Hydroxyl-radical-dependent DNA damage by ambient particulate matter from contrasting sampling locations

Exposure to ambient particulate matter (PM) has been reported to be associated with increased respiratory, cardiovascular, and malignant lung disease. Previously we have shown that PM can induce oxidative DNA damage in A549 human lung epithelial cells. The aims of the present study were to investigate the variability of the DNA-damaging properties of PM sampled at different locations and times and to relate the observed effects to the hydroxyl-radical (OH)-generating activities of these samples. Weekly samples of coarse (10-2.5 microm) and fine (<2.5 microm) PM from four sites (Nordrheim Westfalen, Germany) were analyzed for hydrogen-peroxide-dependent OH formation using electron paramagnetic resonance and formation of 8-hydroxydeoxyguanosine (8-OHdG) in calf thymus DNA using an immuno-dot-blot assay. DNA strand breakage by fine PM in A549 human lung epithelial cells was quantified using the alkaline comet assay. Both PM size distribution fractions elicited OH generation and 8-OHdG formations in calf thymus DNA. Significantly higher OH generation was observed for PM sampled at urban/industrial locations and for coarse PM. Samples of fine PM also caused DNA strand breakage in A549 cells and this damage could be prevented using the hydroxyl-radical scavengers 5,5-dimethyl-1-pyrroline-N-oxide and dimethyl sulfoxide. The observed DNA strand breakage appeared to correlate with the hydroxyl-radical-generating capacities of the PM samples but with different profiles for rural versus urban/industrial samples. In conclusion, when considered at equal mass, OH formation of PM shows considerable variability with regard to the sampling location and time and is correlated with its ability to cause DNA damage.     

California Wildfires of 2008: Coarse and Fine Particulate Matter Toxicity

Background

During the last week of June 2008, central and northern California experienced thousands of forest and brush fires, giving rise to a week of severe fire-related particulate air pollution throughout the region. California experienced PM_10–2.5 (particulate matter with mass median aerodynamic diameter > 2.5 μm to < 10 μm; coarse ) and PM_2.5 (particulate matter with mass median aerodynamic diameter < 2.5 μm; fine) concentrations greatly in excess of the air quality standards and among the highest values reported at these stations since data have been collected.

Objectives

These observations prompt a number of questions about the health impact of exposure to elevated levels of PM_10–2.5 and PM_2.5 and about the specific toxicity of PM arising from wildfires in this region.

Methods

Toxicity of PM_10–2.5 and PM_2.5 obtained during the time of peak concentrations of smoke in the air was determined with a mouse bioassay and compared with PM samples collected under normal conditions from the region during the month of June 2007.

Results

Concentrations of PM were not only higher during the wildfire episodes, but the PM was much more toxic to the lung on an equal weight basis than was PM collected from normal ambient air in the region. Toxicity was manifested as increased neutrophils and protein in lung lavage and by histologic indicators of increased cell influx and edema in the lung.

Conclusions

We conclude that the wildfire PM contains chemical components toxic to the lung, especially to alveolar macrophages, and they are more toxic to the lung than equal doses of PM collected from ambient air from the same region during a comparable season.     

Potential confounding of particulate matter on the short-term association between ozone and mortality in multisite time-series studies

BACKGROUND: A critical question regarding the association between short-term exposure to ozone and mortality is the extent to which this relationship is confounded by ambient exposure to particles. OBJECTIVES: We investigated whether particulate matter < 10 and < 2.5 microm in aerodynamic diameter (PM(10) and PM(2.5)) is a confounder of the ozone and mortality association using data for 98 U.S. urban communities from 1987 to 2000. METHODS: We a) estimated correlations between daily ozone and daily PM concentrations stratified by ozone or PM levels; b) included PM as a covariate in time-series models; and c) included PM as a covariate as in d), but within a subset approach considering only days with ozone below a specified value. RESULTS: Analysis was hindered by data availability. In the 93 communities with PM(10) data, only 25.0% of study days had data on both ozone and PM(10). In the 91 communities with PM(2.5) data, only 9.2% of days in the study period had data on ozone and PM(2.5). Neither PM measure was highly correlated with ozone at any level of ozone or PM. National and community-specific effect estimates of the short-term effects of ozone on mortality were robust to inclusion of PM(10) or PM(2.5) in time-series models. The robustness remains even at low ozone levels (< 10 ppb) using a subset approach. CONCLUSIONS: Results provide evidence that neither PM(10) nor PM(2.5) is a likely confounder of observed ozone and mortality relationships. Further investigation is needed to investigate potential confounding of the short-term effects of ozone on mortality by PM chemical composition.     

