The mutagenic hazards of settled house dust: a review

Abstract

Given the large proportion of time people spend indoors, the potential health risks posed by chemical contaminants in the indoor environment are of concern. Research suggests that settled house dust (SHD) may be a significant source for indoor exposure to hazardous substances including polycyclic aromatic hydrocarbons (PAHs). Here, we summarize the literature on the mutagenic hazards of SHD and the presence of PAHs in dust. We assess the extent to which PAHs are estimated to contribute to the mutagenicity of SHD, and evaluate the carcinogenic risks associated with exposures to PAHs in SHD. Research demonstrates that SHD has a Salmonella TA98 mutagenic potency of 1000–7000 revertants/g, and contains between 0.5 and 500 μg/g of PAHs. Although they only account for a small proportion of the variability, analyses of pooled datasets suggest that cigarette smoking and an urban location contribute to higher levels of PAHs. Despite their presence, our calculations show that PAHs likely account for less than 25% of the overall mutagenic potency of dust. Nevertheless, carcinogenic PAHs in dust can pose potential health risks, particularly for children who play and crawl on dusty floors, and exhibit hand-to-mouth behaviour. Risk assessment calculations performed in this study reveal that the excess cancer risks from non-dietary ingestion of carcinogenic PAHs in SHD by preschool aged children is generally in the range of what is considered acceptable (1 × 10⁻⁶ to 2 × 10⁻⁶). Substantially elevated risk estimates in the range 1.5 × 10⁻⁴ to 2.5 × 10⁻⁴ correspond only to situations where the PAH content is at or beyond the 95th percentile, and the risk estimates are adjusted for enhanced susceptibility at early life stages. Analyses of SHD and its contaminants provide an indication of indoor pollution and present important information for human exposure assessments.

Introduction

Much attention has been placed on researching, monitoring and regulating air pollution in the outdoor environment. As a result, there exists a general misconception that air pollution by chemical contaminants is an outdoor phenomenon. In reality, numerous studies have noted that indoor air can be many times more contaminated than outdoor air [1]. Moreover, people spend the majority of their time indoors. For example, Canadians spend as much as 70% of their time at home and up to 90% of their time indoors [2]. These percentages are easily exceeded for mothers, children, the elderly and the infirm. As a result, the health risks posed by contaminants in the indoor environment are of significant concern, and the potential hazards of indoor pollutants are now being more widely acknowledged. For instance, organizations such as the United States Environmental Protection Agency (US EPA) have recently ranked indoor pollution as a high priority risk to human health [3].

Pollutants in the indoor environment can include radiation (e.g., radon gas), biological contaminants (e.g., bacteria, molds, viruses, dust mites), chemical contaminants (e.g., pesticides, metals, flame retardants, plasticizers), combustion products (e.g., environmental tobacco smoke, carbon monoxide, nitrogen dioxide) and others [4]. Many of these contaminants adsorb to particulate matter suspended in indoor air that later settles out as house dust.

Research investigating human exposures to priority pollutants have suggested that settled house dust (SHD) may be a significant source for indoor exposures [5]. Exposure to these pollutants in the indoor environment has been associated with numerous adverse health effects including allergenic and immune system effects, respiratory effects, cardiovascular and nervous system effects, irritating effects of the skin and mucous membranes, cancer and reproductive effects [6]. Exposure to dust and its associated contaminant load may be of particular concern for children who tend to play or crawl on the floor and place objects in their mouths that have been in intimate contact with dusty floors or carpets [7].

Studies investigating exposure to toxic contaminants in SHD have often focussed on lead [8], [9], [10], [11], [12], [13] and pesticides [7], [14], [15], [16], [17], [18]. However, combustion products such as the polycyclic aromatic hydrocarbons (PAHs) have also been detected in dust, and these substances may pose additional health concerns [19], [20], [21], [22], [23], [24], [25], [26], [27], [28], [29], [30], [31], [32], [33], [34], [35], [36], [37], [38], [39]. PAHs are ubiquitous in the indoor and outdoor environment, and a number of these compounds have been classified as mutagens and/or possible or probable human carcinogens [40].

Although several studies have investigated the PAH composition of SHD, only one published study [41] has investigated the mutagenic hazards of SHD. As a result, there is a paucity of information on the mutagenic hazards of indoor dust. Given the large proportion of time spent indoors and the potential for enhanced risks in children, the hazards associated with exposure to indoor dust warrant further investigation. The objectives of this review are: (1) to review the limited data on the mutagenicity of SHD, (2) to compile published data on PAH levels in SHD, and analyze relationships between these levels and various attributes of the households (e.g., location, presence of smokers, type of flooring), (3) to assess the potential contributions of frequently measured PAHs to the overall mutagenic hazards of SHD, and (4) to estimate the carcinogenic risks associated with exposure to PAHs in SHD.

