Search

Background Particle matter (PM) has been associated with increased morbidity and mortality rates across the world. This study was designed to test the hypotheses that pyrotechnic firework displays introduce significant amounts of toxic metals into the atmosphere and are hazardous to human health. Size-selective emissions from 10 different fireworks displays were collected during particle generation in a dynamic, stainless steel chamber and tested for toxicity in cells. A subset of 2 particle types were tested in vivo in mice. At doses that did not produce cytotoxicity in an LDH assay, in vitro reactive oxygen species (ROS) formation was measured in bronchial epithelial airway (BEAS-2B) and human pulmonary microvascular endothelial (HPMEC-ST1.6R) cell lines treated with size-fractionated particles from the emissions of fireworks. Results Significant increases in ROS, in both cell types, were dependent upon the type of firework but not particle size. The in vitro ROS activity was correlated with lung inflammation produced in groups of mice treated by oropharyngeal aspiration with 0, 50, or 100 μg fireworks PM10/mouse. Trace metal analyses of the PM10 samples showed significant differences in metal content among fireworks type. Interestingly, the PM10 sample for the fireworks type producing the greatest in vitro ROS response in BEAS-2B cells contained ~ 40,000 and ~ 12,000 ppm of lead and copper, respectively. This sample also produced the greatest inflammatory response (i.e., increased neutrophils in bronchoalveolar lavage fluid) in mice. Conclusions These findings demonstrate that pyrotechnic display particles can produce adverse effects in mammalian cells and lungs, thus suggesting that further research is needed to expand our understanding of the contribution of metal content to the adverse health effects of fireworks particles. This information will lead to the manufacture of safer fireworks.

In this review, we elucidate the central role played by fossil fuel combustion in the health-related effects that have been associated with inhalation of ambient fine particulate matter (PM2.5). We especially focus on individual properties and concentrations of metals commonly found in PM air pollution, as well as their sources and their adverse health effects, based on both epidemiologic and toxicological evidence. It is known that transition metals, such as Ni, V, Fe, and Cu, are highly capable of participating in redox reactions that produce oxidative stress. Therefore, particles that are enriched, per unit mass, in these metals, such as those from fossil fuel combustion, can have greater potential to produce health effects than other ambient particulate matter. Moreover, fossil fuel combustion particles also contain varying amounts of sulfur, and the acidic nature of the resulting sulfur compounds in particulate matter (e.g., as ammonium sulfate, ammonium bisulfate, or sulfuric acid) makes transition metals in particles more bioavailable, greatly enhancing the potential of fossil fuel combustion PM2.5 to cause oxidative stress and systemic health effects in the human body. In general, there is a need to further recognize particulate matter air pollution mass as a complex source-driven mixture, in order to more effectively quantify and regulate particle air pollution exposure health risks.

[Figure: see text].

Background & aims Emerging evidence supports ambient fine particulate matter (PM2.5) exposure is associated with insulin resistance (IR) and hepatic lipid accumulation. In this study, we aimed to evaluate the sex-dependent vulnerability in response to PM2.5 exposure and investigate the underlying mechanism by which PM2.5 modulates hepatic lipid metabolism. Methods Both male and female C57BL/6 mice were randomly assigned to ambient PM2.5 or filtered air for 24 weeks via a whole body exposure system. High-coverage quantitative lipidomics approaches and liquid chromatography-mass spectrometry techniques were performed to measure hepatic metabolites and hormones in plasma. Metabolic studies, histological analyses, as well as gene expression levels and molecular signal transduction analysis were applied to examine the effects and mechanisms by which PM2.5 exposure-induced metabolic disorder. Results Female mice were more susceptible than their male counterparts to ambient PM2.5 exposure-induced IR and hepatic lipid accumulation. The hepatic lipid profile was changed in response to ambient PM2.5 exposure. Levels of hepatic triacylglycerols (TAGs), free fatty acids (FFAs) and cholesterol were only increased in female mice from PM group compared to control group. Plasmalogens were dysregulated in the liver from PM2.5-exposed mice as well. In addition, exposure to PM2.5 led to enhanced hepatic ApoB and microsomal triglyceride transport protein expression in female mice. Finally, PM2.5 exposure inhibited hypothalamus-pituitary-adrenal (HPA) axis and decreased glucocorticoids levels, which may contribute to the vulnerability in PM2.5-induced metabolic dysfunction. Conclusions Ambient PM2.5 exposure inhibited HPA axis and demonstrated sex-associated differences in its effects on IR and disorder of hepatic lipid metabolism. These findings provide new mechanistic evidence of hormone regulation in air pollution-mediated metabolic abnormalities of lipids and more personalized care should be considered in terms of sex-specific risk factors.

In this study, factor analysis and mass regression were used to identify four fine particulate matter sources and estimate their contributions to the ambient air pollution in Beijing. The identified sources were traffic re-suspended soil, mixed industrial sources, oil combustion, and secondary sulfate. The estimated source contributions were then introduced into two models as exposure variables to explore the relationships between cardiovascular responses in mice and PM exposures. We observed that PM2.5 has a small negative acute effect on heart rate, but the individual source factors showed much more significant effects. Traffic re-suspended soil had the most significant effect on heart rate, with a positive contribution on the day of exposure and a negative one on day lag 1. Acute heart rate variability outcomes were better explained by the total PM2.5 than by the source components. Chronic effects were observed as a decreased heart rate but an increased number of heart rate variability outcomes.

Air pollution is a complex mixture of gaseous, volatile, and particulate matter (PM) containing inorganic and organic species. There is now abundant evidence in epidemiological and toxicological studies that air pollution contributes to the development and exacerbation of diseases of respiratory, cardiovascular, and other organs, and associated mortality. Studies showed that equal masses of PM could induce disparate health effects, suggesting that particle sizes and components may be at fault. The fine and ultrafine PM is considered to be particularly important because the small particles can be easily inhaled. Possible biological mechanisms of action leading to adverse effects include the production of inflammatory mediators in the lung causing systemic inflammation, interaction with neural receptors causing interference with the central nervous system regulation of cardiovascular function, and particle translocation via the bloodstream to other organs. This chapter reviews whether some components of the PM mixture are of a greater public health concern than others, and presents compelling evidence that trace elements are most strongly linked to the adverse effects. Air pollution has wide-ranging and harmful effects on human health and is a major issue for the global community. Further research should explore the effects of source-specific PM with more advanced approaches to exposure modeling, measurements, and statistics, which would lead to more effective legislation and interventions for greater benefits to public health.

