Christopher D. Simpson

Woodsmoke Health Effects: A Review

The sentiment that woodsmoke, being a natural substance, must be benign to humans is still sometimes heard. It is now well established, however, that wood-burning stoves and fireplaces as well as wildland and agricultural fires emit significant quantities of known health-damaging pollutants, including several carcinogenic compounds. Two of the principal gaseous pollutants in woodsmoke, CO and NOx, add to the atmospheric levels of these regulated gases emitted by other combustion sources. Health impacts of exposures to these gases and some of the other woodsmoke constituents (e.g., benzene) are well characterized in thousands of publications. As these gases are indistinguishable no matter where they come from, there is no urgent need to examine their particular health implications in woodsmoke. With this as the backdrop, this review approaches the issue of why woodsmoke may be a special case requiring separate health evaluation through two questions. The first question we address is whether woodsmoke should be regulated and/or managed separately, even though some of its separate constituents are already regulated in many jurisdictions. The second question we address is whether woodsmoke particles pose different levels of risk than other ambient particles of similar size. To address these two key questions, we examine several topics: the chemical and physical nature of woodsmoke; the exposures and epidemiology of smoke from wildland fires and agricultural burning, and related controlled human laboratory exposures to biomass smoke; the epidemiology of outdoor and indoor woodsmoke exposures from residential woodburning in developed countries; and the toxicology of woodsmoke, based on animal exposures and laboratory tests. In addition, a short summary of the exposures and health effects of biomass smoke in developing countries is provided as an additional line of evidence. In the concluding section, we return to the two key issues above to summarize (1) what is currently known about the health effects of inhaled woodsmoke at exposure levels experienced in developed countries, and (2) whether there exists sufficient reason to believe that woodsmoke particles are sufficiently different to warrant separate treatment from other regulated particles. In addition, we provide recommendations for additional woodsmoke research.

Composition and distribution of polycyclic aromatic hydrocarbon contamination in surficial marine sediments from Kitimat Harbor, Canada

Surficial marine sediments from 20 sites within the Kitimat fjord system were analyzed for polycylic aromatic hydrocarbons (PAHs). Levels of the sum of the 16 USEPA priority pollutant PAHs varied from below detection limits (ca. 1 microg x g-1) to over 10 000 microg x g-1. Sediment PAH levels were highest in the immediate vicinity of a large aluminum smelter at the head of Kitimat Arm, and declined rapidly with increasing distance from the smelter. However, even at some of the more distant sites which are geographically isolated from the smelter PAH levels were elevated. The PAH distribution in the fjord system is consistent with a combination of aeolian and fluvial transport of PAHs emitted by the aluminum smelter at the head of Kitimat Arm. The mixture of PAHs present was qualitatively similar in all samples analyzed, including those from the distant sites. All aspects of the PAH composition are consistent with combustion generated PAHs. A correlation between PAH levels and sediment organic carbon was observed; however, this was only significant for highly contaminated sites in the harbor. This probably reflects the high organic content of particulate emissions from the smelter, rather than equilibrium partitioning of PAHs to sediment organic carbon within the harbor itself.

Source Apportionment of Indoor, Outdoor, and Personal PM2.5 in Seattle, Washington, Using Positive Matrix Factorization

Abstract As part of a large exposure assessment and health-effects panel study, 33 trace elements and light-absorbing carbon were measured on 24-hr fixed-site filter samples for particulate matter with an aerodynamic diameter <2.5 μm (PM2.5) collected between September 26, 2000, and May 25, 2001, at a central outdoor site, immediately outside each subjects residence, inside each residence, and on each subject (personal sample). Both two-way (PMF2) and three-way (PMF3) positive matrix factorization were used to deduce the sources contributing to PM2.5. Five sources contributing to the indoor and outdoor samples were identified: vegetative burning, mobile emissions, secondary sulfate, a source rich in chlorine, and a source of crustal-derived material. Vegetative burning contributed more PM2.5 mass on average than any other source in all microenvironments, with average values estimated by PMF2 and PMF3, respectively, of 7.6 and 8.7 μg/m3 for the outdoor samples, 4 and 5.3 μg/m3 for the indoor samples, and 3.8 and 3.4 μg/m3 for the personal samples. Personal exposure to the combustion-related particles was correlated with outdoor sources, whereas exposure to the crustal and chlorine-rich particles was not. Personal exposures to crustal sources were strongly associated with personal activities, especially time spent at school among the child subjects.

Determination of levoglucosan in atmospheric fine particulate matter.