The US EPA defines house dust as “a complex mixture of biologically-derived material (animal dander, fungal spores, etc.), particulate matter deposited from the indoor aerosols, and soil particles brought in by foot traffic … The indoor abundance depends on the interplay of deposition from the airborne state, re-suspension due to activities, direct accumulation and infiltration” [42]. The precise composition of a house dust sample is a function of numerous factors including environmental and seasonal factors, ventilation and air filtration, homeowner activities, and indoor and outdoor source activities. The penetration of outdoor particles into the indoor environment has been shown to be a significant source of indoor particles [43], [44], [45], [46]. In the outdoor environment, natural sources of dust particles include pollen, soil, forest fire emissions and volcanic debris. Anthropogenic sources of outdoor dust particles include fossil fuel combustion (e.g., coal, oil), wood combustion, waste incineration, and a variety of industrial processes (e.g., iron founding, construction). In the indoor environment, dust sources include skin, hair, mites, fibres from clothing and furnishings, cooking emissions, heating emissions and cigarette smoke [47]. This variety of indoor and outdoor sources yields a complex matrix that can be extremely heterogeneous in nature with temporal and spatial variability in particle size, particle shape, particle composition, and contaminant concentration. Consequently, the composition of SHD can differ considerably between rooms of a given house, as well as between houses, and among geographic locations in a study area [20].

Most dust particles range from micrometers to millimetres in size and are generally classified as either fine or coarse particles. Although no standard exists, a common practice is to define fine particles as those less than 2.5 μm, while coarse particles are those greater than 2.5 μm [47]. Dust particle size is of particular importance as it influences the deposition and re-suspension of dust in the indoor environment. Particles greater than 30 μm tend to fall and form SHD [47], while particles less than 30 μm tend to remain airborne and only constitute approximately 10% of SHD [31], [48], [49]. The settling and re-suspension of dust is readily influenced by air flow patterns and activities taking place in the sampling area [50], [51].

The physical–chemical characteristics and composition of house dust plays an important role in determining the types of contaminants that are associated with dust particles. The adsorption and adherence of chemical contaminants to particulate material depends on the type and size of the particles as well as the surface texture, polarity and lipophilicity [19]. Studies have revealed the presence of many chemical contaminants adsorbed to dust particles including: pesticides, smoke residues, PAHs, PCBs, flame retardants, plasticizers, heavy metals and asbestos [19], [20], [21], [22]. Equilibrium concentrations on dust particles generally far exceed those in the gaseous portion of indoor air [52], thus dust and its associated fine particulate matter tends to become a sink for semi-volatile organic compounds [19]. Furthermore, these compounds have the potential to persist and accumulate in indoor dust, as they are not subjected to the same degradation processes that occur outdoors. Compounds associated with indoor dust particles are protected from sunlight, fluctuations in temperature and humidity, high rates of microbial degradation, and the overall effects of weathering [53].

Some of the general characteristics of SHD are presented in Table 1. It should be noted however, that due to the complex nature of SHD and the numerous factors that influence its composition, actual values for specific dust characteristics (i.e., deposition rate, particle size distribution and loss on ignition) may vary considerably from the values shown in Table 1 depending on the location that is being sampled. For a more detailed overview of the sources and properties of SHD, the reader is referred to the recent publication by Morawska and Salthammer [47].

Researchers investigating dust contamination have devised a number of passive and active dust sampling techniques. Passive techniques may involve setting out stationary “dust fall” jars or non-electrostatic plates and simply letting dust accumulate for a given period of time. Active sampling techniques can include: surface wiping, press sampling, sweeping, or vacuuming. Each of these methods has been devised to measure specific parameters such as the total dust loading or dust available for dermal adsorption. No one sampling method can collect dust equally well from all surfaces, and the optimal collection method will depend on the surface to be sampled and the goal of the study. A comprehensive review of the various sampling techniques is provided by Lioy et al. [20].

In an effort to obtain the most reliable information with the highest possible reproducibility, two standard methods for sampling SHD have been established; one by the American Society for Testing and Materials (ASTM), and the other by the German Association of Engineers (VDI). The ASTM method D 5438-00 makes use of the High Volume Small Surface Sampler (HVS3), a modified vacuum cleaner that collects particles greater than 5 μm using various cyclones [54]. The VDI 4300 Part 8 guideline describes methods for a number of sampling techniques (e.g., commercial vacuum cleaners, surface wipes, deposition collection) in order to optimize sampling to the specific situation [55]. This guideline also distinguishes between “old dust” which is dust of unknown age, and “new dust” which is generally 1–2 weeks old. The collection methods employed in many published studies do not adhere to any rigid standards. This introduces unfortunate variability (e.g., in particle size distribution), which complicates cross-study data analysis and interpretation.

Reviews by Butte and Heinzow [19], Roberts and Dickey [52], and Roberts et al. [5] provide an overview of dust sampling studies to date. They also summarize the occurrence of various chemical contaminants in dust and assess potential exposure rates.