Background With the number of annual global travellers reaching 1.2 billion, many individuals encounter greater levels of air pollution when they travel abroad to megacities around the world. This study’s objective was to determine if visits to cities abroad with greater levels of air pollution adversely impact cardiopulmonary health. Methods A total of 34 non-smoking healthy adult participants who travelled abroad to selected cities from the New York City (NYC) metropolitan area were pre-trained to measure lung function, blood pressure and heart rate (HR)/HR variability (HRV) and record symptoms before, during and after travelling abroad. Outdoor particulate matter (PM)2.5 concentrations were obtained from central monitors in each city. Associations between PM exposure concentrations and cardiopulmonary health endpoints were analysed using a mixed effects statistical design. Results East and South Asian cities had significantly higher PM2.5 concentrations compared with pre-travel NYC PM2.5 levels, with maximum concentrations reaching 503 μg/m3. PM exposure–related associations for lung function were statistically significant and strongest between evening Forced Expiratory Volume in the first second (FEV1) and same-day morning PM2.5 concentrations; a 10-μg/m3 increase in outdoor PM2.5 was associated with a mean decrease of 7 mL. Travel to a highly polluted city (PM2.5 > 100 μg/m3) was associated with a 209-ml reduction in evening FEV1 compared with a low polluted city (PM2.5 Conclusions Exposure to increased levels of PM2.5 in cities abroad caused small but statistically significant acute changes in cardiopulmonary function and respiratory symptoms in healthy young adults. These data suggest that travel-related exposure to increased PM2.5 adversely impacts cardiopulmonary health, which may be particularly important for travellers with pre-existing respiratory or cardiac disease.

Environmental factors can act as facilitators of chronic non-communicable diseases. Ambient noise and air pollution collectively outrank all other environmental risk factors in importance, contributing to over 75% of the disease and disability burden associated with known environmental risk factors. In the first part of this review, we discussed the global burden and epidemiologic evidence supporting the importance of these novel risk factors as facilitators of cardiometabolic disease. In this part, we will discuss pathophysiological mechanisms responsible for noise and air pollution-mediated effects. Akin to traditional cardiovascular risk factors, a considerable body of evidence suggests that these environmental agents induce low-grade inflammation, oxidative stress, vascular dysfunction, and autonomic nervous system imbalance, thereby facilitating the development of diseases such as hypertension and diabetes. Through their impact on traditional risk factors and via additional novel mechanisms, environmental risk factors may have much larger impact on cardiovascular events than currently appreciated. In the second part of this review, we discuss deficiencies and gaps in knowledge and opportunities for new research.

Indoor air pollution from bituminous coal combustion has been linked to the extremely high lung cancer rates of nonsmoking women in Xuan Wei County, Yunnan Province, China. Venting the smoke outdoors by installing chimneys was found to be effective at reducing the lung cancer risk in a cohort study of 21,232 farmers in central Xuan Wei. However, the lung cancer mortality rates in all 1.2 million residents of Xuan Wei have been increasing dramatically over the last four decades. It was higher than that in Yunnan Province and China overall, with significant heterogeneities in the geographic patterns of Xuan Wei. Intervention measures targeting certain types of coal or certain carcinogenic components in coal smoke need to be explored. To inform targeted intervention policies, it is essential to pinpoint the specific substance (particulate matter, organic extract, PAHs, free radicals, crystalline silica, and inorganic matter) that might account for the carcinogenicity of bituminous coal smoke. Exploring the underlying carcinogenesis mechanisms would also contribute to the intervention and control of the lung cancer epidemic in Xuan Wei, China. Here we review the suspected carcinogens and carcinogenesis mechanisms and discuss future research directions towards a better understanding of the etiology of lung cancer in Xuan Wei, China.

Background: In Xuan Wei, the lung cancer mortality rate is five times higher than the country average, and continues to increase despite interventions to reduce indoor coal burning air pollution. T...

Recent epidemiological evidence suggests that exposure to particulates may be a factor in the etiology of metabolic syndrome (MetS). In this novel study, we investigated the relationship between particulate levels and prevalence of MetS component abnormalities (hypertension, hyperglycemia, obesity) in a recruited cohort (N = 2025) in Jeddah, Saudi Arabia. We observed significant associations between a 10 μg/m3 increase in PM2.5 and increased risks for MetS (Risk Ratio (RR): 1.12; 95% Confidence Interval (CI): 1.06–1.19), hyperglycemia (RR: 1.08; 95% CI: 1.03–1.14), and hypertension (RR: 1.09; 95% CI: 1.04–1.14). PM2.5 from soil/road dust was found to be associated with hyperglycemia (RR: 1.12; 95% CI: 1.06–1.19) and hypertension (RR: 1.11; 95% CI: 1.05–1.18), while PM2.5 from traffic was associated with hyperglycemia (RR: 1.33; 95% CI: 1.05–1.71). We did not observe any health associations with source-specific mass exposures. Our findings suggest that exposure to specific elemental components of PM2.5, especially Ni, may contribute to the development of cardiometabolic disorders.

