Cytogenetic analysis using fluorescence in situ hybridization (FISH) to evaluate occupational exposure to carcinogens

Chromosomal aberrations determined by conventional method or fluorescence in situ hybridization (FISH) technique with whole chromosome painting are used as biomarkers of effect. Groups occupationally exposed to 1,3-butadiene (BD), acrylonitrile, ethyl benzene and benzene in petrochemical industry, and carcinogenic polycyclic aromatic hydrocarbons (c-PAHs) from ambient air were followed by conventional method and FISH painting for chromosomes # 1 and # 4, in total 383 subjects, including controls. No effect was observed by either method with exposure to 1,3-butadiene < 1mg/m(3) and acrylonitrile < 0.3mg/m(3). Ethyl benzene and benzene exposure significantly increased chromosomal aberrations by both methods, which decreased after the implementation of preventive measures. The genomic frequency of translocations by FISH calculated as FG/100 was significantly increased in city policemen versus control group exposed to c-PAHs from ambient air (1.72+/-1.57 versus 1.25+/-1.11, P<0.05). The method of FISH with whole chromosome painting seems to be more sensitive to detect chromosomal injury by occupational exposure to carcinogens than conventional method.     

Exposure to secondhand smoke at home and in public places in Syria: a developing country's perspective

This study employs sensitive methods to address the issue of exposure to secondhand smoke among children and women in an understudied developing country setting (Syria). The study combines data collected by the Syrian Center for Tobacco Studies as part of two international studies conducted in 2006: the Secondhand Smoke Exposure among Women and Children study (Johns Hopkins) and the Global Air Monitoring Study (Roswell Park Cancer Institute). We employed objective measures (hair nicotine, and ambient household nicotine assessed by passive monitors) to assess children's and mothers' exposure to secondhand smoke at home, and used the TSI SidePak personal aerosol monitor to sample respirable suspended particles less than 2.5 microm diameter (PM(2.5)) in the air in public places (40 restaurants/cafés in Aleppo). In homes, the mean ambient nicotine level (+/- standard deviation, SD) was 2.24 +/- 2.77 microg/m(3). Mean level of hair nicotine was 11.8 ng/mg among children (n = 54), and was higher if the mother was a smoker (19.4 +/- 23.6 ng/mg) than nonsmoker (5.2 +/- 6.9 ng/mg) (p < .05). Mean hair nicotine among nonsmoking mothers (n = 23) was 1.17 +/- 1.56 ng/mg. Children's hair nicotine level was strongly correlated with ambient household nicotine and number of cigarettes smoked daily in the house (r = .54 and r = .50, respectively, p < .001), and also was related to having a father who smoked in the children's presence. In public places, average PM(2.5) in the monitored 40 hospitality venues was 464 microg/m(3) and correlated with smoker density measured as cigarettes-waterpipes/100 m(3) (r = .31, p = 0.049). Thus, children in Syria are exposed to high levels of secondhand smoke at home, in which mothers' smoking plays a major role. Also, levels of respirable hazardous particles are high in public hospitality venues, putting customers and workers at serious health risks. Efforts to limit exposure of children and women at home and to adopt clean air policies should become a public health priority in Syria and the Arab region.     

DNA adducts and oxidative DNA damage induced by organic extracts from PM2.5 in an acellular assay

The genotoxic activities of complex mixtures of organic extracts from the urban air particles collected in various localities of the Czech Republic, which differed in the extent and sources of air pollution, were compared. For this purpose, PM2.5 particles were collected by high volume samplers in the most polluted area of the Czech Republic - Ostrava region (localities Bartovice, Poruba and Karvina) and in the locality exhibiting a low level of air pollution - Trebon - a small town in the non-industrial region of Southern Bohemia. To prepare extractable organic matter (EOM), PM2.5 particles were extracted by dichloromethane and c-PAHs contents in the EOMs were determined. As markers of genotoxic potential, DNA adduct levels and oxidative DNA damage (8-oxo-7,8-dihydro-2′-deoxyguanosine, 8-oxodG, levels) induced by EOMs in an acellular assay of calf thymus DNA coupled with ³²P-postlabeling (DNA adducts) and ELISA (8-oxodG) in the presence and absence of microsomal S9 fraction were employed. Twofold higher DNA adduct levels (17.20 adducts/10⁸ nucleotides/m³ vs. 8.49 adducts/10⁸ nucleotides/m³) were induced by EOM from Ostrava-Bartovice (immediate proximity of heavy industry) compared with that from Ostrava-Poruba (mostly traffic emissions). Oxidative DNA damage induced by EOM from Ostrava-Bartovice was more than fourfold higher than damage induced by EOM from Trebon (8-oxodG/10⁸ dG/m³: 0.131 vs. 0.030 for Ostrava-Bartovice vs. Trebon, respectively). Since PM2.5 particles collected in various localities differ with respect to their c-PAHs content, and c-PAHs significantly contribute to genotoxicity (DNA adduct levels), we suggest that monitoring of PM2.5 levels is not a sufficient basis to assess genotoxicity of respirable aerosols. It seems likely that the industrial emissions prevailing in Ostrava-Bartovice represent a substantially higher genotoxic risk than mostly traffic-related emissions in Ostrava-Poruba. B[a]P and c-PAH contents in EOMs are the most important factors relating to their genotoxic potential.     

