Exposure and Risk from Ambient Particle-Bound Pollution in an Airshed Dominated by Residential Wood Combustion and Mobile Sources

Abstract

A major field study was conducted in Boise, Idaho, during the heating season of 1986 to 1987 as part of the Integrated Air Cancer Project. Filter samples were systematically collected in residences and in the ambient air across the community to characterize the particle-bound pollutants. The extractable organic matter (EOM) from the filter samples was apportioned to its source of origin, either residential wood combustion (RWC) or mobile sources (MS). Two composite samples, with apportioned contributions from RWC and MS, were prepared from the Boise ambient samples and tested for tumor-initiation potency. A comparative potency lung cancer risk estimate has been made based on the two ambient composite samples from this airshed. In addition, a microenvironmental exposure model was developed from the Boise data and from national survey data to estimate the exposure to EOM from RWC and MS. In this paper, the microenvironmental model is extrapolated to provide an estimate of the average annual exposure and dose in Boise to EOM from RWC and MS. The annual model considers actual pollutant levels in Boise, historical changes in RWC usage and meteorological dilution factors and the likely activities in the various microenvironmental zones and their resultant inhalation rates. Combined with the lifetime risk estimates, the average annual dose suggests a risk of about 4 x 10 4 based upon the composite ambient samples. Despite the fact that RWC accounts for 73% of the EOM on an annual average basis, it accounts for only about 20% of the estimated lifetime risk.-Environ Health Perspect 102(Suppl 4): 75-84 (1994).

Roles of oxidative stress in signaling and inflammation induced by particulate matter

“…Additionally, in developing countries, sugar cane plantations are burnt before harvesting, thus releasing air pollutants (Arbex et al 2004;Zhang and Smith 2007), whose levels may result high enough to cause adverse health effects similar to those produced by urban pollution (Arbex et al 2000(Arbex et al , 2007Cançado et al 2006;Mazzoli-Rocha et al 2008). Finally, it seems that emissions by mobile sources (as cars, trucks, buses, locomotives, and so forth) contribute more importantly to the risk of lung cancer than wood smoke (Cupitt et al 1994) since they respond for approximately 60% of benzene emissions (US EPA 2005).…”

Mutagenicity of the organic fraction of World Trade Center dust

“…Exposure to mutagenic EOM is associated with increased cancer risk from a variety of complex mixtures and combustion emissions ( Cupitt et al, 1994 ; DeMarini & Linak, 2022 ), including particles from outdoor air ( IARC, 2016 ), coal emissions and woodsmoke ( IARC, 2010 ), and diesel exhaust ( IARC, 2014 ). As shown in Figure 5 , the potential lung cancer risk resulting from a lifetime exposure to 1 μg EOM/m 3 has been determined for the EOMs from various combustion emissions, including cigarette smoke, roofing tar, and coke oven emissions ( Albert et al, 1983 ).…”

“…As shown in Figure 5 , the potential lung cancer risk resulting from a lifetime exposure to 1 μg EOM/m 3 has been determined for the EOMs from various combustion emissions, including cigarette smoke, roofing tar, and coke oven emissions ( Albert et al, 1983 ). Using the comparative potency bioassay method, Cupitt et al (1994) found a nearly perfect correlation between the EOM-based lung cancer risk of Albert et al (1983) ( Figure 5 ) and the carcinogenic potency of the EOMs on mouse skin. They used the resulting linear curve to extrapolate and predict the EOM-associated lung cancer risk for various air samples for which the carcinogenic potency of the EOM had been determined on mouse skin, and we have done the same for the EOM from highly carcinogenic smoky coal emissions as shown in Figure 2 of DeMarini and Linak (2022) .…”

“… EOM-based risk for lung cancer; data from Albert et al (1983) . Cupitt et al (1994) show the high correlation of these data with the carcinogenic potency of the EOMs on mouse skin, generating a standard curve from which an estimate of lung cancer risk can be made using the carcinogenic potency of EOMs on mouse skin. Such estimates have been made for air samples ( Cupitt et al, 1994 ) and smoky coal emissions ( DeMarini & Linak, 2022 ).…”