This study provides the first comprehensive analysis of the seasonal variations and weekday/weekend differences in fine (PM2.5) and coarse (PM2.5–10) particulate matter mass concentrations, elemental constituents, and potential source origins in Jeddah, Saudi Arabia. Air quality samples were collected over one year, from June 2011 to May 2012 at a frequency of three times per week, and analyzed. The average mass concentrations of PM2.5 (21.9 µg/m3) and PM10 (107.8 µg/m3) during the sampling period exceeded the recommended annual average levels by the World Health Organization (WHO) for PM2.5 (10 µg/m3) and PM10 (20 µg/m3), respectively. Similar to other Middle Eastern locales, PM2.5–10 is the prevailing mass component of atmospheric particulate matter at Jeddah, accounting for approximately 80% of the PM10 mass. Considerations of enrichment factors, absolute principal component analysis (APCA), concentration roses, and backward trajectories identified the following source categories for both PM2.5 and PM2.5–10: 1) soil/road dust; 2) incineration; and 3) traffic; and for PM2.5 only, 4) residual oil burning. Soil/road dust accounted for a major portion of both the PM2.5 (27%) and PM2.5–10 (77%) mass, and the largest source contributor for PM2.5 was from residual oil burning (63%). Temporal variations of PM2.5–10 and PM2.5 were observed, with the elevated concentration levels observed for mass during the spring (due to increased dust storm frequency), and on weekdays (due to increased traffic). The predominant role of windblown soil and road dust in both the PM2.5 and PM2.5–10 masses in this city may have implications regarding the toxicity of these particles versus those in the western world where most PM health assessments have been made in the past. These results support the need for region-specific epidemiological investigations to be conducted and considered in future PM standard setting.

This study’s aim was to investigate the post-effect of an air quality improvement on systemic inflammation and circulating microparticles in asthmatic patients during, and 2 months after, the Beijing Olympics 2008. We measured the levels of circulating inflammatory cytokines and microparticles in the peripheral blood from asthma patients and healthy controls during (phase 1), and 2 months after (phase 2) the Beijing 2008 Olympic Games. The concentrations of circulating cytokines (including TNFα, IL-6, IL-8, and IL-10) were still seen reduced in phase 2 when compared with those in phase 1. The number of circulating endothelial cell-derived microparticles was significantly lower during the phase 2 than that during phase 1 in asthma patients. The level of plasma lipopolysaccharide-binding protein (LBP) was significantly decreased in asthmatics in phase 2. The level of norepinephrine was significantly higher in phase 2 than that in phase 1 in plasma from both asthma patients and healthy subjects. There were no significant differences in the gene profile for the toll-like receptor (TLR) signaling from peripheral blood mononuclear cells. In vitro, microvesicles from patients with asthma impaired the relaxation to bradykinin and contraction to acetylcholine, whereas microparticles from healthy subjects did not. These data suggested that reduction in systemic pro-inflammatory responses and circulating LBP and increased level of norepinephrine in asthma patients persisted even after 2 months of the air pollution intervention. These changes were independent of the TLR signaling pathway. Circulating microparticles might be associated with airway smooth muscle dysfunction.

Recent studies have demonstrated that mobile sampling can improve the spatial granularity of land use regression (LUR) models. Mobile sampling campaigns deploying low-cost (

The purpose of this study was to investigate the effects of chronically inhaled particulate matter 2.5) on inflammatory cell populations in the lung and systemic circulation. A prominent component of air pollution exposure is a systemic inflammatory response that may exaggerate chronic diseases such as atherosclerosis and insulin resistance. T cell response was measured in wild-type C57B/L6, Foxp3-green fluorescent protein (GFP) “knockin,” and chemokine receptor 3 knockout (CXCR3−/−) mice following 24–28 wk of PM2.5or filtered air. Chronic PM2.5exposure resulted in increased CXCR3-expressing CD4+and CD8+T cells in the lungs, spleen, and blood with elevation in CD11c+macrophages in the lung and oxidized derivatives of 1-palmitoyl-2-arachidonyl-sn-glycero-3-phosphorylcholine in wild-type mice. CXCR3 deficiency decreased T cells in the lung. GFP+regulatory T cells increased with PM2.5exposure in the spleen and blood of Foxp3-GFP mice but were present at very low levels in the lung irrespective of PM2.5exposure. Mixed lymphocyte cultures using primary, PM2.5-treated macrophages demonstrated enhanced T cell proliferation. Our experiments indicate that PM2.5potentiates a proinflammatory Th1 response involving increased homing of CXCR3+T effector cells to the lung and modulation of systemic T cell populations.

Background Previous studies have reported relationships between adverse respiratory health outcomes and residential proximity to traffic pollution, but have not shown this at a personal exposure level. Objective We compared, among inner-city children with asthma, the associations of adverse asthma outcome incidences with increased personal exposure to particulate matter mass ≤ 2.5 μm in aerodynamic diameter (PM2.5) air pollution versus the diesel-related carbonaceous fraction of PM2.5. Methods Daily 24-hr personal samples of PM2.5, including the elemental carbon (EC) fraction, were collected for 40 fifth-grade children with asthma at four South Bronx schools (10 children per school) during approximately 1 month each. Spirometry and symptom scores were recorded several times daily during weekdays. Results We found elevated same-day relative risks of wheeze [1.45; 95% confidence interval (CI), 1.03–2.04)], shortness of breath (1.41; 95% CI, 1.01–1.99), and total symptoms (1.30; 95% CI, 1.04–1.62) with an increase in personal EC, but not with personal PM2.5 mass. We found increased risk of cough, wheeze, and total symptoms with increased 1-day lag and 2-day average personal and school-site EC. We found no significant associations with school-site PM2.5 mass or sulfur. The EC effect estimate was robust to addition of gaseous pollutants. Conclusion Adverse health associations were strongest with personal measures of EC exposure, suggesting that the diesel “soot” fraction of PM2.5 is most responsible for pollution-related asthma exacerbations among children living near roadways. Studies that rely on exposure to PM mass may underestimate PM health impacts.