Winter urban air particles from Rome (Italy): effects on the monocytic-macrophagic RAW 264.7 cell line

Epidemiological data show an association between exposure to elevated levels of particulate matter (PM), in particular the fine fraction (<2.5 microm in diameter), and an increase in cardiovascular mortality and respiratory symptoms. The aim of this study was to compare the in vitro toxicity of coarse and fine particulate matter collected with a cascade impactor during winter in an urban area of Rome in relation to their physicochemical characterization (size distribution and chemical composition) as assessed by analytical electron microscopy (SEM/EDX). The X-ray microanalysis data of single particles of coarse and fine matter were analyzed by hierarchical cluster analysis to determine the principal component of the two granulometric fractions. The main chemical difference between the two fractions was the greater abundance of carbonaceous particles in the fine fraction. We compared the ability of coarse and fine fractions, carbon black (CB), and residual oil fly ash (ROFA) to induce arachidonic acid release and tumor necrosis factor-alpha (TNF-alpha) production in the monocytic-macrophagic RAW 264.7 cell line at concentrations of 30 and 120 microg/mL. Our results showed that CB and ROFA were consistently less effective than both fractions of urban particles at inducing an inflammatory reaction in RAW 264.7 cells. Both PM fractions dose-dependently increased TNF-alpha production in RAW 264.7 cells after 5 and 24h of incubation, and only the TNF-alpha production induced by coarse particles at 30 microg/mL decreased significantly (P<0.01) after 24h of treatment. In our in vitro model the winter fine fraction was more reactive than the winter coarse fraction, in contrast to a previously examined summer sample. In the summer sample, coarse particles produced higher levels of inflammatory mediators than fine particles and the CB was consistently less effective than the urban particles. The different behaviors between summer and winter urban fractions may be due to their different physicochemical characteristics; in fact, the comparison of the two samples' characterization by SEM/EDX and X-ray photoelectron spectroscopy (XPS) analysis showed that in winter the carbonaceous particles are more abundant than in summer and that winter particles carry a greater quantity of organic compounds. We suggest that the higher concentration of organic compounds on fine carbonaceous particles may partially explain the higher activation of RAW 264.7 cells by fine particles.     

The effects of particulate matter sources on daily mortality: a case-crossover study of Barcelona, Spain

Background: Dozens of studies link acute exposure to particulate matter (PM) air pollution with premature mortality and morbidity, but questions remain about which species and sources in the vast PM mixture are responsible for the observed health effects. Although a few studies exist on the effects of species and sources in U.S. cities, European cities—which have a higher proportion of diesel engines and denser urban populations—have not been well characterized. Information on the effects of specific sources could aid in targeting pollution control and in articulating the biological mechanisms of PM.Objectives: Our study examined the effects of various PM sources on daily mortality for 2003 through 2007 in Barcelona, a densely populated city in the northeast corner of Spain.Methods: Source apportionment for PM ≤ 2.5 μm and ≤ 10 µm in aerodynamic diameter (PM_2.5 and PM₁₀) using positive matrix factorization identified eight different factors. Case-crossover regression analysis was used to estimate the effects of each factor.Results: Several sources of PM_2.5, including vehicle exhaust, fuel oil combustion, secondary nitrate/organics, minerals, secondary sulfate/organics, and road dust, had statistically significant associations (p < 0.05) with all-cause and cardiovascular mortality. Also, in some cases relative risks for a respective interquartile range increase in concentration were higher for specific sources than for total PM_2.5 mass.Conclusions: These results along with those from our multisource models suggest that traffic, sulfate from shipping and long-range transport, and construction dust are important contributors to the adverse health effects linked to PM.     

