Benzene exposure in childhood: Role of living environments and assessment of available tools

Abstract

Benzene is a widespread air pollutant and a well-known human carcinogen. Evidence is needed regarding benzene intake in the pediatric age group. We investigated the use of urinary (u) trans,trans-muconic acid (t,t-MA), S-phenylmercapturic acid (SPMA), and unmodified benzene (UB) for assessing exposure to low concentrations of environmental benzene and the role of living environment on benzene exposure in childhood.

u-t,t-MA, u-SPMA, u-UB and u-cotinine were measured in urine samples of 243 Italian children (5–11 years) recruited in a cross-sectional study. Analytical results were compared with data obtained from questionnaires about participants' main potential exposure factors.

u-UB, u-t,t-MA and u-SPMA concentrations were about 1.5-fold higher in children living in urban areas than in those in the rural group. Univariate analyses showed that u-UB was the only biomarker able to discriminate secondhand smoke (SHS) exposure in urban and rural children (medians = 411.50 and 210.50 ng/L, respectively); these results were confirmed by the strong correlation between u-UB and u-cotinine in the SHS-exposed group and by multivariate analyses. A regression model on u-SPMA showed that the metabolite is related to residence area (p < 0.001), SHS exposure (p = 0.048) and gender (p = 0.027).

u-UB is the best marker of benzene exposure in children in the present study, and it can be used as a good carcinogen-derived biomarker of exposure to passive smoking, especially related to benzene, when urine sample is collected at the end of the day. In addition, it is important to highlight that SHS resulted the most important contributor to benzene exposure, underlining the need for an information campaign against passive smoking exposure.

Introduction

In recent decades, the potential adverse effects on human health of pollution of living environments have caused great concern worldwide (WHO, 2006). In this context, one of the most important health-based European Union priority substances is benzene (Bruinen de Bruin et al., 2008), a well-known human carcinogen classified in group 1 (carcinogenic to humans) by the International Agency for Research on Cancer (IARC) since 1982. Strong evidence links benzene exposure with lymphohematopoietic cancers, particularly acute myeloid leukemia (International Agency for Research on Cancer (IARC), 1982, Lamm et al., 2009).

For this reason the use of benzene—an organic compound historically employed in numerous production and synthesis processes—has been progressively reduced and is rigorously regulated by occupational exposure limits and by air quality standards set by the European legislation for the general environment (European Communities, 2000).

However, benzene exposure still occurs today because of its presence in petrochemical solvents, automobile gasoline, fuel, and their emissions. Environmental tobacco smoke (ETS) is another important source of benzene (Johnson et al., 2007).

Benzene is a widespread, diffused air pollutant in outdoor and indoor environments. Its adverse health effects for the general population cannot be neglected, especially in the context of exposure to low concentrations for a prolonged period.

Children are considered a high-risk population for both acute and chronic effects of environmental hazards because they are much more susceptible than adults are (Weaver et al., 1998, Barton et al., 2005, Duderstadt, 2006, van Leeuwen et al., 2008). Children's increased vulnerability is due to several factors, such as exposure, physiological characteristics, and pharmacokinetics. With regard to exposure, children absorb more from their surroundings than adults, even when exposed to the same concentrations of environmental contaminants. For example, per kilogram body weight, the daily intake of air has been estimated to be 2.3 times higher in children than in adults, intake of fluids 4.8 times higher, and intake of food 6.1 times higher (Armstrong et al., 2002). Moreover, one must consider differences in the biologically effective doses that reach target organs in children and adults. Thus, if the exposure to environmental pollution starts during childhood, the risk of adverse health effects with long latency becomes very high (Wild and Kleinjans, 2003).

For these reasons, the World Health Organization (WHO) Task Force for the Protection of Children's Environmental Health, in the Bangkok statement, declared that children cannot be considered “little adults” with regard to the risk of adverse health effects resulting from exposure at an early age and exposure assessment tools (Anderson et al., 2000).

Research has yielded conflicting findings with respect to the link between benzene exposure in childhood and the risk of lymphohematopoietic cancer. However, in these studies, researchers considered only secondhand smoke (SHS) exposure, not other sources of benzene, and the possibility of cancers in adulthood after SHS exposure during childhood (Chang, 2009).

Several exposure assessment studies have shown that children are exposed to low environmental concentrations of benzene. Many studies conducted on adults who are not professionally exposed to benzene suggest that urinary trans,trans-muconic acid (u-t,t-MA), urinary S-phenylmercapturic acid (u-SPMA) and urinary unmodified benzene (u-UB) serve as good exposure markers for benzene (Waidyanatha et al., 2001, Fustinoni et al., 2005, Johnson et al., 2007, Barbieri et al., 2008, Lovreglio et al., 2010), although their abilities to discriminate different levels of exposure (especially at low levels) are currently under evaluation.

Only a few research studies are available in the literature on the specific magnitude of children's exposure to benzene (Minoia et al., 1996, Weaver et al., 1996, Duarte-Davidson et al., 2001, Amodio-Cocchieri et al., 2001, Kouniali et al., 2003, Adgate et al., 2004, Bahrami and Edwards, 2006, Ruchirawat et al., 2007). These studies were conducted using predictive models of daily benzene intake in different exposure scenarios or by monitoring levels of benzene in the air and/or biological exposure indices, such as u-UB, u-t,t-MA, u-SPMA, and urinary phenol. At present, no research on children's exposure to low doses of benzene has been performed using u-UB, u-t,t-MA, and u-SPMA as biomarkers.

Due to the current lack of research in this area, there is a significant need to better evaluate benzene exposure during childhood and to determine which tools to use for assessment purposes.

The objectives of the present research were:

• To evaluate the abilities of u-UB, u-t,t-MA, and u-SPMA to assess exposure to low concentrations of environmental benzene in the pediatric age group; and

• To investigate the impacts of living environment and cohabitants' habits on benzene exposure in childhood.