Personal exposures to fine particulate matter air pollution (PM(2.5)), and to its traffic-related fraction, were investigated in a group of urban children with asthma. The relationships of personal and outdoor school-site measurements of PM(2.5) and elemental carbon (EC) were characterized for a total of 40 fifth-grade children. These students, from four South Bronx, NY schools, each carried air pollution monitoring equipment with them for 24 h per day for similar to 1 month. Daily EC concentrations were estimated using locally calibrated reflectance of the PM(2.5) samples. Personal EC concentration was more closely related to outdoor school-site EC (median subject-specific: r=0.64) than was personal PM(2.5) to school-site PM(2.5) concentration (median subject-specific: r=0.33). Regression models also showed a stronger, more robust association of school site with personal measurements for EC than those for PM(2.5). High traffic pollution exposure was found to coincide with the weekday early morning rush hour, with higher personal exposures for participants living closer to a highway (

The aggressive traffic interventions and emission control measures implemented to improve air quality during the 2008 Beijing Olympic Games created a valuable case study to evaluate the effectiveness of these measures on mitigating air pollution and protecting public health. In this paper, we report the results from our field campaign in summer 2008 on the on-road emission factors of carbon monoxide, black carbon (BC) and ultrafine particles (UFP) as well as the ambient BC concentrations. The fleet average emission factors for light-duty gasoline vehicles (LDGV) showed considerable reduction in the Olympic year (2008) compared to the pre-Olympic year (2007). Our measurement of Black Carbon (BC), a primary pollutant, at different elevations at the ambient site suggests consistent decrease in BC concentrations as the height increased near the ground level, which indicates that the nearby ground level sources, probably dominated by traffic, contributed to a large portion of BC concentrations in the lower atmospheric layer in Beijing during summertime. These observations indicate that people living in near ground levels experience higher exposures than those living in higher floors in Beijing. The BC diurnal patterns on days when traffic control were in place during the Olympic Games were compared to those on non-traffic-control days in both 2007 and in 2008. These patterns strongly suggest that diesel trucks are a major source of summertime BC in Beijing. The median BC concentration on Olympic days was 3.7 μg m−3, which was dramatically lower than the value on non-traffic-control days, indicating the effectiveness of traffic control regulations in BC reduction in Beijing.

On 11 September 2001, the explosion and the collapse of the World Trade Center (WTC) Twin Towers in New York City (NYC), USA, generated a massive release of dust and inhalable toxic substances to the atmosphere as a result of the pulverization of various building materials, furniture, and computers. Many concerns were raised as Particulate Matter (PM) levels in Lower Manhattan might not meet the current National Ambient Air Quality Standards (NAAQS) (65 μg m −3 ). The current study aims to provide a first estimate of the scale of population exposures during this episode. Data collected from existing monitoring stations in September showed the occurrence of a series of high peaks of PM 2.5 registered in the Lower Manhattan area after the 11 September. An interpolation technique was used within a Geographical Information Systems (GIS) environment to estimate outdoor PM 2.5 concentrations over NYC. Monthly average of 24 h outdoor PM 2.5 concentration of Lower Manhattan was 20.2 μg m −3 and did not exceed the NAAQS value. PM 2.5 concentrations in indoor micro-environments were simulated by a deterministic micro-environmental model (INTAIR) and linear regression equations. Three typical population groups were identified for the NYC area—home-makers, office/shop-workers, and students/children—and their 12 h nighttime and daytime exposures were estimated from 14 September until the end of September, either as mean exposure (daytime and nighttime) or as exposure weighted by residential population distribution (nighttime only). Average nighttime and daytime exposures of the Lower Manhattan population were calculated to be 37.3 and 23.6 μg m −3 , respectively (daily average: 30.45 μg m −3 ), in which the various group movements and activities, smoking habits of individuals, and special population movements due to access restrictions and risk avoidance behaviors were considered. Within the study period, assuming the real nighttime population distribution followed the residential population pattern, approximate one quarter of the population was exposed to 20–30 μg m −3 PM 2.5 ; one half of the Lower Manhattan population was exposed to 10–20 and 30–60 μg m −3 ; around one fifth of the population was exposed to over 60 μg m −3 during nighttime. The results indicated that although the outdoor PM 2.5 concentration was lower than the NAAQS value, personal exposure levels, which were generally higher than the outdoor PM 2.5 concentration, might still be a reason of concern.

The objective of this study is to characterize the ambient air quality of the South Bronx, New York City (NYC), having high concentrations of diesel trucks and waste transfer facilities. We employed a mobile laboratory for continuous measurements of concentrations of fine particulate matter (PM2.5), black carbon (BC), and gaseous pollutants at 6 locations for three–four weeks each during the period of April 2001–February 2003. Integrated 24-hr PM2.5 samples were also collected for elemental and PAHs analyses. South Bronx PM2.5 and BC levels were compared to those at Bronx PS 154 (NYSDEC site) and at Hunter College in the Lower Manhattan. Although the median daily PM2.5 concentrations agreed within 20%, the median hourly BC concentrations were higher at all South Bronx sites ranging from 2.2 to 3.8m gm � 3 , compared to 1.0–2.6m gm � 3 at Hunter College. Continuous Aethelometer measurements at additional 27 sampling sites in the South Bronx were conducted along major highways. BC concentrations varied within each site, depending on time-of-day, with a large spatial variability from site-to-site. Daily median BC concentrations varied from 1.7 to 12m gm � 3 on the weekdays, and were lower (0.50–2.9m gm � 3 ) on the weekends. Elemental concentrations were higher at all South Bronx sites than those at Hunter College for all measured elements but Ni and V, and at the Hunts Point, an industrial location, were approximately 2.5-fold higher. The average sum of 35 PAHs was 225 ng m � 3 , which is 4.5 times larger than representative regional concentrations in Jersey City, NJ. Among the individual PAHs, 3,6-dimethylphenanthrene had the highest concentrations, and the overall PAH fingerprint differed from signal for Jersey City. Our data indicates that highways encircling the South Bronx are having a measurable adverse influence on residents’ exposure to pollutants compared to other NYC areas. r 2004 Elsevier Ltd. All rights reserved.

