Low-level exposure to ambient particulate matter is associated with systemic inflammation in ischemic heart disease patients
Department of Environmental Health, National Institute for Health and Welfare, Kuopio, Finland. Environmental Research
(Impact Factor: 4.37).
04/2012; 116:44-51. DOI: 10.1016/j.envres.2012.04.004
Short-term exposure to ambient air pollution is associated with increased cardiovascular mortality and morbidity. This adverse health effect is suggested to be mediated by inflammatory processes. The purpose of this study was to determine if low levels of particulate matter, typical for smaller cities, are associated with acute systemic inflammation. Fifty-two elderly individuals with ischemic heart disease were followed for six months with biweekly clinical visits in the city of Kotka, Finland. Blood samples were collected for the determination of inflammatory markers interleukin (IL)-1Β, IL-6, IL-8, IL-12, interferon (IFN)γ, C-reactive protein (CRP), fibrinogen, myeloperoxidase and white blood cell count. Particle number concentration and fine particle (particles with aerodynamic diameters <2.5μm (PM 2.5)) as well as thoracic particle (particles with aerodynamic diameters <10μm (PM 10)) mass concentration were measured daily at a fixed outdoor measurement site. Light-absorbance of PM 2.5 filter samples, an indicator of combustion derived particles, was measured with a smoke-stain reflectometer. In addition, personal exposure to PM 2.5 was measured with portable photometers. During the study period, wildfires in Eastern Europe led to a 12-day air pollution episode, which was excluded from the main analyses. Average ambient PM 2.5 concentration was 8.7μg/m 3. Of the studied pollutants, PM 2.5 and absorbance were most strongly associated with increased levels of inflammatory markers; most notably with C-reactive protein and IL-12 within a few days of exposure. There was also some evidence of an effect of particulate air pollution on fibrinogen and myeloperoxidase. The concentration of IL-12 was considerably (227%) higher during than before the forest fire episode. These findings show that even low levels of particulate air pollution from urban sources are associated with acute systemic inflammation. Also particles from wildfires may exhibit pro-inflammatory effects.
Available from: Gavin Pereira
- "For the two studies that investigated birth weight, results were inconsistent (Holstius et al., 2012; Prass et al., 2012). All three cohort studies reported significant adverse associations between wildfires and health: systemic inflammation (Huttunen et al., 2012), bone marrow content (Tan et al., 2000), and physical strength and overall health (Frankenberg et al., 2005). Diarrhea and diabetes were mentioned as health outcomes of interest in multiple studies (Aditama 2000; Jalaludin et al., 2000; Lee et al., 2009; Viswanathan et al., 2006), but only two reported the results (Lee et al., 2009; Viswanathan et al., 2006). "
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Climate change is likely to increase the threat of wildfires, and little is known about how wildfires affect health in exposed communities. A better understanding of the impacts of the resulting air pollution has important public health implications for the present day and the future.
We performed a systematic search to identify peer-reviewed scientific studies published since 1986 regarding impacts of wildfire smoke on health in exposed communities. We reviewed and synthesized the state of science of this issue including methods to estimate exposure, and identified limitations in current research.
We identified 61 epidemiological studies linking wildfire and human health in communities. The U.S. and Australia were the most frequently studied countries (18 studies on the U.S., 15 on Australia). Geographic scales ranged from a single small city (population about 55,000) to the entire globe. Most studies focused on areas close to fire events. Exposure was most commonly assessed with stationary air pollutant monitors (35 of 61 studies). Other methods included using satellite remote sensing and measurements from air samples collected during fires. Most studies compared risk of health outcomes between 1) periods with no fire events and periods during or after fire events, or 2) regions affected by wildfire smoke and unaffected regions. Daily pollution levels during or after wildfire in most studies exceeded U.S. EPA regulations. Levels of PM10, the most frequently studied pollutant, were 1.2 to 10 times higher due to wildfire smoke compared to non-fire periods and/or locations. Respiratory disease was the most frequently studied health condition, and had the most consistent results. Over 90% of these 45 studies reported that wildfire smoke was significantly associated with risk of respiratory morbidity.
Exposure measurement is a key challenge in current literature on wildfire and human health. A limitation is the difficulty of estimating pollution specific to wildfires. New methods are needed to separate air pollution levels of wildfires from those from ambient sources, such as transportation. The majority of studies found that wildfire smoke was associated with increased risk of respiratory and cardiovascular diseases. Children, the elderly and those with underlying chronic diseases appear to be susceptible. More studies on mortality and cardiovascular morbidity are needed. Further exploration with new methods could help ascertain the public health impacts of wildfires under climate change and guide mitigation policies.
Available from: Edvinas Krugly
- "Recent air quality studies indicate a rising worldwide concern due to the significant contribution of biomass combustion to ambient air pollution (Glasius et al., 2008; Gustafson et al., 2008; Hell en et al., 2008) and underline the importance of using efficient wood combustion technologies to improve the air quality in residential areas (Bari et al., 2010, 2011; Gonçalves et al., 2012; Huttunen et al., 2012; Kaivosoja et al., 2012; Meyer, 2012; Piazzalunga et al., 2013). While the above presented studies addressed quantitative estimate of the contribution from the residential heating to the ambient air quality, very few have aimed at the investigation of the contribution of the products of fuel combustion to the indoor air quality. "
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ABSTRACT: Emissions from the fuel combustion in the energy production are causes of concern due to associated health risks, but little information is available on the impact of residential fuel burning on indoor air quality, where most of the human exposure occurs. In this complex study, concentrations of size-segregated particulate matter (PM), monocyclic and polycyclic aromatic compounds (MAHs and PAHs) at indoor and outdoor sites in six urban homes in the city of Kaunas, Lithuania, were determined over winter and summer sampling campaigns, specifically targeting the impact of the local fuel burning to the indoor air quality. PM levels observed in Kaunas during winter measurement campaign were higher compared to those in many other European settlements utilizing biomass for energy production. The particle size distribution analysis revealed that the major part of the PM mass in winter period consisted of fine particles (PM2.5). Both MAH and PAH levels were higher in winter. The indoor to outdoor ratios (I/O) of MAHs and PAHs revealed specific patterns depending on the presence of emissions sources indoors. Irrespectively of the season, I/O values were <1, suggesting that in case of the absence of an indoor pollution, the dominant source of organic compounds was from the outdoor environment. In homes with no PAH source inside, the I/O ratio equalled ranged from 0.05 to 0.36, suggesting the penetrated portion of outdoor combustion particles to the indoor air.
Available from: Kate Rittenhouse-Olson
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ABSTRACT: Abstract Inflammatory response is implicated as a biologic mechanism that links particulate matter (PM) air pollution with health effects. C-reactive protein (CRP), an important acute-phase reactant with profound proinflammatory properties, is used clinically as an indicator of the presence and intensity of inflammation. In vitro and in vivo animal studies suggest that CRP levels increase in response to PM exposure, but there was no consistency in epidemiologic studies. Herein, a systematic review was conducted to examine the association between PM exposure and serum CRP levels in humans. Elevated CRP levels were consistently found among children, and CRP elevations were also observed among healthy adults, albeit requiring higher peak levels of PM exposure. PM-induced CRP responses were not consistently found in adults with chronic inflammatory conditions, perhaps because of the use of anti-inflammatory medications in this population. Of the eight examined randomized trials, only one trial with a longer intervention period supported the effect of PM exposure on CRP concentrations. To provide conclusive evidence, further epidemiologic studies are needed to better quantify the magnitude of CRP level changes in response to PM with well-defined study populations and better control of various confounding factors.
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