This paper presents a summary of fireplace particle size and organic speciation data gathered to date in an ongoing project. Tests are being conducted in a residential wood combustion (RWC) laboratory on three factory-built fireplaces. RWC wood smoke particles <10 μm (PM10) consist primarily of a mixture of organic compounds that have condensed into droplets; therefore, the size distribution and total mass are influenced by temperature of the sample during its collection. During the series 1 tests (15 tests), the dilution tunnel used to cool and dilute the stack gases gave an average mixed gas temperature of 47.3 °C and an average dilution ratio of 4.3. Averages for the PM2.5 (particles <2.5 μm) and PM10 fractions were 74 and 84%, respectively. For the series 2 tests, the dilution tunnel was modified, reducing the average mixed gas temperatures to 33.8 °C and increasing the average dilution ratio to 11.0 in tests completed to date. PM2.5 and PM10 fractions were 83 and 91%, respectively. Since typical winter time mixed gas temperatures would usually be less than 10 °C, these size fraction results (even from the series 2 tests) probably represent the lower bound; the PM10 and PM2.5 size fractions might be higher at typical winter temperatures. The particles collected on the first stage (cutpoint ≈ 11.7 μm) were light gray and appeared to include inorganic ash. Particles collected on the remainder of the stages were black and appeared to be condensed organics because there was noticeable lateral bleeding of the collected materials into the filter substrate. Total particulate emission rates ranged from 10.3 to 58.4 g/h; corresponding emission factors ranged from 3.3 to 14.9 g/kg of dry wood burned. A wide range of Environmental Protection Agency (EPA) Method 8270 semivolatile organic compounds were found in the emissions; of the 17 target compounds quantified, major constituents are phenol, 2-methylphenol, 4-methylphenol, 2,4-dimethylphenol, and naphthalene.

As part of the Integrated Air Cancer Project, the U.S. Environmental Protection Agency (EPA) has conducted field emission measurement programs in Raleigh, North Carolina, and Boise, Idaho, to identify the potential mutagenic impact of residential wood burning and motor vehicles on ambient and indoor air. These studies included the collection of emission samples from chimneys serving wood burning appliances. Parallel projects were undertaken in instrumented woodstove test laboratories to quantify woodstove emissions during operations typical of in-house usage but under more controlled conditions. Three woodstoves were operated in test laboratories over a range of burnrates, burning eastern oak, southern yellow pine, or western white pine. Two conventional stoves were tested at an altitude of 90 m. One of the conventional stoves and a catalytic stove were tested at an altitude of 825 m. Decreasing burnrate increased total particulate emissions from the conventional stoves while the catalytic stove's total particulate emissions were unaffected. There was no correlation of total particulate emissions with altitude whereas total polynuclear aromatic hydrocarbon (PAH) emissions were higher at the lower altitude. Mutagenicity of the catalytic stove emissions was higher than emissions from the conventional stove. Emissions from burning pine were more mutagenic than emissions from oak.

Studies in animals have shown that a wide range of airborne particulates including cigarette smoke, acid aerosols, metals, organic compounds, and combustion products can interfere with the normal defense processes of the lung to enhance susceptibility to respiratory infection or exacerbate allergic diseases. Such detrimental effects are less easy to quantify in humans because of the difficulties in obtaining comprehensive exposure history and health status in large populations and because of the inherent dangers of inducing disease in clinical studies. In this article we describe examples of how air pollutants affect lung disease in experimental animal systems. This information can be used to predict the health risk of simple and complex exposures and to lend insight into the mechanisms of air pollution toxicity.