The South Bronx is a low-income, minority community in New York City. It has one of the highest asthma rates in the country, which community residents feel is related to poor air quality. Community residents also feel that the air quality data provided by the New York State Department of Environmental Conservation (DEC) through its network of monitoring stations do not reflect the poor quality of the air they breathe. This is due to the fact that these monitoring stations are located 15 m above ground. In the year 2001 this project collected air quality data at three locations in the study area. They were collected close to ground-level at a height of 4 m by a mobile laboratory placed in a van as part of the South Bronx Environmental Health and Policy Study. This paper compares data collected by the project with data from DEC's monitoring stations in Bronx County during the same periods. The goal of the comparison is to gain a better understanding of differences in measured air quality concentrations at these different heights. Although there is good agreement in the data among DEC stations there are some important differences between ground-level measurements and DEC data. For PM 2.5 the measured concentrations by the van were similar to those recorded by DEC stations. In the case of ozone, the concentrations recorded at ground level were similar or lower than those recorded by DEC stations. For NO 2 , however, the concentrations recorded at ground level were over twice as high as those recorded by DEC. In the case of SO 2 , ground level measurements were substantially higher in August but very similar in the other two periods. CO concentrations measured at ground-level tend to be 60–90% higher than those recorded by DEC monitoring stations. Despite these differences, van measurements of SO 2 and CO concentrations were well below EPA standards.

The attack on the World Trade Center (WTC) created an acute environmental disaster of enormous magnitude. This study characterizes the environmental exposures resulting from destruction of the WTC and assesses their effects on health. Methods include ambient air sampling; analyses of outdoor and indoor settled dust; high-altitude imaging and modeling of the atmospheric plume; inhalation studies of WTC dust in mice; and clinical examinations, community surveys, and prospective epidemiologic studies of exposed populations. WTC dust was found to consist predominantly (95%) of coarse particles and contained pulverized cement, glass fibers, asbestos, lead, polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), and polychlorinated furans and dioxins. Airborne particulate levels were highest immediately after the attack and declined thereafter. Particulate levels decreased sharply with distance from the WTC. Dust pH was highly alkaline (pH 9.0-11.0). Mice exposed to WTC dust showed only moderate pulmonary inflammation but marked bronchial hyperreactivity. Evaluation of 10,116 firefighters showed exposure-related increases in cough and bronchial hyperreactivity. Evaluation of 183 cleanup workers showed new-onset cough (33%), wheeze (18%), and phlegm production (24%). Increased frequency of new-onset cough, wheeze, and shortness of breath were also observed in community residents. Follow-up of 182 pregnant women who were either inside or near the WTC on 11 September showed a 2-fold increase in small-for-gestational-age (SGA) infants. In summary, environmental exposures after the WTC disaster were associated with significant adverse effects on health. The high alkalinity of WTC dust produced bronchial hyperreactivity, persistent cough, and increased risk of asthma. Plausible causes of the observed increase in SGA infants include maternal exposures to PAH and particulates. Future risk of mesothelioma may be increased, particularly among workers and volunteers exposed occupationally to asbestos. Continuing follow-up of all exposed populations is required to document the long-term consequences of the disaster.

Particulate matter (PM*), an ambient air criteria pollutant, is a complex mixture of chemical components; particle sizes range from nanometer-sized molecular clusters to dust particles that are too large to be aspirated into the lungs. Although particle composition is believed to affect health risks from PM exposure, our current health-based air quality standards for PM are limited to (1) the mass concentrations of PM2.5 (particles 2.5 microm or smaller in aerodynamic diameter), which are largely attributable to combustion products; and (2) PM10 (10 microm or smaller), which includes larger-sized mechanically generated dusts. Both of these particle size fractions are regulated under the National Ambient Air Quality Standards (NAAQS) and both have been associated with excess mortality and morbidity. We conducted four studies as part of HEI's integrated National Particle Component Toxicity (NPACT) Initiative research program. Since 1999, the Chemical Speciation Network (CSN), managed by the U.S. Environmental Protection Agency (U.S; EPA), has routinely gathered air monitoring data every third or sixth day for the concentrations of numerous components of PM2.5. Data from the CSN enabled us to conduct a limited time-series epidemiologic study of short-term morbidity and mortality (Ito study); and a study of the associations between long-term average pollutant concentrations and annual mortality (Thurston study). Both have illuminated the roles of PM2.5 chemical components and source-related mixtures as potentially causal agents. We also conducted a series of 6-month subchronic inhalation exposure studies (6 hours/day, 5 days/week) of PM2.5 concentrated (nominally) 10 x from ambient air (CAPs) with apolipoprotein E-deficient (ApoE(-/-)) mice (a mouse model of atherosclerosis) (Chen study). The CAPs studies were conducted in five different U.S. airsheds; we measured the daily mass concentrations of PM2.5, black carbon (BC), and 16 elemental components in order to identify their sources and their roles in eliciting both short- and long-term health-related responses. In addition, from the same five air-sheds we collected samples of coarse (PM10-2.5), fine (PM2.5-0.2), and ultrafine (PM0.2) particles. Aliquots of these samples were administered to cells in vitro and to mouse lungs in vivo (by aspiration) in order to determine their comparative acute effects (Gordon Study). The results of these four complementary studies, and the overall integrative analyses, provide a basis for guiding future research and for helping to determine more targeted emission controls for the PM components most hazardous to acute and chronic health. Application of the knowledge gained in this work may therefore contribute to an optimization of the public health benefits of future PM emission controls. The design of each NPACT study conducted at NYU was guided by our scientific hypotheses, which were based on our reviews of the background literature and our experience in conducting studies of associations between ambient PM and health-related responses. These hypotheses guided the development and conduct of the four studies. Hypothesis 1. Coarse, fine, and ultrafine PM are each capable of producing acute health effects of public health concern, but the effects may differ according to particle size and composition. (Applies to all studies.) Hypothesis 2. Long-term PM2.5 exposures are closely associated with chronic health effects. (Applies to studies 1 and 4.) Hypothesis 3. The source-apportionment techniques that we have developed and refined in recent years provide a useful basis for identifying major categories of sources of PM in ambient air and specific chemical components that have the greatest impacts on a variety of acute and chronic health effects. (Applies to all studies.) Hypothesis 4. The health effects due to ambient PM exposures can best be seen in sensitive subgroups within overall human populations and in animal models of such populations. (Applies to studies 1, 3, and 4.) Overall, the studies have demonstrated that the toxicity of PM is driven by a complex interaction of particle size range, geographic location, source category, and season. These findings suggest that the components of PM--associated with certain categories of sources--are responsible for the observed adverse health effects. Most importantly, the responsible components and source categories vary with the health-related endpoints being assessed. Across all studies, fossil-fuel combustion source categories were most consistently associated with both short- and long-term adverse effects of PM2.5 exposure. The components that originate from the Residual Oil Combustion and Traffic source categories were most closely associated with short-term effects; and components from the Coal Combustion category were more closely associated with long-term effects.