Two-years of fine and ultrafine particles measurements in Rome, Italy

Long-term aerosol measurements have been conducted at two sites in Rome, Italy, April 2001 through March 2003, in a traffic-oriented site, and at an urban background site, close to the city center. The main objective was to establish validated and consistent data sets of particle number concentrations (PNC) in Rome to be used for epidemiological analyses of cardiovascular health effects. Particle number concentrations were measured by a condensation particle counter (CPC 3022A, TSI). Other pollutants (PM10, PM2.5, CO, NO2, NO, NOx, O3) were simultaneously measured at the traffic-oriented site. During the study period, the mean (standard deviation) 24-h PNC values were 4.69 x 10(4) (1.99 x 10(4)) cm(-3) and 2.46 x 10(4) (1.10 x 10(4)) cm(-3), respectively, at the traffic-oriented site and at the urban background site. Mean (standard deviation) 24-h mass concentration of PM2.5 was 23.1 (11.9) microg m(-3), while for PM10 it was 41.3 (17.9) microg m(-3). Higher values for all the pollutants, except ozone, were recorded during the winter period in comparison with the summer period, and a higher variability of the results was also observed during cold months. The comparison between the daily PNC measured at the two sites showed a good correlation (r = .74). CO (r = .77), NO (r = .82), and NOx (r = .83) were all highly correlated with PNC (simultaneous obs. number 576). The diurnal and seasonal pattern of PNC can be attributed to the combined effect of motor vehicle emissions and meteorological conditions.     

Effects of concentrated fine ambient particles on rat plasma levels of asymmetric dimethylarginine

The health effects of ambient fine particulate matter (PM(2.5)) and its potential impact on vascular endothelial function have not been thoroughly investigated. As endothelial dysfunction plays an important role in the pathogenesis of atherosclerosis and its complications, we examined the effects of concentrated fine ambient particles (CAPs) on the plasma level of asymmetric dimethylarginine (ADMA) in a pilot study. ADMA is a circulating endogenous inhibitor of nitric oxide synthase (NOS) that is associated with impaired vascular function and increased risk for cardiovascular events. A mobile air research laboratory (AirCARE 1) was used to provide "real-world" CAPs exposures for this study conducted in Detroit, MI. Fourteen Brown Norway rats were exposed to filtered air (FA) (n = 7) or CAPs (0.1-2.5 microm) (n = 7) for 3 consecutive days (8 h/day) in July 2002. Rats were exposed during these periods to average particle mass concentrations of 354 microg/m(3). Rat plasma samples were collected 24 h postexposure. Plasma concentrations of ADMA were significantly elevated in rats exposed to CAPs versus those exposed to FA (mean +/- standard deviation = 1.49 +/- 0.18 vs. 1.29 +/- 0.26 microM, p =.05 by one-tailed t-test). Analyses of meteorological data and CAPs trace element composition suggest that local particle emission sources contributed largely to overall mass of CAPs. Results of this pilot study suggest that exposure to PM(2.5) at high concentrations may trigger an acute increase in circulating ADMA level. This finding has implications for the regulation of vasomotor tone by particulate pollutants and the propensity for adverse cardiovascular events.     