A comparison of particulate matter from biomass-burning rural and non-biomass-burning urban households in northeastern China

BACKGROUND: Biomass fuel is the primary source of domestic fuel in much of rural China. Previous studies have not characterized particle exposure through time-activity diaries or personal monitoring in mainland China. OBJECTIVES: In this study we characterized indoor and personal particle exposure in six households in northeastern China (three urban, three rural) and explored differences by location, cooking status, activity, and fuel type. Rural homes used biomass. Urban homes used a combination of electricity and natural gas. METHODS: Stationary monitors measured hourly indoor particulate matter (PM) with an aerodynamic diameter < or = 10 microm (PM10) for rural and urban kitchens, urban sitting rooms, and outdoors. Personal monitors for PM with an aerodynamic diameter < or = 2.5 microm (PM2.5) were employed for 10 participants. Time-activity patterns in 30-min intervals were recorded by researchers for each participant. RESULTS: Stationary monitoring results indicate that rural kitchen PM10 levels are three times higher than those in urban kitchens during cooking. PM10 was 6.1 times higher during cooking periods than during noncooking periods for rural kitchens. Personal PM2.5 levels for rural cooks were 2.8-3.6 times higher than for all other participant categories. The highest PM2.5 exposures occurred during cooking periods for urban and rural cooks. However, rural cooks had 5.4 times higher PM2.5 levels during cooking than did urban cooks. Rural cooks spent 2.5 times more hours per day cooking than did their urban counterparts. CONCLUSIONS: These findings indicate that biomass burning for cooking contributes substantially to indoor particulate levels and that this exposure is particularly elevated for cooks. Second-by-second personal PM2.5 exposures revealed differences in exposures by population group and strong temporal heterogeneity that would be obscured by aggregate metrics.     

Induction of IL-6 and inhibition of IL-8 secretion in the human airway cell line Calu-3 by urban particulate matter collected with a modified method of PM sampling

Exposure to particulate matter (PM) induces inflammatory cytokines. In the present study, we evaluated the secretion of IL-6 and IL-8 by an airway cell line exposed to PM with a mean aerodynamic size equal to or less than 10 or 2.5 μm (PM₁₀ and PM_2.5, respectively) collected in Mexico City, using a modified high-volume sampling method avoiding the use of solvents or introducing membrane components into the samples. PM was collected on cellulose-nitrate (CN) membranes modified for collection on high-volume samplers. Composition of the particles was evaluated by particle-induced X-ray emission (PIXE) and scanning electron microscopy. The particles (10-160 μg/cm²) were tested on Calu-3 cells. Control cultures were exposed to LPS (10 ng/mL to 100 μg/mL) or silica (10-160 μg/cm²). IL-6 and IL-8 secretions were evaluated by ELISA. An average of 10 mg of PM was recovered form each cellulose-nitrate filter. No evidence of contamination from the filter was found. Cells exposed to PM₁₀ presented an increase in the secretion of IL-6 (up to 400%), while IL-8 decreased (from 40% to levels below the detection limit). A similar but weaker effect was observed with PM_2.5. In conclusion, our modified sampling method provides a large amount of urban PM free of membrane contamination. The urban particles induce a decrease in IL-8 secretion that contrasts with the LPS and silica effects. These results suggest that the regulation of IL-8 expression is different for urban particles (complex mixture containing combustion-related particles, soil and biologic components) than for biogenic compounds or pure mineral particles.     

Early childhood lower respiratory illness and air pollution

BACKGROUND: Few studies of air pollutants address morbidity in preschool children. In this study we evaluated bronchitis in children from two Czech districts: Teplice, with high ambient air pollution, and Prachatice, characterized by lower exposures. OBJECTIVES: Our goal was to examine rates of lower respiratory illnesses in preschool children in relation to ambient particles and hydrocarbons. METHODS: Air monitoring for particulate matter < 2.5 microm in diameter (PM(2.5)) and polycyclic aromatic hydrocarbons (PAHs) was conducted daily, every third day, or every sixth day. Children born May 1994 through December 1998 were followed to 3 or 4.5 years of age to ascertain illness diagnoses. Mothers completed questionnaires at birth and at follow-up regarding demographic, lifestyle, reproductive, and home environmental factors. Longitudinal multivariate repeated-measures analysis was used to quantify rate ratios for bronchitis and for total lower respiratory illnesses in 1,133 children. RESULTS: After adjustment for season, temperature, and other covariates, bronchitis rates increased with rising pollutant concentrations. Below 2 years of age, increments in 30-day averages of 100 ng/m(3) PAHs and of 25 microg/m(3) PM(2.5) resulted in rate ratios (RRs) for bronchitis of 1.29 [95 % confidence interval (CI), 1.07-1.54] and 1.30 (95% CI, 1.08-1.58), respectively; from 2 to 4.5 years of age, these RRs were 1.56 (95% CI, 1.22-2.00) and 1.23 (95% CI, 0.94-1.62), respectively. CONCLUSION: Ambient PAHs and fine particles were associated with early-life susceptibility to bronchitis. Associations were stronger for longer pollutant-averaging periods and, among children > 2 years of age, for PAHs compared with fine particles. Preschool-age children may be particularly vulnerable to air pollution-induced illnesses.     