Objectives Studies have shown that chronic exposure to ambient fine particulate matter (less than 2.5 µm in aerodynamic diameter, PM2.5) pollution induces insulin resistance through alterations in inflammatory pathways. It is critical to study how the immune system responds to this stimulant, which has been linked to cardiovascular and autoimmune diseases, but few studies have been focused on such involvement of both neutrophils and monocytes in a timely manner. We hypothesized that the neutrophil was involved in the inflammatory response to air pollution. Methods and Results C57BL/6 mice were exposed to PM2.5 or filtered air (6 hours/day, 5 days/week) for 5, 14, and 21 days, respectively, in Columbus, OH. At the end of each of the exposure periods, we investigated the inflammatory response through flow cytometry, histology, intravital microscopy, and real-time PCR. PM2.5-exposed mice demonstrated a significant inflammatory response after 5 days of exposure. In the lung tissue and bronchoalveolar lavage fluid, monocytes/macrophages showed a transient response, while neutrophils showed a cumulative response. In addition, exposure to PM2.5 resulted in elevation of the monocyte chemoattractant protein 1 (MCP-1) cytokine, a monocyte/macrophage attractant in blood, at an early stage of exposure. Conclusions These findings suggest that PM2.5 exposure induces the inflammatory responses from both macrophages and neutrophils involvement.

Background It has been well recognized that toxicity of fine ambient air particulate matter (PM2.5) may depend on its chemical constituents, including components such as soluble metals that may theoretically exert distinctive effects. We have recently demonstrated an important effect of PM2.5 on metabolic function. Since transition metals, such as nickel (Ni), represent an important component of exposure in certain environments, and may significantly influence the toxicity of inhalational exposure, we investigated the effects of Ni as a variable component of ambient PM2.5 exposure. Methods Male ApoE knockout mice were exposed to filtered air (FA), fine-sized nickel sulfate particles alone (Ni) at 0.44 μ g/m3, concentrated ambient air PM2.5 (CAPs) at a mean of 70 μ g/m3, or CAPs+Ni in Tuxedo, NY, 6 hours/day, 5 days/week, for 3 months. Results Exposure to Ni, irrespective of co-exposure to CAPs, resulted in body weight gain, while exposure to CAPs+Ni significantly enhanced fasting glucose and worsened insulin resistance measures (HOMA-IR), when compared with exposure to CAPs alone. CAPs+Ni exposure induced a significant decrease in phosphorylation of AMP-activated protein kinase (AMPK) α. Exposure to Ni or CAPs+Ni significantly induced microcirculatory dysfunction and increased monocytic cell infiltration into lung and adipose, and decreased uncoupling protein 1 expression at gene and protein levels and several brown adipocyte-specific genes in adipose tissue. Conclusions Ni exposure has effects on metabolic and inflammatory parameters that are comparable to that of CAPs. Additionally, Ni synergistically exacerbates CAPs-induced adverse effects on some of, but not all of, these parameters, that may be mediated via the AMPK signaling pathway. These findings have important implications for inhaled transition metal toxicity that may exert synergistic effects with other PM2.5 components.

Traffic noise and air pollution together represent the two most important environmental risk factors in urbanized societies. The first of this two-part review discusses the epidemiologic evidence in support of the existence of an association between these risk factors with cardiovascular and metabolic disease. While independent effects of these risk factors have now clearly been shown, recent studies also suggest that the two exposures may interact with each other and with traditional risk factors such as hypertension and type 2 diabetes. From a societal and policy perspective, the health effects of both air pollution and traffic noise are observed for exposures well below the thresholds currently accepted as being safe. Current gaps in knowledge, effects of intervention and their impact on cardiovascular disease, will be discussed in the last section of this review. Increased awareness of the societal burden posed by these novel risk factors and acknowledgement in traditional risk factor guidelines may intensify the efforts required for effective legislation to reduce air pollution and noise.

The main purpose of this study was to identify policy maker opinions and attitudes towards children's environmental health (CEH), potential barriers to child-specific protective legislation and implementation in northwest China, and evaluate knowledge and attitudes about CEH before and after an educational conference. We conducted seventy-two interviews with regional officials, researchers and non-governmental organization representatives from five provinces, and surveyed participants (forty-seven) before and after an educational conference in northwest China about CEH. Interviews identified general consensus among participants of the adverse effects of air pollution on children, yet few participants knew of policies to protect them. Barriers identified included limited funding and enforcement, weak regional governments and absence of child-specific policy-making. After the conference, substantially greater self-efficacy was identified for lead, mercury, air pollution and polychlorinated biphenyls (+0.57-0.72 on a 1-5 Likert scale, p = 0.002-0.013), and the scientific knowledge for the role of environment in children's health (+0.58, p = 0.015), and health care provider control (+0.52, p = 0.025) were rated more strongly. We conclude that policy makers in Northwest China appreciate that children are uniquely vulnerable, though additional regulations are needed to account for that vulnerability. Further research should examine effectiveness of the intervention on a larger scale and scope, and evaluate the usefulness of such interventions in translating research into improved care/reduced exposure to environmental hazards.

Exposure to particulate matter (PM) air pollution produces inflammatory damage to the cardiopulmonary system. This toxicity appears to be inversely related to the size of the PM particles, with the ultrafine particle being more inflammatory than larger sizes. Exposure to PM has more recently been associated with neurotoxicity. This study examines if the size-dependent toxicity reported in cardiopulmonary systems also occurs in neural targets. For this study, PM ambient air was collected over a 2 week period from Sterling Forest State Park (Tuxedo, New York) and its particulates sized as Accumulation Mode, Fine (AMF) (>0.18-1μm) or Ultrafine (UF) (12.5μg/ml) but was only significant at the highest concentration of AMF (50μg/ml). To examine if PM size-dependent neurotoxicity was retained in the presence of other cell types, dissociated brain cultures of embryonic rat striatum were exposed to AMF (80μg/ml) or UF (8.0μg/ml). After 24h exposure, a significant increase of reactive nitrogen species (nitrite) and morphology suggestive of apoptosis occurred in both treatment groups. However, morphometric analysis of neuron specific enolase staining indicated that only the UF exposure produced significant neuronal loss, relative to controls. Together, these data suggest that the inverse relationship between size and toxicity reported in cardiopulmonary systems occurs in cultures of isolated dopaminergic neurons and in primary cultures of the rat striatum.