Exposure to SHD and associated contaminants may occur via dermal adsorption, inhalation, and non-dietary ingestion. Dermal absorption of dust may occur following contact with dust that has settled on furniture, floors or other objects. Dust particles less than 100–200 μm are most effectively retained by the skin [31]. It is estimated that approximately 28 mg of SHD per day adsorb to children's hands, while 51 mg adsorb to the hands of adults [56]. In non-occupational settings, this route of exposure is thought to be less significant than inhalation and non-dietary ingestion [29].

Inhalation of dust can occur when dust is suspended or re-suspended by activities such as vacuuming, cleaning, playing, or simply walking through a room [50]. It is estimated that young children inhale between 0.15 and 0.34 mg of dust per day, while adults inhale approximately 0.81 mg per day [56]. Inhaled dust particles greater than 10 μm are generally trapped by the nose, throat or upper respiratory tract, whereas particles less than 2.5 μm have the ability to penetrate deep into the respiratory system where they are less likely to be eliminated [47]. These finer particles, which often contain higher levels of PAHs [31], likely pose a toxic hazard to exposed individuals.

Non-dietary ingestion of SHD generally occurs through accidental ingestion of particles that have adhered to food or skin. This route of exposure is thought to be of particular concern for children who frequently put their hands, toys and other objects into their mouths [7]. It is estimated that young children ingest between 50 and 100 mg of dust per day compared to adults who ingest an estimated 0.56 mg per day [56]. A small percentage of children are known to exhibit pica behaviour, which involves the intentional eating of non-food items. These children may ingest up to 10 g of soil and dust per day [57].

Other than our current work examining SHD samples from homes in the Ottawa area, to our knowledge only one study has investigated the mutagenic hazards of SHD. In their study of 29 houses in Washington state, Roberts et al. [41] examined the mutagenicity of dust collected from homes in high and low pollution areas. A microtiter Escherichia coli K-12 DNA repair assay and the Salmonella mutagenicity assay (TA98 only) were used to assess the genotoxicity of the dust extracts.

Statistically significant increases were noted for both assays. Specifically, 20 out of 29 samples gave statistically significant positive responses in the DNA repair assay. Ten out of 29 samples yielded significantly elevated levels of Salmonella mutagenicity in the absence of metabolic activation, and 5 out of 29 samples showed significantly elevated levels of Salmonella mutagenicity in the presence of metabolic activation (S9). Salmonella (TA98) mutagenic potency values ranged from 1190 to 6570 revertants/g without S9 and from 1340 to 4180 revertants/g with S9. Eight of the dust extracts produced elevated responses for both the DNA repair assay and the Salmonella mutagenicity assay. In addition, both tests revealed an increase in mutagenic activity with decreasing particle size.

Roberts et al. also examined correlations between the mutagenicity of the dust samples and information contained in the corresponding homeowner surveys. The authors found a statistically significant correlation between the age of the carpet and the magnitude of the Salmonella mutagenicity with metabolic activation. They also found a significant correlation between vehicle traffic density and the Salmonella mutagenicity without metabolic activation. The latter relationship suggests that direct-acting mutagenic combustion by-products such as nitro-substituted PAHs produced outdoors (e.g., diesel emissions) may be entering the indoor environment. The study did not investigate the chemical composition of the dust. Hence, no correlations could be made between the level of mutagenicity and the concentration of any mutagenic compounds present in the dust.

Preliminary Salmonella mutagenicity analyses of SHD collected from 65 houses in the Ottawa area confirm mutagenic potency values with TA98 range from 780 to 3678 revertants/g (N = 13 positive results) without S9, and 2299 to 7213 revertants/g (N = 23 positive results) with S9 activation (Maertens, unpublished data). These values are similar to the values published in the study by Roberts et al., and it appears that the Salmonella TA98 mutagenic activity of SHD extracts tends to be in the 1000–7000 revertants/g range. Comparisons between the mutagenic potency of indoor dust and other particulate matrices reveals that settled dust tends to be more mutagenic than most outdoor soils, including those collected from contaminated industrial sites, but less mutagenic than suspended particulate matter collected from either indoor or outdoor air (Table 2). Geometric mean mutagenic potency values for contaminated soils from industrial sites tend to be in the 1000 revertants/g range, although individual values for heavily contaminated soils can yield 10⁵ revertants/g [58]. Although the potency of suspended particulate material collected in both indoor and outdoor environments can vary a great deal, organic extracts of these samples often yield potency values greater than 10⁵ TA98 revertants/g [59]. This relative ranking of mutagenic potency seems reasonable since settled dust contains deposited particulates from both indoor and outdoor air, as well as tracked-in soil particles [50]. The relatively low mutagenic potency of SHD in comparison to suspended particles in indoor or outdoor air is likely due to the dilution of SHD with large particles of inert material and textile fibers that are non-mutagenic. In a similar fashion, the lower levels of mutagenic potency of soil particles is almost certainly accounted for, at least in part, by the presence of large amounts of inert material of geological origin.