Abstract A microanalytical method suitable for the quantitative determination of the sugar anhydride levoglucosan in low-volume samples of atmospheric fine particulate matter (PM) has been developed and validated. The method incorporates two sugar anhydrides as quality control standards. The recovery standard sedoheptulosan (2,7-anhydro-β-D-altro-heptulopyranose) in 20 μL solvent is added onto samples of the atmospheric fine PM and aged for 1 hr before ultrasonic extraction with ethylacetate/ triethylamine. The extract is reduced in volume, an internal standard is added (1,5-anhydro-D-mannitol), and a portion of the extract is derivatized with 10% by volume N-trimethylsilylimidazole. The derivatized extract is analyzed by gas chromatography/mass spectrometry (GC/MS). The recovery of levoglucosan using this procedure was 69 ± 6% from five filters amended with 2 μg levoglu-cosan, and the reproducibility of the assay is 9%. The limit of detection is ∼0.1 μg/mL, which is equivalent to ∼3.5 ng/m3 for a 10 L/min sampler or ∼8.7 ng/m3 for a 4 L/min personal sampler (assuming 24-hr integrated samples). We demonstrated that levoglucosan concentrations in collocated samples (expressed as ng/m3) were identical irrespective of whether samples were collected by PM with aerodynamic diameter ≤2.5 μm or PM with aerodynamic diameter ≤10 μm impactors. It was also demonstrated that X-ray fluorescence analysis of samples of atmospheric PM, before levoglucosan determinations, did not alter the levels of levoglucosan.

Changes in Lung Function and Airway Inflammation Among Asthmatic Children Residing in a Woodsmoke-Impacted Urban Area

Fine particulate matter (PM2.5) is associated with respiratory effects, and asthmatic children are especially sensitive. Preliminary evidence suggests that combustion-derived particles play an important role. Our objective was to evaluate effect estimates from different PM2.5 exposure metrics in relation to airway inflammation and lung function among children residing in woodsmoke-impacted areas of Seattle. Nineteen children (ages 6–13 yr) with asthma were monitored during the heating season. We measured 24-h outdoor and personal concentrations of PM2.5 and light-absorbing carbon (LAC). Levoglucosan (LG), a marker of woodsmoke, was also measured outdoors. We partitioned PM2.5 exposure into its ambient-generated (Eag) and nonambient (Ena) components. These exposure metrics were evaluated in relation to daily changes in exhaled nitric oxide (FENO), a marker of airway inflammation, and four lung function measures: midexpiratory flow (MEF), peak expiratory flow (PEF), forced expiratory volume in the first second (FEV1), and forced vital capacity (FVC). Eag, but not Ena, was correlated with combustion markers. Significant associations with respiratory health were seen only among participants not using inhaled corticosteroids. Increases in FENO were associated with personal PM2.5, personal LAC, and Eag but not with ambient PM2.5 or its combustion markers. In contrast, MEF and PEF decrements were associated with ambient PM2.5, its combustion markers, and Eag, but not with personal PM2.5 or personal LAC. FEV1 was associated only with ambient LG. Our results suggest that lung function may be especially sensitive to the combustion-generated component of ambient PM2.5, whereas airway inflammation may be more closely related to some other constituent of the ambient PM2.5 mixture.

Methodology for the determination of priority pollutant polycyclic aromatic hydrocarbons in marine sediments

The development and application of a simple method for the isomer specific determination of polycyclic aromatic hydrocarbons (PAHs) in marine sediments is described. The method involves Soxhlet extraction of the sample with methylene chloride, a one-step cleanup on a Florisil column, and analysis by using capilliary gas chromatography with flame ionisation detection (GC-FID). Using this method, quantitative recoveries from spiked sediment samples were obtained for all of the 16 USEPA priority pollutant PAHs, with the exception of naphthalene. This method allows for substantial time and cost savings when compared to current isomer specific analytical methodologies, and will find application where availability of resources and instrumentation is limited.