Background Prior studies have demonstrated a link between air pollution and metabolic diseases such as type II diabetes. Changes in adipose tissue and its mitochondrial content/function are closely associated with the development of insulin resistance and attendant metabolic complications. We investigated changes in adipose tissue structure and function in brown and white adipose depots in response to chronic ambient air pollutant exposure in a rodent model. Methods Male ApoE knockout (ApoE-/-) mice inhaled concentrated fine ambient PM (PM < 2.5 μm in aerodynamic diameter; PM2.5) or filtered air (FA) for 6 hours/day, 5 days/week, for 2 months. We examined superoxide production by dihydroethidium staining; inflammatory responses by immunohistochemistry; and changes in white and brown adipocyte-specific gene profiles by real-time PCR and mitochondria by transmission electron microscopy in response to PM2.5 exposure in different adipose depots of ApoE-/- mice to understand responses to chronic inhalational stimuli. Results Exposure to PM2.5 induced an increase in the production of reactive oxygen species (ROS) in brown adipose depots. Additionally, exposure to PM2.5 decreased expression of uncoupling protein 1 in brown adipose tissue as measured by immunohistochemistry and Western blot. Mitochondrial number was significantly reduced in white (WAT) and brown adipose tissues (BAT), while mitochondrial size was also reduced in BAT. In BAT, PM2.5 exposure down-regulated brown adipocyte-specific genes, while white adipocyte-specific genes were differentially up-regulated. Conclusions PM2.5 exposure triggers oxidative stress in BAT, and results in key alterations in mitochondrial gene expression and mitochondrial alterations that are pronounced in BAT. We postulate that exposure to PM2.5 may induce imbalance between white and brown adipose tissue functionality and thereby predispose to metabolic dysfunction.

While many studies found associations between ambient particulate matter (PM) and morbidity or mortality outcomes, it is unclear whether these associations are dependent on the composition of PM, which varies with the source of that PM. We addressed this knowledge gap by conducting a time-series PM-health effects assessment that specifically investigated the role of source-apportioned fine PM (PM2.5) on the oxidant generation capacity that might be responsible for respiratory and cardiovascular health outcomes. Daily PM2.5 composition speciation and blakc carbon (BC) measurements, conducted in rural New York for 303 days between March 2003 and January 2005, were analyzed by a factor analysis source apportionment model, and five source categories (transported aerosol/secondary sulfate, resuspended soil, metals, residual oil combustion, industrial/incineration) were identified. After the exposure of human epithelial cells (BEAS-2B) to our PM2.5 samples, cellular NFkB activation showed a relatively significant association with the Ni concentration averaging 38 ng/m3, and weaker but still significant correlations with Ba (13 ng/m3), Mn (9 ng/m3), and Fe (500 ng/m3). The single-source category regression analysis of NF-κB signal showed a significant association only with the metals source Thus, three metals, which together constitute only 60 ng/m3 to the PM2.5 mass (107 ug/m3), appear to be more influential on lung cell responses than BC (6 ug/m3) and sulfate ions (36 ug/m3) that are present at much higher mass concentrations.

Background— There is a strong link between urbanization and type 2 diabetes mellitus. Although a multitude of mechanisms have been proposed, there are no studies evaluating the impact of ambient air pollutants and the propensity to develop type 2 diabetes mellitus. We hypothesized that exposure to ambient fine particulate matter (2.5 ) exaggerates diet-induced insulin resistance, adipose inflammation, and visceral adiposity. Methods and Results— Male C57BL/6 mice were fed high-fat chow for 10 weeks and randomly assigned to concentrated ambient PM 2.5 or filtered air (n=14 per group) for 24 weeks. PM 2.5 -exposed C57BL/6 mice exhibited marked whole-body insulin resistance, systemic inflammation, and an increase in visceral adiposity. PM 2.5 exposure induced signaling abnormalities characteristic of insulin resistance, including decreased Akt and endothelial nitric oxide synthase phosphorylation in the endothelium and increased protein kinase C expression. These abnormalilties were associated with abnormalities in vascular relaxation to insulin and acetylcholine. PM 2.5 increased adipose tissue macrophages (F4/80 + cells) in visceral fat expressing higher levels of tumor necrosis factor-α/interleukin-6 and lower interleukin-10/ N -acetyl-galactosamine specific lectin 1. To test the impact of PM 2.5 in eliciting direct monocyte infiltration into fat, we rendered FVBN mice expressing yellow fluorescent protein (YFP) under control of a monocyte-specific promoter (c- fms , c- fms YFP ) diabetic over 10 weeks and then exposed these mice to PM 2.5 or saline intratracheally. PM 2.5 induced YFP cell accumulation in visceral fat and potentiated YFP cell adhesion in the microcirculation. Conclusion— PM 2.5 exposure exaggerates insulin resistance and visceral inflammation/adiposity. These findings provide a new link between air pollution and type 2 diabetes mellitus.

