An Assessment of Risk From Particulate Released From Outdoor Wood Boilers: Brown, David R. et al; Human and Ecological Risk Assessment: Vol.13, Sept. 30, 2006 Excerpt from Page 197-199
Wood smoke particulate and ambient air particulate toxicity have been reviewed elsewhere (e.g., Boman et al 2003; Naeher et al. 2005; Butterfield et al. 1989; Cupitt et al. 1994; Dominici et al 2006; Koenig et al. 1993; ALA 2001; Zelikoff et al. 2002).
As a brief overview, the following health effects have been linked (ibid.) to wood smoke.
1. Airway changes including hyper responsiveness, lower air way respiratory infections, and inflammation.
2. Bronchiolitis, hyperplasia, and hypertrophy including increase in lung cancer risk.
3. Shortness of breath and moderate to severe cough in asthmatics and waking up with a cough.
4. Inflammation of the middle ear marked by pain, fever and dizziness.
5. Significant decreases in lung function including Forced Ventilatory Capacity (FVC) and 1 minute ventilatory rate (FEV1).
6. A pattern of increased symptoms and chronic illness in children based in part on a compromised immune system.
Current ambient exposure episodes to PM^sub 2.5^ in the Northeast U.S. increase hospitalization rates for cardiovascular and respiratory disease. More specifically, some of the well established health effects of ambient paniculate matter include the following (USEPA 2006; Burnett et al. 2000; Delfino et al. 2002; Dockery 2001; Steib et al. 2003):
1. Epidemiology studies report increased cardiovascular events, exacerbation of asthma, and chronic obstructive pulmonary disease as well as links to cancer (Pope et al. 2002).
2. Case report studies show increased admission to emergency rooms for both respiratory and cardiovascular events.
3. Some clinical studies demonstrate a protective effect for anti- inflammatory medications.
4. Statistical analyses of some national mortality data show an increase in mortality in areas with higher particulate materials in the ambient air.
Particulate matter exposures also produce biochemical actions at the cellular level (Naeher et al. 2005). These biochemical studies suggest plausible modes of action, the release of bioactive materials. This effect that occurs at low doses strongly indicates that direct irritation of the respiratory tract is not the sole basis for a portion of the many health actions. Furthermore, health effects from PM occur after exposures of 2 to 4 h or less in duration of wood smoke at the 12 to 29 g/m^sup 3^ range (Koenig et al 1993).
Quantitative PM^sub 2.5^ ambient air studies as a quantitative measure for wood smoke
The strongest dose-response information for action between particulate and health effects is found in the reports based on ambient measures of PM^sub 2.5^. Peters et al. (2001) and Gent et al. (2003) demonstrated that health actions occur after PM exposures of 2 h or less. Peters found an increase in myocardial infarctions 2 h after an increase of 25 g/m^sup 3^ over background (odds ratio 1.48) and another 24 h later after a 20 g/m^sup3^ increase in PM^sub 2.5^ over background (Odds ratio 1.69). Similarly, Gent et al. (2003) showed that, within 1 h, groups of children with severe asthma showed 35% increase in wheezing and 47% increase in chest tightness after 50 ppb ozone and 12 to 18 g/m^sup 3^ PM^sub 2.5^ (odds ratio for chest tightness is 1.24). Dockery and coworkers (1993) found that exposures in the 11 to 29 g/m^sup 3^ PM (measured as annual PM levels) range revealed a dose-related difference between six cities for the following conditions:
* All cause of death (odds ratio 1.26 (CI^sup 4^ 1.08-1.47))
* Lung Cancer (odds ratio 1.37 (0.81-2.31))
* Cardiopulmonary (odds ratio 1.37 (1.11-1.68))
The actions appear to be specific for the cardiopulmonary system and cancer because the odds ratio for "all other causes" studied was 1.01 (CI 0.79-1.30) ; moreover, there were 2-h and 24-h lags between the increase in PM and the health outcome.
The dose levels showing the above actions are in the 15 to 30 g/ m^sup 3^ range. This compares with the 12 to 29 g/m^sup 3^ median values found in wood stove data. Zanobetti and Schwartz's (2003) analysis (and reanalysis) of morbidity found similarly high relative risks. These findings show that increased PM^sub 2.5^ (at levels of 12 to 30 g/m^sup 3^) for 2 to 4 h can induce cardiopulmonary effects in humans.
Several reports that analyzed exposures to wood smoke in regions with extensive wood burning show that human exposure is related to four variables:
1. The amount of emissions released to the ambient air;
2. The dilution in the ambient air prior to a human inhalation;
3. The amount in indoor air due to penetration from the surrounding ambient air and the time that lapses before indoor air levels off-gas to the outdoors; and
4. The behavioral activity of the persons exposed.
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