Impact of air pollution and genotype variability on DNA damage in Prague policemen

DNA integrity was analyzed in the lymphocytes of 65 non-smoking city policemen during January and September 2004 using the comet assay combined with excision repair enzymes. Information about inhalation exposure was obtained by (1) stationary monitoring of PM2.5 and carcinogenic polycyclic aromatic hydrocarbons (cPAHs) during the sampling periods and (2) personal exposure monitoring of cPAHs 48h before blood sampling. The data were completed by a lifestyle questionnaire. Regardless of the season of the year, policemen working outdoors (exposed group) exhibited higher levels of DNA damage than those working indoors (controls). Within the exposed group, the levels of both unspecified and oxidative DNA damage detected in January significantly exceeded those found in September. The controls did not show analogous inter-seasonal variability. The winter levels of oxidative DNA damage positively correlated with exposure to cPAHs, probably reflecting increased oxidative stress as a result of high concentrations of PM2.5. In comparison with the wild type genotype, the carriers of at least one mutated allele, CYP1A1*2C (Ile/Val), MTHFR 2656 or MS 2656, and the EPHX1-medium phenotype appeared to be more susceptible specifically to the induction of oxidative DNA damage, while the p53 MspI mutation predisposed the carrier to a higher incidence of both breaks and oxidative lesions in DNA. In contrast, GSTM1-null and vitamin C tended rather to protect DNA integrity.     

The alarm reaction of coho salmon parr is impaired by the carbamate fungicide IPBC

To determine whether the carbamate fungicide IPBC alters the olfactory-mediated behavioral and physiologic alarm responses of coho salmon parr (Oncorhynchus kisutch), groups of coho were exposed to skin extract (an alarm pheromone source) under a variety of conditions. In the 3min following skin extract exposure, freezing behavior was significantly increased (In the 3 min following skin extract exposure, freezing behavior was significantly increased under darkness (IR lighting) but not ambient lighting (25.3+/-2.6% and 7.5+/-5.7%, respectively; Delta calculated as: [(time (s) after/time (s) before)-1]x100%), and so IR was used for further experiments. Physiologically, following skin extract exposure, plasma cortisol concentration was increased at 0.5h (58.1+/-14.6ng/ml versus 4.32+/-1.31ng/ml, exposed versus control), hematocrit (Hct) was increased at 2h (50.4+/-1.0% versus 41.7+/-1.6%), and leucocrit (Lct) was decreased at 0.5 and 2h (0.534+/-0.114 and 0.13+/-0.01% versus 1.23+/-0.20%). After 0.5h exposures to 0, 1, 10 and 100microg/l IPBC and skin extract, the time spent dashing (>5cm/s) increased significantly (323+/-118%) in the first minute after skin extract exposure, but was absent in IPBC-exposed coho. Freezing behavior increased after skin extract exposure with control and 1microg/l IPBC exposures (11.0+/-3.0% and 17.7+/-11.0%, respectively), but was absent after 10microg/l and decreased after 100microg/l IPBC. Physiologically, Hct and plasma lactate concentration were significantly increased above controls after 1microg/l IPBC exposure (Hct: 45.7+/-1.6% versus 34.0+/-1.6%, lactate: 12.8+/-1.2mM versus 3.30+/-1.2mM). After 10microg/l exposure, IPBC alone elicited a stress response similar to skin extract. However in the 100microg/l treatment group the stress parameters were not different from controls. These findings suggest that the behavioral and physiologic alarm responses of juvenile salmonids may be impaired by acute exposure to > or =1microg/l IPBC.     

Biological monitoring of low benzene exposure in Italian traffic policemen

A comparative evaluation of urinary biomarkers was carried out to characterize benzene exposure in a group of 100 traffic policemen of the city of Parma (Italy). All subjects were monitored once, in two consecutive days characterized by similar climatic conditions but preceded by two windy days. Benzene ambient concentration measured by municipal air monitoring stations was 1 microg/m(3) (Day 1) and 2 microg/m3 (Day 2). Personal exposure to ambient concentrations of benzene, toluene, ethylbenzene and xylene (BTEX) was assessed by using Radiello((R)) passive-diffusive samplers in a subgroup of 24 workers. Benzene metabolites, t,t-muconic acid (t,t-MA) and S-phenylmercapturic acid (S-PMA) were determined by isotopic dilution liquid chromatography-tandem mass spectrometry on spot urine samples collected at the end of the shift. Urinary benzene (U-B) was determined by solid-phase microextraction gas chromatography-mass spectrometry. Airborne benzene concentration expressed as median [and interquartile range] was 6.07 [0.28-9.53] microg/m(3), as assessed by personal sampling. Urinary concentrations of biomarkers in the whole group were 41.8 [34.1-89.8] microg/g creatinine for t,t-MA, 0.67 [0.23-1.32] microg/g creatinine for S-PMA, and 0.16 [0.13-0.26] microg/l for U-B. Smokers eliminated significantly higher concentrations of unchanged BTEX and benzene metabolites than non-smokers (p < 0.05). When traffic policemen were distinguished into indoor (n=31) and outdoor workers, no significant differences were observed for either airborne benzene or urinary biomarkers. Significantly lower concentrations of S-PMA and U-B were determined in samples collected at Day 1 as compared to Day 2 (p < 0.0001 and p = 0.003, respectively) suggesting that these biomarkers are enough sensitive and specific to detect changes in airborne benzene concentration even at few microg/m(3).     

