Predictors of coarse particulate matter and associated endotoxin concentrations in residential environments
Introduction
There is a growing interest in understanding human exposure to coarse particulate matter (PM), i.e., particles with an aerodynamic diameter between 2.5 and 10 μm (PM10–2.5). Recent epidemiological studies have found some evidence of an association between short-term exposure to high concentrations of ambient coarse PM and increased morbidity, and mortality risk, primarily due to cardiovascular and respiratory diseases, and venous thromboembolic disease (Host et al., 2008, Graff et al., 2009, Malig and Ostro, 2009, Linares et al., 2010, Martinelli et al., 2012, Qiu et al., 2012, Karakatsani et al., 2012). Long-term exposure to high levels of coarse PM have recently been found to be associated with significant cognitive decline in older women (Weuve et al., 2012). Moreover, it has been reported that coarse PM tends to deposit in the upper airways in the bronchiolar region (Heyder et al., 1986, Kim et al., 1996), causing significant lung inflammation with the release of pro-inflammatory cytokines by lung cells (Schins et al., 2004, Brunekreef and Forsberg, 2005, Alexis et al., 2006) and may therefore be relevant for asthmatic responses and irritation. Despite this, limited information is available to establish the linkage between indoor and outdoor sources, exposure and toxicity of coarse PM and their relation to adverse health outcomes (Monn and Becker, 1999, Brunekreef and Forsberg, 2005, U.S. EPA, 2009).
An important environment for exposure to coarse PM is the indoor residential environment. As studies of time-activity patterns have shown that Canadian adults spend an average of 64% of their time in indoor residential environments (Leech et al., 2001, Wheeler et al., 2011a), activities and sources within the home may contribute considerably to their exposure. In residences, coarse PM concentrations can be increased by several personal activities such as smoking, dusting, cleaning, washing, as well as by the number of occupants, the amount of carpet, re-suspension of indoor particles, and outdoor particle concentrations (Long et al., 2000, Rojas-Bracho et al., 2000, Morawska and Salthammer, 2003, Wheeler et al., 2011b). Ambient coarse PM is generally formed by a wide range of natural (e.g., windblown dust, sea-salt, plant debris, forest fires) and anthropogenic sources, including mechanical disruption (e.g., crushing, grinding, abrasion of surfaces), non-exhaust traffic emissions (e.g., abrasion of brake, tire and road surface), construction and demolition, agriculture, road dust resuspension and industrial fugitive emissions (Yin and Harrison, 2008, Wegesser et al., 2009, Edgerton et al., 2009, Moore et al., 2010, Lagudu et al., 2011).
A variety of biological substances (pollen, fungi and endotoxin) can also attach to the surface of coarse particles (Monn and Becker, 1999, Soukup and Becker, 2001, Schins et al., 2004). Bacterial endotoxins are lipopolysaccharides derived from the cell wall of gram-negative bacteria (Douwes et al., 2000). They are adsorbed on the surface of particles and are found to be mostly associated with coarse PM (Soukup and Becker, 2001, Schins et al., 2004). When inhaled, endotoxin can contribute to asthma exacerbation in children (Rizzo et al., 1997), and increased prevalence and severity of asthma in adults (Michel et al., 1996, Thorne et al., 2005). A number of studies have demonstrated the association of endotoxin exposure with proinflammatory cytokine production (Monn and Becker, 1999, Becker and Soukup, 1999), increased lung inflammation, airway responsiveness and systemic immune cell populations (Michel et al., 1996), and lung function modification by CD14/−260 genotype (Bakolis et al., 2012).
