Health risk assessment on human exposed to environmental polycyclic aromatic hydrocarbons pollution sources

Abstract

To assess how the human exposure to environmental carcinogenic polycyclic aromatic hydrocarbons (PAHs) pollution sources generated from industrial, traffic and rural settings, we present a probabilistic risk model, appraised with reported empirical data. A probabilistic risk assessment framework is integrated with the potency equivalence factors (PEFs), age group-specific occupancy probability and the incremental lifetime cancer risk (ILCR) approaches to quantitatively estimate the exposure risk for three age groups of adults, children, and infants. The benzo[a]pyrene equivalents based PAH concentrations in rural, traffic, and industrial areas associated with age group-specific occupancy probability at different environmental settings are used to calculate daily exposure level through inhalation and dermal contact pathways. Risk analysis indicates that the inhalation-ILCR and dermal contact-ILCR values for adults follow a lognormal distribution with geometric mean 1.04 × 10^− 4 and 3.85 × 10^− 5 and geometric standard deviation 2.10 and 2.75, respectively, indicating high potential cancer risk; whereas for the infants the risk values are less than 10^− 6, indicating no significant cancer risk. Sensitivity analysis indicates that the input variables of cancer slope factor and daily inhalation exposure level have the greater impact than that of body weight on the inhalation-ILCR; whereas for the dermal-ILCR, particle-bound PAH-to-skin adherence factor and daily dermal exposure level have the significant influence than that of body weight.

Introduction

Human cancer causes of skin, lungs, and bladder have always been associated with polycyclic aromatic hydrocarbons (PAHs) (Boffetta et al., 1997). The relationship between cancer and the environment is largely conditioned by investigations involving PAH exposures (Armstrong et al., 2004). Several individual PAHs such as benzo[a]pyrene (B[a]P), chrysene, indeno[1,2,3-c,d]pyrene, and benzo[b]fluoranthene have produced carcinogenic, mutagenic, and genotoxic effects in animal experiments (Thyssen et al., 1981, Deutsch-Wenzel et al., 1983). Somers et al., 2002, Somers et al., 2004 have also found out that air pollution enriched with PAHs has been shown to include heritable (paternal germ-line) mutations in mice.

More recently, PAHs have been associated with elevated levels of DNA adducts (PAH-DNA adducts) and P53 mutations in persons who smoke or are exposed to PAH in the workplace and ambient air (Alexandrov et al., 2002, Gaspari et al., 2003). Perera et al. (2002) has also indicated that airborne PAHs have been implicated in human reproductive effects, PAH-DNA adducts in newborns as well as preterm birth and intrauterine growth restriction. Although exposure to environmental PAHs has been based on the assumption that inhalation was the primary route (Venkataraman and Raymond, 1998), dermal contact is increasingly taken into account (ATSDR, 1990, Tsai et al., 2001).

The risk associated with human exposure to atmospheric PAHs is highest in cities, considering the density of population, increasing vehicular traffic, and scarce dispersion of the atmospheric pollutants. In Taiwan region, several significant contributor to PAHs sources had been sampled such as stationary industrial combustion: steel and iron industries (Yang et al., 2002) with a mean total-PAHs concentrations measured to be 1020 μg m^− 3, traffic vehicles exhaust: motorcycle (Yang et al., 2005) and highway toll station (Tsai et al., 2004) with a mean total-PAHs concentrations ranged from 8280–12300 ng m^− 3. Fang et al., 2004a, Fang et al., 2004b, Fang et al., 2004c indicated that mean total PAHs levels at industrial, urban, and rural areas in central Taiwan region ranged from 1232–1650, 700–1740, and 610–831 ng m^− 3, respectively.

However, occurrence of PAHs in ambient air causes particular concern due to the continuous nature of exposures and the size of populations at risk, especially in urban, suburban and industrial areas. Therefore, in light of the mutagenicity, carcinogenicity and ubiquity of some PAHs in the atmosphere, the setting of air quality standards and guidelines to limit human exposure should be of primary concern for public health policy. However, it is complicated to derive scientifically the standards or guidelines based on relatively limited empirical data, owing to the difficulties in interpreting heterogeneous experimental and epidemiological findings (Tsai et al., 2001).

Currently, no information on the human cancer risk assessment for specific-age groups related to environmental PAHs pollution sources is available in Taiwan region. Furthermore, identification of the most dangerous environmental PAHs and their mode of action in producing specific health effects remain uncertain and difficult to quantify the exposure risk precisely. To reduce the potential risk of harmful negative health consequences and problems, we suggest that risk analyses be taken seriously to characterize the impact of PAHs in the human environment. Fang et al., 2004a, Fang et al., 2004b, Fang et al., 2004c have been reported the relevant measurements of PAHs in industrial, urban, and rural areas and these measurements were sufficiently to motivate the most serious kind of concern for personal exposure to environmental carcinogenic PAHs. We were stimulated to develop a probabilistic risk assessment framework to evaluate the carcinogenic risk from personal exposure to environmental PAHs in industrial, urban, and rural areas.

The objective of this study is to develop an integrated environmental exposure risk model that incorporates inhalation and dermal contact from atmospheric PAHs existing in industrial, urban, and rural areas in Taiwan region. The risk model is intended to apply to general Taiwanese population. A detailed sensitivity and uncertainty analyses are conducted, and the results are used to identify critical input variables requiring further study. We employed a quantitative risk assessment method used for PAHs based on B[a]P equivalent concentration from animal studies. Several studies have also documented the impact that the outdoor air (Ando et al., 1996, Li and Ro, 2000, Naumova et al., 2002), and more specifically traffic (Kingham et al., 2000, Fisher et al., 2000), has on the quality of indoor air. We were extended our risk analysis to include PAH levels in indoor air in light of these findings.