Effects of concentrated ambient particles on heart rate, blood pressure, and cardiac contractility in spontaneously hypertensive rats

Epidemiological studies have shown that particulate matter (PM) air pollution is associated with cardiovascular mortality and morbidity, especially for particles with aerodynamic diameters under 2.5 microm (PM(2.5)). Recent studies have revealed an association between PM pollution and autonomic functions including heart rate (HR), blood pressure (BP), and heart-rate variability. However, the association and linking mechanisms have not been clearly demonstrated in animal studies. Utilizing a novel approach that employs a mixed-effects model to overcome the problems of variations in diseased animals and circadian cycles, we have previously demonstrated an association between concentrated PM(2.5) and changes of HR and BP in pulmonary hypertensive rats. The objective of this study is to test the plausibility of this methodology and to demonstrate the particle effects under different pathophysiology. The feasibility of cardiac contractility (measured as QA interval, QAI) as an indicator for PM toxicology was also explored. Four spontaneously hypertensive (SH) rats were repeatedly exposed to concentrated PM(2.5) during spring and summer. The mass concentration of particles during the 5 h of exposure was 202.0 +/- 68.8 (mean +/- SE) and 141.0 +/- 54.9 microg/m(3) for spring and summer experiments, respectively. During spring exposures, the maximum increase of HR and mean BP noted at the end of exposure were 51.6 bpm (p <.001) and 8.7 mm Hg (p =.002), respectively. The maximum decrease of QAI noted at the same time was 1.6 ms (p =.001). Though a similar pattern was demonstrated during summer exposures, the responses were less prominent. We conclude that concentrated PM(2.5) may increase HR and mean BP and decrease QAI in SH rats. Our results also show that QAI may be used as an indicator in PM toxicology.     

The effect of coarse ambient particulate matter on first, second, and overall hospital admissions for respiratory disease among the elderly

The objective of this article is to examine differences in the effect of ambient particulate matter on first, second, and overall hospital admissions for respiratory disease among the elderly. We studied 8989 adults 65 yr of age or older living in the greater Vancouver area who were admitted to hospital for any acute respiratory disease (ICD-9 codes 460-519) between June 1, 1995, and March 31, 1999. Time-series analysis was used to evaluate the association between respiratory admissions and daily measures of particulate matter (PM10, PM2.5, and PM10 - 2.5) in urban air, after adjustment for gaseous copollutants (CO, O3, NO2, and SO2) and meteorological variables. Repeated admissions for respiratory disease were common among the elderly. Approximately 30% of the subjects were readmitted to hospital after the first admission; 9% had more than 2 admissions for respiratory disease during the 4-yr study period. PM10 - 2.5 was significantly associated with the second and overall admissions for respiratory disease, but not with the first admission. The adjusted relative risks for an increment of 4.2 microg/m(3) in -day average PM10 - 2.5 concentrations were 1.03 (95% confidence interval: 0.98-1.09) for the first admission, 1.22 (1.10-1.36) for the second admission, and 1.06 (1.02, 1.11) for overall admissions. There was no significant association between PM2.5 and hospital admissions for respiratory disease among the elderly. Our data suggest that (1) people with a history of respiratory admissions are at a higher risk of respiratory disease in relation to particulate air pollution in urban areas, (2) analyses based on overall rather than repeated hospital admissions lead to lower estimates of the risk of respiratory disease associated with particulate air pollution, and (3) PM10 - 2.5 has a larger effect on respiratory admissions than PM2.5.     

