluene, styrene, and m,p-xylene [₄]. In addition, atopic symptoms were associated with excretion of those volatile hydrocarbon metabolites [₄]. Rolle-Kampczyk et al found an association between eczema and exposure to toluene and between eczema and increased excretion of the benzene metabolite [₄]. They suggested that evaluation of external biomarker for volatile hydrocarbon exposures could supplement the knowledge on internal process for volatile hydrocarbon allergy [₄].

This aim of this work is to study the correlation between urine phenol, metabolite of benzene, and eosinophil count in the subjects occupationally exposed to benzene.

Materials and Methods

1. Subjects and Specimen Collection

2. Statistical Analysis

Results

The averages (mean ± SD) of urine phenol level and eosinophil count of the volunteer subjects were 13.3 ± 3.2 mg/gCreatinine and 129.9 ± 18.7 cells/mm³, respectively. The regression analyses show no significant correlation between urine phenol level and eosinophil count in volunteer subjects (r = 0.07, P = 0.67, Figure 1)

Figure 1

Figure 1: Scattergram for the correlation between urine phenol levels and eosinophil counts in volunteer subjects.

Discussion

Lehmann et al performed a study to investigate the association between indoor exposure to volatile organic compounds (VOC), prevalence of allergic sensitization and cytokine secretion profile of peripheral T cells in 3 year old children [₇]. They noted that exposure to benzene was associated with higher percentages of IL-4 producing CD3+ T cells [₇]. Both an increase in IL-4 producing type 2 T cells and a reduction of IFN-gamma producing type 1 T cells may contribute to a type 2 skewed memory in response to allergens [₇]. There is also a previous report, which found correlation between benzene concentration in the air at work places and the change in the polymorphonuclear enzymes levels[₈]. In addition, Lee et al noted that hydroquinone (HQ), a mjor metabolit of benzene, might enhance allergic immune responses by enhancing IL-4 mRNA expression, IL-4 gene promoter activity and also immunoglobulin E from eosinophil [₉]. However, there have been no correlative studies between the level of benzene metabolite, phenol in urine and the eosinophil. Here, we performed the study to answer that question. The author designed the study to examine the subjects, traffic wardens [₁₀], who would possibly be at risk for such an effect.

According to our study, we detected no significant correlation between the urine phenol and eosinophil counts in our volunteers. This result agrees with the finding of Nicolai et al that no volatile hydrocarbon pollutant was associated with allergic sensitisation when monitored by measurements of specific immunoglobulin E [₁₁]. Although some recent epidemiologic studies indicate correlations between existing of allergic symptoms and the exposure to benzene [₃,₄, ₆], we did not demonstrate the correlation between the standard biomarker for benzene exposure, urine phenol level and the basic blood marker for allergy, eosinophil count.

However, some discussion on the limitations of this study should be maid. Firstly, the small number of subjects can limit the generalization of the data. Secondly, it should concern the lack of eosinophil counts on the same patients in the absence of exposure to phenols. This point may be important if “baseline” eosinophil counts vary from patient to patient. Therefore, further studies with larger sample size focusing in the details of pathogenesis of white blood cell disorders and allergogenesis are necessary. The long-term pre-post benzene exposure following up is also recommended.

Acknowledgement

Correspondence to

Viroj Wiwanitkit Department of Laboratory Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok Thailand 10330 Tel: 662-2564136, Email: wviroj@pioneer.netserv.chula.ac.th