Recent studies have suggested a link between inhaled particulate matter (PM) exposure and atherogenesis. We investigated tissue factor (TF) expression with ambient fine particulate matter (diameter < 2.5 microm, PM(2.5)) exposure and in response to in vitro exposure to fine and ultrafine PM in cultured human bronchial epithelial cells, vascular smooth muscle cells (hSMCs), and monocytes. ApoE-/- mice, fed with normal chow (NC) or high-fat chow (HFC), were exposed to concentrated PM(2.5) or filtered air (FA) for 6 mo (6 h/day, 5 day/wk, n = 28). Following in vivo ultrasound bio-microscopy (UBM) assessment of plaque area, macrophage infiltration (CD68) and TF expression in the aorta were quantified. Cultured cells were incubated with size-fractionated PM from cascade impactors, or with standard reference PM material (SRM, number 1649a) and assayed for TF protein, mRNA, and activity. UBM-derived plaque areas were 7 +/- 1% larger in the PM(2.5)-HFC than the FA-HFC group (p = .04), but not significantly different between the PM(2.5)-NC and FA-NC groups (p = .07). Immunohistochemistry revealed increased TF (15 +/- 3% vs. 8 +/- 2%, p < .01) and macrophage infiltration (19 +/- 2% vs. 14 +/- 3%, p < .01) in the plaques of PM(2.5)-HFC compared with FA-HFC groups. Impactor-collected PM(2.5) and ultrafine particles consistently increased TF protein in bronchial epithelial cells, monocytes, and hSMCs. TF mRNA expression increased rapidly (within 1 h) in response to SRM PM. We conclude that in vivo and in vitro exposure to ambient air PM(2.5) induces TF expression.

It is readily understandable that Dutton of the International Nickel Company (INCO) would like to separate the nickel emissions from the 381-m INCO smelter stack from the highly statistically significant Ni-associated effects on heart rate and heart rate variability that we observed on 14 of 103 consecutive weekdays of exposure in our laboratory (located within the Sterling Forest State Park) in a mouse model of atherosclerosis (Lippmann et al. 2006). Indeed, it is possible that some closer source of Ni could have been responsible for the effects. However, as we noted in our article, the back trajectories on the 14 days with unusually elevated Ni concentrations did not pass over any known industrial sources or large urban areas, but did pass over or near the distant point source of Ni at the INCO smelter in Sudbury, Ontario, Canada. It is also noteworthy that the 14 back trajectories, illustrated in Figure 2 of our article (Lippmann et al. 2006), approached Sterling Forest from a variety of directions, ranging from the NW to the NNE, making it highly unlikely that that their metals compositions were influenced by a significant source within a 100-mi radius. Furthermore, both the directions of the incoming winds and the combination of unusually high Ni and lower than normal vanadium on those 14 days, as compared with the other 89 days of observation, seemed to preclude the major sources of Ni being the Port of New York, the New York City metropolitan area, or other coastal regions where residual oil is used to generate heat and electrical power. It is well known that residual oil combustion effluents are high in both Ni and V. We commend Dutton on identifying a mislabeled key in Figure 4 of our article (Lippmann et al. 2006) that occurred during the preparation of the print version. As he noted, the original manuscript published online was correctly labeled. (See the Erratum on p. A294.) Dutton provided no supporting reference for his comment that “2-year inhalation exposures of rodents to nickel sulfate at levels 600 times higher than those used by Lippmann et al. (2006) were without effect on mortality ….” Based on the 600× concentration difference, we assume he was referring to a National Toxicology Program (NTP) report (NTP 1996). It should be noted that healthy B6C3F1 mice were exposed in this study, and that healthy B6 mice had much greater survival times than seven other inbred mice strains when exposed to nickel sulfate by Prows et al. (2003). Dutton also states that “there is no statistical relationship between NMMAPS [National Mortality and Morbidity Air Pollution Study] CVR [cardiovascular risk] mortality rates and Ni emission rates.” Again, no reference was cited. Even if his statement was supported by a negative study, it relates to emissions and not concentrations. In our article (Lippmann et al. 2006), we showed that the annual average PM10 (particulate matter < 10 μm in aerodynamic diameter) NMMAPS mortality coefficients for 60 NMMAPS cities were significantly associated with annual average ambient Ni and V concentrations in those same cities. Finally, we take exception to Dutton’s comment that implies that we lack sufficient expertise in atmospheric science. The only issue in our article that relates to atmospheric science is our use of HYSPLIT back trajectories, and we fail to see how we misused them.

ContextRecent studies have suggested a link between inhaled particulate matter exposure in urban areas and susceptibility to cardiovascular events; however, the precise mechanisms remain to be determined.ObjectiveTo test the hypothesis that subchronic exposure to environmentally relevant particulate matter, even at low concentrations, potentiates atherosclerosis and alters vasomotor tone in a susceptible disease model.Design, Setting, and ParticipantsBetween July 21, 2004, and January 12, 2005, 28 apolipoprotein E−/− (apoE−/−) mice were, based on randomized assignments, fed with normal chow or high-fat chow and exposed to concentrated ambient particles of less than 2.5 μm (PM2.5) or filtered air (FA) in Tuxedo, NY, for 6 hours per day, 5 days per week for a total of 6 months.Main Outcome MeasuresComposite atherosclerotic plaque in the thoracic and abdominal aorta and vasomotor tone changes.ResultsIn the high-fat chow group, the mean (SD) composite plaque area of PM2.5 vs FA was 41.5% (9.8%) vs 26.2% (8.6%), respectively (P

The collapse of the World Trade Center (WTC) on September 11, 2001, generated large amounts of dust and smoke that settled in the surrounding indoor and outdoor environments in southern Manhattan. Sixteen dust samples were collected from undisturbed locations inside two uncleaned buildings that were adjacent to Ground Zero. These samples were analyzed for morphology, metals, and organic compounds, and the results were compared with the previously reported outdoor WTC dust/smoke results. We also analyzed seven additional dust samples provided by residents in the local neighborhoods. The morphologic analyses showed that the indoor WTC dust/smoke samples were similar to the outdoor WTC dust/smoke samples in composition and characteristics but with more than 50% mass in the53-microm size fraction. This was in contrast to the outdoor samples that contained50% of mass above53 microm. Elemental analyses also showed the similarities, but at lower concentrations. Organic compounds present in the outdoor samples were also detected in the indoor samples. Conversely, the resident-provided convenience dust samples were different from either the WTC indoor or outdoor samples in composition and pH, indicating that they were not WTC-affected locations. In summary, the indoor dust/smoke was similar in concentration to the outdoor dust/smoke but had a greater percentage of mass53 microm in diameter.