An acellular assay to assess the genotoxicity of complex mixtures of organic pollutants bound on size segregated aerosol. Part I: DNA adducts

An acellular assay consisting of calf thymus DNA with/without rat liver microsomal S9 fraction was used to study the genotoxicity of complex mixtures of organic air pollutants bound to size segregated aerosols by means of DNA adduct analysis. We compared the genotoxicity of the organic extracts (EOMs) from three size fractions of aerosol ranging from 0.17 μm to 10 μm that were collected by high volume cascade impactors in four localities of the Czech Republic differing in the extent of the environmental pollution: (1) small village in proximity of a strip mine, (2) highway, (3) city center of Prague and (4) background station. The total DNA adduct levels induced by 100 μg/ml of EOMs were analyzed by ³²P-postlabelling analysis with a nuclease P1 method for adduct enrichment. The main finding of the study was most of the observed genotoxicity was connected with a fine particulate matter fraction (<1 μm). The concentrations of carcinogenic polycyclic aromatic hydrocarbons (c-PAHs) in EOMs indicate that fine fractions (0.5–1 μm) bound the highest amount of c-PAHs in all aerosol sampling sites, which might be related to the higher specific surface of this fraction as compared with a course fraction (1–10 μm) and higher mass as compared with a condensational fraction (0.17–0.5 μm). As for aerosol mass, both fine and condensational fractions are effective carriers of c-PAHs. Similarly, the DNA adduct levels per m³ of air were highest for the fine fraction, while the condensational fraction (strip mine site and city center) revealed the highest DNA adduct levels in cases where aerosol mass is taken into consideration. A strong correlation was found between the c-PAHs and DNA adduct levels induced by EOMs in all the localities and for various size fractions (R² = 0.98, p < 0.001). It may be concluded that the analysis of total DNA adducts induced in an acellular assay with/without metabolic activation represents a relatively simple method to assess the genotoxic potential of various complex mixtures.     

Pulmonary retention of particulate matter is associated with airway inflammation in allergic rats exposed to air pollution in urban Detroit

A collaborative research study was conducted in order to improve our understanding of the source-to-receptor pathway for ambient fine particulate matter (aerodynamic diameter < or = 2.5 mu m; PM2.5) and subsequently to investigate the identity and sources of toxic components in PM2.5 responsible for adverse health effects in allergic humans. This research used a Harvard fine particle concentrator to expose Brown Norway rats, with and without ovalbumin-induced allergic airway disease, to concentrated air particles (CAPs) generated from ambient air in an urban Detroit community where the pediatric asthma rate was three times higher than the national average. Rats were exposed to CAPs during the exposure periods in July (mean = 676 microg/m3) and September (313 microg/m3) of 2000. Twenty-four hours after exposures lung lobes were either lavaged with saline to determine cellularity and protein in bronchoalveolar lavage fluid (BALF), or removed for analysis by inductively coupled plasma-mass spectrometry (ICP-MS) to detect ambient PM2.5-derived trace element retention. PM2.5 trace elements of anthropogenic origin, lanthanum (La), vanadium (V), manganese (Mn), and sulfur (S), were recovered from the lung tissues of CAPs-exposed rats. Recovery of those pulmonary anthropogenic particles was further increased in rats with allergic airways. In addition, eosinophils and protein in BALF were increased only in allergic animals exposed to CAPs. These results demonstrate preferential retention in allergic airways of air particulates derived from identified local combustion sources after a short-term exposure. Our findings suggest that the enhancement of allergic airway responses by exposure to PM2.5 is mediated in part by increased pulmonary deposition and localization of potentially toxic elements in urban air.     

Pro-inflammatory effects of Dunkerque city air pollution particulate matter 2.5 in human epithelial lung cells (L132) in culture