Blood Manganese as an Exposure Biomarker: State of the Evidence

Despite evidence of adverse health effects resulting from exposure to manganese (Mn), biomarkers of exposure are poorly understood. To enhance understanding, mean blood Mn (MnB) and mean air Mn (MnA) were extracted from 63 exposure groups in 24 published papers, and the relationship was modeled using segmented regression. On a log/log scale, a positive association between MnA and MnB was observed among studies reporting MnA concentrations above about 10 μg/m3, although interpretation is limited by largely cross-sectional data, study design variability, and differences in exposure monitoring methods. Based on the results of the segmented regression, we hypothesize that below the concentration of about 10 μg/m3, Mn in the body is dominated by dietary Mn, and additional inhaled Mn only causes negligible changes in Mn levels unless the inhaled amount is substantial. However, stronger study designs are required to account for temporal characteristics of the MnA to MnB relationships that reflect the underlying physiology and toxicokinetics of Mn uptake and distribution. Thus, we present an inception cohort study design we have conducted among apprentice welders, and the analytical strengths this study design offers. To determine if blood could be a useful biomarker for Mn to be utilized by industrial hygienists in general industry requires additional time-specific analyses, which our inception cohort study design will allow.

Biological monitoring of smoke exposure among wildland firefighters: A pilot study comparing urinary methoxyphenols with personal exposures to carbon monoxide, particular matter, and levoglucosan

Urinary methoxyphenols (MPs) have been proposed as biomarkers of woodsmoke exposure. However, few field studies have been undertaken to evaluate the relationship between woodsmoke exposure and urinary MP concentrations. We conducted a pilot study at the US Forest Service — Savannah River Site, in which carbon monoxide (CO), levoglucosan (LG), and particulate matter (PM2.5) exposures were measured in wildland firefighters on prescribed burn days. Pre- and post-shift urine samples were collected from each subject, and cross-shift changes in creatinine-corrected urinary MP concentrations were calculated. Correlations between exposure measures and creatine-adjusted urinary MP concentrations were explored, and regression models were developed relating changes in urinary MP concentrations to measured exposure levels. Full-shift measurements were made on 13 firefighters over 20 work shifts in winter 2004 at the US Forest Service Savannah River site, a National Environmental Research Park. The average workshift length across the 20 measured shifts was 701±95 min. LG and CO exposures were significantly correlated for samples where the filter measurement captured at least 60% of the work shift (16 samples), as well as for the smaller set of full-shift exposure samples (n=9). PM2.5 and CO exposures were not significantly correlated, and LG and PM2.5 exposures were only significantly correlated for samples representing at least 60% of the work shift. Creatinine-corrected urinary concentrations for 20 of the 22 MPs showed cross-shift increases, with 14 of these changes showing statistical significance. Individual and summed creatinine-adjusted guaiacol urinary MPs were highly associated with CO (and, to a lesser degree, LG) exposure levels, and random-effects regression models including CO and LG exposure levels explained up to 80% of the variance in cross-shift changes in summed creatinine-adjusted guaiacol urinary MP concentrations. Although limited by the small sample size, this pilot study demonstrates that urinary MP concentrations may be effective biomarkers of occupational exposure to wood smoke among wildland firefighters.

Urinary levoglucosan as a biomarker of wood smoke: results of human exposure studies.

Urinary levoglucosan was investigated as a potential biomarker of wood smoke exposure in two different controlled experimental settings. Nine subjects were exposed to smoke from a campfire in a controlled setting, and four were exposed to smoke from an older-model wood stove. All subjects were asked to provide urine samples before and after exposure, and to wear personal particulate matter with a diameter of ≤2.5 μm (PM2.5) monitors during exposure. Urinary levoglucosan measurements from both studies showed no consistent response to the smoke exposure. A third experiment was conducted to assess the contribution of dietary factors to urinary levoglucosan levels. Nine subjects were asked to consume caramel and provide urine samples before and after consumption. Urinary levoglucosan levels increased within 2 h of caramel consumption and returned to pre-exposure levels within 24 h. These studies suggest that diet is a major factor in determining urinary levoglucosan levels and that recent dietary history needs to be taken into account for future work involving levoglucosan as a biomarker of wood smoke exposure.

Metabolism of pyrene by two clam species, Mya arenaria and Protothaca staminea

Two species of marine clam, Mya arenaria and Protothaca staminea, were exposed to pyrene and 1-hydroxypyrene in small glass aquaria. After 10 days of exposure the clams were sacrificed, and both clam tissue and seawater were assayed for pyrene metabolites by using HPLC, fluorescence spectroscopy, HPLC-ESI-MS, GC-MS and 1H-NMR spectrometry. 1-Pyrenol-1-hydrogensulfate (pyrene-1-sulfate) was identified as the major water soluble metabolite formed from both pyrene and 1-hydroxypyrene by both species of clam. 1-Hydroxypyrene was identified as a minor metabolite of pyrene, and pyrenediol-hydrogen sulfate was identified as a minor metabolite of 1-hydroxypyrene.