Endotoxin is ubiquitous in both indoor and outdoor environments. Several studies have been carried out worldwide to assess endotoxin levels through measurement of settled house dust (Heinrich et al., 2001, Gereda et al., 2001, Su et al., 2002, Perzanowski et al., 2005, Tavernier et al., 2006, Thorne et al., 2009, Madsen et al., 2012, Sordillo et al., 2011, Moniruzzaman et al., 2012, Chen et al., 2012). However, relatively few studies have been conducted to measure endotoxin levels in the ambient air (Park et al., 2000, Heinrich et al., 2003, Morgenstern et al., 2005, Sebastian et al., 2006, Dales et al., 2006, Madsen, 2006, Wheeler et al., 2011b, McNamara et al., 2013, Pavilonis et al., 2013) and simultaneously in both dust and air media (Park et al., 2001, Singh et al., 2011, Mazique et al., 2011, Barnig et al., 2013). These studies have identified several sources of endotoxin including dairy farming, agricultural dusts, pets, pests such as mice and cockroaches, cigarette smoke, humidifiers, carpeted flooring, cotton mills, wood-working plants, dampness and contaminated water systems. However, it remains unclear if there is regional variability in the levels and predictors of endotoxin.
In collaboration with the University of Alberta, a study was undertaken by Health Canada in Edmonton, Alberta in 2010 as part of a series of studies examining residential indoor air quality across Canada. The intent of these studies was to identify/confirm priority indoor air contaminants, determine their sources and to provide data to assist in development/revision of appropriate air quality guidelines and source product regulations, as required, in order to improve indoor air quality. Edmonton is the second largest city in Alberta, and within it's municipal boundaries the city's population was 782,439 in 2009 (Municipal census, 2009). It covers an area of over 680 km2, and is the northernmost North American city with a metropolitan population over 1.1 million. The city is surrounded by a number of industries (coal-fired power plants, petroleum refineries, steel foundries, asphalt roofing and cement manufacturing plants) and agricultural farming lands (Cheng et al., 1998, Zhang, 2005). Edmonton has a dry humid continental climate with wide variations in seasonal temperatures, i.e., cold winters and warm summers. Daily average temperatures range from −11.7 °C in January to 17.5 °C in July. The overall objective of his manuscript is to characterize indoor and outdoor levels and predictors of airborne coarse PM and associated endotoxin in Edmonton homes.
Section snippets
Sampling strategy
Coarse PM concentrations were measured both indoors and outdoors for seven consecutive 24-h periods in 50 homes during winter (January to April) and summer (June to August) 2010, with 26 homes participating in both seasons. Therefore, measurements were conducted in a total of 74 individual homes during the study period. There were nine consecutive seven-day sampling periods per season, with 5–6 homes being measured concurrently per period. Data on relative humidity, temperature, air exchange
Method precision
The indoor and outdoor results from samples collected at 24 homes during the first four 7-day sampling periods in the winter were deemed invalid due to improper laboratory assembly of the sampling units and were excluded. Therefore, for this investigation, data from 50 homes in the summer and 26 homes in the winter were analyzed. More than 50% of the blank PUF filters were below the laboratory detection limit of 4 μg/filter, therefore no blank corrections were applied to the coarse PM
Summary and conclusion
Indoor and outdoor concentrations of coarse PM and associated endotoxin were measured in residences of Edmonton. During the winter, higher outdoor concentrations of coarse PM were observed compared to indoor concentrations. Endotoxin concentrations were found to be higher during summer than winter. From linear mixed models, similar indoor predictors of coarse PM were found in both seasons, including number of people in the home, vacuuming, sweeping or dusting activities and outdoor coarse PM
Acknowledgment
The authors are grateful to the study participants as well as Health Canada staff (Keith Van Ryswyk, Ryan Kulka, Hongyu You, Mélissa St-Jean and Tae Maen Shin), field technicians, study and laboratory personnel at the University of Alberta; and Alberta Research Council and Paracel Laboratories personnel. We would also like to acknowledge the guidance and help provided by Ninon Lyrette. This study was funded by Health Canada under contract # 4500220223.
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Cited by (0)
- 1
Current address: WHO European Centre for Environment and Health, Bonn, Germany.
- 2
Current address: Centre for Ecosystem Management, School of Natural Sciences, Edith Cowan University, 270 Joondalup Drive, Joondalup, WA 6027, Australia.