Exposure to urban airborne particulate matter (PM) has been associated with adverse health effects. The majority of research articles published on air pollution PM relate to PM10. However, increasing emphasis and stringent regulations have been placed on PM2.5. The mechanisms for PM-induced adverse health effects are not well understood, but inflammation seems to be of importance. We focused our attention also on the capacity of air pollution PM2.5 to induce cytotoxic and inflammatory responses in human epithelial lung cells (L132) in culture. Particulate matter was collected in Dunkerque, a French seaside city characterized by the proximity of industrial activity and heavy motor vehicle traffic. Size distribution results showed that the cumulative frequency of PM2.5 was 92.15% and their specific surface area was 1 m2 g(-1). Inorganic and organic chemicals usually associated with the natural environment but also so-called anthropogenic elements were found in PM, suggesting that much of the PM was derived from wind-borne dust from the industrial complex and the heavy diesel motor vehicle. We observed PM concentration-dependent cytotoxic effects in L132 cells (LC10 = 18.84 microg PM ml(-1); LC50 = 75.36 microg PM ml(-1)). We showed that exposure to Dunkerque City's PM2.5 induced significant increases (in a concentration- and time-dependent manner) in protein secretion and/or gene expression of inflammatory cytokines (i.e. TNF-alpha, IL-1beta, IL-8, GM-CSF, IL-6, TGF-beta1). We hypothesized also that the occurrence of the acute inflammatory response might rely on the capacity of such air pollutants to generate oxidative species, which have been implicated in the stringent regulation of the cytokine network. Hence, we suggest that the development of inflammatory effects that worsen over time stems from the cytotoxicity in Dunkerque City's PM2.5-exposed L132 cells in culture.     

Inflammatory mediators induced by coarse (PM2.5-10) and fine (PM2.5) urban air particles in RAW 264.7 cells

Increased incidence of mortality and morbidity due to cardiopulmonary complications has been found to associate with elevated levels of urban air particles with an aerodynamic diameter <10 micron, PM10 and <2.5 micron, PM2.5. Respirable particles reach the lower respiratory tract where they are phagocytized by alveolar macrophages. Depending on particle composition, exposed macrophages may produce inflammatory mediators. A cascade impactor sampler was used to collect size-fractionated urban air particles. Particulate matter from the city of Rome (Italy) were collected onto stainless steel plates, and recovered using alcohol. The murine monocytic/macrophagic RAW 264.7 cell line was used to compare the ability of PM2.5-10, PM2.5 and carbon black to cause cell injury, such as arachidonic acid (AA) release, tumour necrosis factor alpha (TNF alpha) and interleukin (IL)-6 production. All test particles have been used at the same concentrations 30 and 120 microg/ml. Treatment with PM2.5-10 and PM2.5 induced significant AA release after 5 h of exposure at both concentrations, while carbon black was effective only at the higher concentration. After 5 h of incubation, PM2.5-10 and PM2.5 at 120 microg/ml induced 10 times the amount of TNF alpha than carbon black particles. The urban air particles-stimulated TNF alpha production decreased after 24 h of incubation while carbon black-stimulated TNF alpha was not. IL-6 production was induced by PM2.5 and by PM2.5-10 but not by carbon black. Carbon black was consistently less effective than the urban particles, suggesting that, the contaminants adsorbed on the particles are responsible for the release of inflammatory mediators.     

Damage effects of dust storm PM2.5 on DNA in alveolar macrophages and lung cells of rats.

The aim of the present study was to investigate in vitro toxicological effects of PM2.5 suspensions, their water-soluble fraction and solvent-extractable organics from dust storm on the viability and DNA of rat alveolar macrophages and in vivo toxicological effects of PM2.5 suspensions on DNA of lung cells of rats. PM2.5 samples from dust storm and normal weather were collected in Baotou city, Inner Mongolia Autonomous Region, and Wuwei city, Gansu Province, China, in March, 2004. DNA damage was detected with single cell gel electrophoresis technique and cytotoxicity was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction assay. The results showed that: (1) In vitro, PM2.5 suspensions, their water-soluble fraction and solvent-extractable organics from both dust storm and normal weather caused a decrease of the cell viability and an increase of DNA damage of rat alveolar macrophages in a dose-response manner; for both Baotou city and Wuwei city, the samples of normal weather showed higher DNA damage than those of dust storm at the highest treated dosage; for both normal weather PM2.5 and dust storm PM2.5, their solvent-extractable organics showed higher DNA damage than the water-soluble fraction. (2) In vivo, PM2.5 from both dust storm and normal weather caused an increase of DNA damage of rat lung cells in a dose-response manner. (3) Baotou city is one of the heavy industrial cities, while Wuwei is one of agricultural cities in Northwest region of China. The effects induced by normal weather samples in Baotou city slightly higher than those in Wuwei city on DNA damage, though there was no significant difference was found between two cities. These results lead to conclusions that dust storm PM2.5 as well as normal weather PM2.5 could lead to DNA damage and the organic compounds and the insoluble particle-core might be the main contributors to DNA damage. Our results suggest that the risk of health effects may be greater during dust storms because dust storm PM2.5 whose airborne mass were much higher. Further studies are needed to determine the components of dust storm particles that may contribute to the particle toxicity.     