Correlation between suspended particles in the environmental air and causes of disease among inhabitants: cross-sectional studies using the vital statistics and air pollution data in Japan

To identify the diseases that correlate with suspended particle concentration in the ambient air, a cross-sectional epidemiological study was conducted using the annual vital statistics and air pollution estimates of 1881 points throughout Japan. The concentration of suspended particulate matters (SPMs) 10 microm or less in diameter were hypothetically converted to PM(2.5) values (converted PM(2.5) or cPM(2.5)) by using a conversion factor obtained from 25 estimates in Japan. Among various causes of death, a significant correlation was observed between both the SPM and cPM(2.5) (SPM/cPM(2.5)) levels and the age-adjusted death rates of ischemic heart disease or hypertensive heart disease in both genders. Correlation was noted with pneumonia, asthma, chronic bronchitis/emphysema, or lung cancer only in females. Unexpectedly, breast, endometrial, and ovarian cancer also showed significant increases in mortality rates related to the SPM/cPM(2.5) level, suggesting a role for suspended particles in the ambient air with or without gaseous component as a possible endocrine-disrupting, estrogenic agent. Multivariate regression analysis of confounding factors, smoking rate, population density, and hormone-related factors revealed consistent significance of SPM/cPM(2.5) in these diseases.     

北京市某区餐厅室内空气细颗粒物浓度水平现况研究

目的了解餐厅室内空气细颗粒物（PM2.5）的污染现状,揭示各影响因素的作用,为卫生标准及政策法规的制定提供科学依据。方法采用分层抽样方法选择北京市某区42家餐厅,使用AM-510智能防爆粉尘仪进行餐厅室内外细颗粒物浓度的检测,同时记录餐厅内人员数量、吸烟者数量等情况,比较不同类别餐厅、室内外细颗粒物浓度的差异,分析影响因素与室内细颗粒物浓度的关系。结果 42家餐厅室内、外PM2.5平均浓度分别为194μg/m3、76μg/m3,室内比室外高155.26%;有吸烟的餐厅室内PM2.5平均浓度高于室外206μg/m3（228.89%）且差异有统计学意义,无吸烟的餐厅室内与室外水平基本相当;中式正餐厅吸烟比例、PM2.5浓度水平高于中式快餐厅和西式快餐厅且差异有统计学意义,而中式快餐厅和西式快餐厅室内外PM2.5浓度水平相当;大、中、小型餐厅吸烟比例、PM2.5浓度水平差异无统计学意义;餐饮业量化分级管理的A、B、C级餐厅吸烟比例、PM2.5浓度水平差异亦无统计学意义;经Spearman非参数相关分析,室内与室外PM2.5浓度存在正相关且有统计学意义,室内无吸烟的餐厅该相关关系更为紧密,而有吸烟的餐厅室内与室外PM2.5浓度无相关关系,以无吸烟餐厅的PM2.5浓度为应变量（y）,其室外PM2.5浓度为自变量（x）进行一元线性回归分析,回归方程为y（μg/m3）=0.828x＋9.456（R2=0.862,F=100.327,P〈0.001）;餐厅室内PM2.5浓度与吸烟支数密度存在正相关关系（r=0.814,P〈0.001）。结论餐厅内细颗粒物污染严重;吸烟和室外空气PM2.5浓度是影响餐厅室内PM2.5浓度的主要因素。