Analysis of PM2.5 using the Environmental Benefits Mapping and Analysis Program (BenMAP)

As epidemiological work from around the world continues to tie PM2.5 to serious adverse health effects, including premature mortality, the U.S. Environmental Protection Agency (U.S. EPA) has developed a number of policies to reduce air pollution, including PM2.5. To assist in the benefit-cost analyses of these air pollution control policies, the U.S. EPA has developed the Environmental Benefits Mapping and Analysis Program (BenMAP). BenMAP is meant to (1) provide a flexible tool for systematically analyzing impacts of changes in environmental quality in a timely fashion, (2) ensure that stakeholders can understand the assumptions underlying the analysis, and (3) adequately address uncertainty and variability. BenMAP uses a "damage-function" approach to estimate the health benefits of a change in air quality. The major components of the damage-function approach are population estimates, population exposure, adverse health effects, and economic costs. To demonstrate BenMAP's ability to analyze PM2.5 pollution control policy scenarios, we assess two sample applications: (1) benefits of a national-level air quality control program, and (2) benefits of attaining two annual PM2.5 standards in California (annual average standards of 15 microg/m3 and 12 microg/m3). In the former, we estimate a scenario where control of PM2.5 emissions results in $100 billion of benefits annually. In the analysis of alternative standards, we estimate that attaining the more stringent standard (12 microg/m3) would result in approximately 2000 fewer premature deaths each year than the 15 microg/m3 achieves. BenMAP has a number of features to help clarify the analysis process. It allows the user to record in a configuration all of the choices made during an analysis. Configurations are especially useful for recreating already existing policy analyses. Also, BenMAP has a number of reporting options, including a set of mapping tools that allows users to visually inspect their inputs and results.     

Fine particulate air pollution and total mortality among elderly Californians, 1973-2002

Fine particulate air pollution has been associated with increases in long-term mortality in selected cohort studies, and this association has been influential in the establishment of air quality regulations for fine particles (PM(2.5)). However, this epidemiologic evidence has been questioned because of methodological issues, conflicting findings, and lack of an accepted causal mechanism. To further evaluate this association, the long-term relation between fine particulate air pollution and total mortality was examined in a cohort of 49, 975 elderly Californians, with a mean age of 65 yr as of 1973. These subjects, who resided in 25 California counties, were enrolled in 1959, recontacted in 1972, and followed from 1973 through 2002; 39, 846 deaths were identified. Proportional hazards regression models were used to determine their relative risk of death (RR) and 95% confidence interval (CI) during 1973-2002 by county of residence. The models adjusted for age, sex, cigarette smoking, race, education, marital status, body mass index, occupational exposure, exercise, and a dietary factor. For the 35, 789 subjects residing in 11 of these counties, county-wide exposure to fine particles was estimated from outdoor ambient concentrations measured during 1979-1983 and RRs were calculated as a function of these PM(2.5) levels (mean of 23.4 microg/m(3)). For the initial period, 1973-1982, a small positive risk was found: RR was 1.04 (1.01-1.07) for a 10-microg/m(3) increase in PM(2.5). For the subsequent period, 1983-2002, this risk was no longer present: RR was 1.00 (0.98-1.02). For the entire follow-up period, RR was 1.01 (0.99-1.03). The RRs varied somewhat among major subgroups defined by sex, age, education level, smoking status, and health status. None of the subgroups that had significantly elevated RRs during 1973-1982 had significantly elevated RRs during 1983-2002. The RRs showed no substantial variation by county of residence during any of the three follow-up periods. Subjects in the two counties with the highest PM(2.5) levels (mean of 36.1 microg/m(3)) had no greater risk of death than those in the two counties with the lowest PM(2.5) levels (mean of 13.1 microg/m(3)). These epidemiologic results do not support a current relationship between fine particulate pollution and total mortality in elderly Californians, but they do not rule out a small effect, particularly before 1983.     

Source-specific fine particles in urban air and respiratory function among adult asthmatics

Fine and ultrafine particles in ambient air are more consistently associated with severe adverse health effects than coarse particles. We assessed whether the effects of PM(2.5) on peak expiratory flow (PEF) and respiratory symptoms in asthma patients differ by the source or the chemical properties of particles. A panel of 57 adult asthmatics was followed for 181 days from November 1996 to April 1997 with 3 daily PEF measurements and diaries. Air quality, including elemental analyses of PM(2.5) filters every 2 days (n= 83), was monitored at a central site. Daily concentrations of PM(2.5) from different sources were estimated using principal component analysis and multiple linear regression. Associations of PM(2.5) from different sources with respiratory endpoints were examined using a generalized least squares autoregressive model after adjustment for covariates. PM(2.5) attributable to local combustion was consistently negatively associated with all measurements of PEF. One interquartile increase (1.3 microg/m(3)) in 5-day average concentrations of PM(2.5) attributable to local combustion was associated with an average 1.14 L/min decline in evening PEF (95% CI: -1.95 to -0.33 L/min). We also observed that PM(2.5) attributable to long-range transport was positively, and soil-derived PM(2.5) negatively, associated with PEF. No consistent associations were observed between source-specific PM(2.5) and respiratory symptoms or between individual chemical elements and any respiratory endpoints. Our results suggest that the negative effects of PM(2.5) on PEF in adult asthmatics are mainly mediated by particles related to local combustion sources.     

Particulate matter (PM(2.5), PM(10-2.5), and PM(10)) and children's hospital admissions for asthma and respiratory diseases: a bidirectional case-crossover study

Epidemiological studies reported adverse effects of air pollution on the prevalence of respiratory diseases in children. The purpose of this study was to examine the association between air pollution and admissions for asthma and other respiratory diseases among children who were younger than 15 yr of age. The study used data on respiratory hospital admissions and air pollutant concentrations, including thoracic particulate matter (PM(10)), fine (PM(2.5)), and coarse (PM(10-2.5)) particulate matter in Zonguldak, Turkey. A bidirectional case-crossover design was used to calculate odds ratios for the admissions adjusted for daily meteorological parameters. Significant increases were observed for hospital admissions in children for asthma, allergic rhinitis (AR), and upper (UPRD) and lower (LWRD) respiratory diseases. All fraction of PM in children showed significant positive associations with asthma admissions. The highest association noted was 18% rise in asthma admissions correlated with a 10-microg/m(3) increase in PM(10-2.5) on the same day of admissions. The adjusted odds ratios for exposure to PM(2.5) with an increment of 10 microg/m(3) were 1.15 and 1.21 for asthma and allergic rhinitis with asthma, respectively. PM(10) exerted significant effects on hospital admissions for all outcomes, including asthma, AR, UPRD, and LWRD. Our study suggested a greater effect of fine and coarse PM on asthma hospital admissions compared with PM(10) in children.     

Particle-associated organic compounds and symptoms in myocardial infarction survivors

CONTEXT: The aerosol components responsible for the adverse health effects of the exposure to particulate matter (PM) have not been conclusively identified, and there is especially little information on the role of particulate organic compounds (POC). Objective: This study evaluated the role of PM and POC with regard to daily symptoms. Methods: One hundred and fifty-three myocardial infarction survivors from Augsburg, Germany, recorded daily occurrence of different symptoms in winter 2003/2004. Ambient concentrations of PM with a diameter <2.5 μm (PM(2.5)), particle number concentration (PNC), PM(2.5)-bound hopanes, and polycyclic aromatic hydrocarbons (PAH) were quantified. Data were analyzed using generalized estimating equations adjusting for meteorological and other time-variant confounders. Results: The odds for avoidance of physically demanding activities due to heart problems increased immediately associated with most POC measures (e.g. 5% per 1.08 ng/m(3) increase in benzo[a]pyrene, 95%-confidence interval (CI):1-9%) and tended to a delayed decrease. After a 2-day delayed decrease associated with hopanes, the odds for shortness of breath increased consistently after 3 days with almost all POC measures (e.g. 4% per 0.21 ng/m(3) increase in 17α(H), 21β(H)-hopane, CI: 1-8%). The odds for heart palpitations marginally increased immediately in association with PNC (8% per 8146 cm(-3) increase in PNC, CI: 0-16%). Conclusions: The study showed an association between PM, particle-bound POC, and daily symptoms. The organic compounds may be causally related with cardiovascular health or act rather as indicators for traffic- and combustion-related particles.