Traffic exposures, air pollution and outcomes in pulmonary arterial hypertension: a UK cohort study analysis.
Sofianopoulou Eleni,Kaptoge Stephen,Gräf Stefan,Hadinnapola Charaka,Treacy Carmen M,Church Colin,Coghlan Gerry,Gibbs J Simon R,Haimel Matthias,Howard Luke S,Johnson Martin,Kiely David G,Lawrie Allan,Lordan James,MacKenzie Ross Robert V,Martin Jennifer M,Moledina Shahin,Newnham Michael,Peacock Andrew J,Price Laura C,Rhodes Christopher J,Suntharalingam Jay,Swietlik Emilia M,Toshner Mark R,Wharton John,Wilkins Martin R,Wort Stephen J,Pepke-Zaba Joanna,Condliffe Robin,Corris Paul A,Di Angelantonio Emanuele,Provencher Steeve,Morrell Nicholas W
The European respiratory journal
While traffic and air pollution exposure is associated with increased mortality in numerous diseases, its association with disease severity and outcomes in pulmonary arterial hypertension (PAH) remains unknown.Exposure to particulate matter with a 50% cut-off aerodynamic diameter ≤2.5 μm (PM), nitrogen dioxide (NO) and indirect measures of traffic-related air pollution (distance to main road and length of roads within buffer zones surrounding residential addresses) were estimated for 301 patients with idiopathic/heritable PAH recruited in the UK National Cohort Study of Idiopathic and Heritable PAH. Associations with transplant-free survival and pulmonary haemodynamic severity at baseline were assessed, adjusting for confounding variables defined Higher estimated exposure to PM was associated with higher risk of death or lung transplant (unadjusted hazard ratio (HR) 2.68 (95% CI 1.11-6.47) per 3 μg·m; p=0.028). This association remained similar when adjusted for potential confounding variables (HR 4.38 (95% CI 1.44-13.36) per 3 μg·m; p=0.009). No associations were found between NO exposure or other traffic pollution indicators and transplant-free survival. Conversely, indirect measures of exposure to traffic-related air pollution within the 500-1000 m buffer zones correlated with the European Society of Cardiology/European Respiratory Society risk categories as well as pulmonary haemodynamics at baseline. This association was strongest for pulmonary vascular resistance.In idiopathic/heritable PAH, indirect measures of exposure to traffic-related air pollution were associated with disease severity at baseline, whereas higher PM exposure may independently predict shorter transplant-free survival.
Susceptibility of individuals with chronic obstructive pulmonary disease to air pollution exposure in Beijing, China: A case-control panel study (COPDB).
Chen Xi,Wang Teng,Qiu Xinghua,Que Chengli,Zhang Hanxiyue,Zhang Lina,Zhu Tong
The Science of the total environment
Exposure to air pollution is one of the major risk factors contributing to the occurrence and development of chronic obstructive pulmonary disease (COPD). However, few studies have investigated the susceptibility of patients with COPD to air pollution. Here, we provided a study protocol. A panel study of a total of 480 samples to compare the response to air pollution exposure between 60 patients with COPD and 60 healthy control subjects has been performed in Beijing (the COPDB study) since May 2016. The health assessment and exposure evaluation methods used in this COPDB study are summarized here. Throat, exhaled breath and condensate, urine, serum, plasma, and blood samples, as well as cardiopulmonary function indexes were repeatedly collected over four visits. Indicators of inflammation, oxidative stress, infection, metabolic changes, and genetic differences were then analyzed. Personal and ambient levels of fine particles and their components, as well as gaseous pollutants were monitored during the follow-up period. Linear mixed-effects models were used to evaluate the associations between changes in biomarkers and exposure to air pollution in both patients with COPD and healthy control subjects. Based on the COPDB study, the susceptibility of COPD patients and underlying mechanisms, involving difference in inflammatory, infection, metabolic, and genetic response to different air pollutants, were investigated. Our preliminary result shows that air pollution-associated changes in heart rate were higher in COPD patients than the healthy controls. More investigations of the underlying mechanisms of the susceptibility are ongoing. This study has been registered in ChiCTR with the number of ChiCTR1900023692.
Exposure to inhaled particulate matter impairs cardiac function in senescent mice.
Tankersley Clarke G,Champion Hunter C,Takimoto Eiki,Gabrielson Kathleen,Bedja Djahida,Misra Vikas,El-Haddad Hazim,Rabold Richard,Mitzner Wayne
American journal of physiology. Regulatory, integrative and comparative physiology
Daily exposure to particulate matter (PM) is known to adversely affect cardiac function and is also known to be exaggerated with senescence. This study tests the hypothesis that cardiac function is uniquely altered by PM exposure in senescent mice. A mechanism for PM-induced cardiac effects is also postulated by examining the activity of nitric oxide synthase (NOS) and the generation of reactive oxygen species (ROS) in heart tissue. Echocardiography is performed in awake 18- and 28-mo-old mice at baseline and immediately following 3-h exposures to either filtered air or carbon black (CB; approximately 400 microg/m3) on 4 days. At 28 mo, left ventricular diameter at end-systole and end-diastole is significantly (P < 0.05) elevated, and fractional shortening is significantly reduced (49 +/- 3% vs. 56 +/- 3%) with CB exposure. In vivo hemodynamic measurements at 28 mo also demonstrate significant (P < 0.05) reductions in ejection fraction and increases in right ventricular and pulmonary vascular pressures following CB exposure. Functional changes at 28 mo are associated with increased ROS production as suggested by enhanced luminol activity. This elevated ROS production with aging and CB exposure is attributable to NOS uncoupling. Measurements of natriuretic peptide (atrial and brain) transcription and matrix metalloproteinase (MMP2 and MMP9) activity in heart tissue are significantly (P < 0.05) amplified with senescence and exposure to CB, pointing to increased cardiac stress and remodeling. These results demonstrate that acute PM exposure reduces cardiac contractility in senescent mice, and this decline in function is associated with increased ROS production linked to NOS uncoupling.
Early life exposure to air pollution induces adult cardiac dysfunction.
Gorr Matthew W,Velten Markus,Nelin Timothy D,Youtz Dane J,Sun Qinghua,Wold Loren E
American journal of physiology. Heart and circulatory physiology
Exposure to ambient air pollution contributes to the progression of cardiovascular disease, particularly in susceptible populations. The objective of the present study was to determine whether early life exposure to air pollution causes persistent cardiovascular consequences measured at adulthood. Pregnant FVB mice were exposed to filtered (FA) or concentrated ambient particulate matter (PM2.5) during gestation and nursing. Mice were exposed to PM2.5 at an average concentration of 51.69 μg/m(3) from the Columbus, OH region for 6 h/day, 7 days/wk in utero until weaning at 3 wk of age. Birth weight was reduced in PM2.5 pups compared with FA (1.36 ± 0.12 g FA, n = 42 mice; 1.30 ± 0.15 g PM2.5, n = 67 P = 0.012). At adulthood, mice exposed to perinatal PM2.5 had reduced left ventricular fractional shortening compared with FA-exposed mice (43.6 ± 2.1% FA, 33.2 ± 1.6% PM2.5, P = 0.001) with greater left ventricular end systolic diameter. Pressure-volume loops showed reduced ejection fraction (79.1 ± 3.5% FA, 35.5 ± 9.5% PM2.5, P = 0.005), increased end-systolic volume (10.4 ± 2.5 μl FA, 39.5 ± 3.8 μl PM2.5, P = 0.001), and reduced dP/dt maximum (11,605 ± 200 μl/s FA, 9,569 ± 800 μl/s PM2.5, P = 0.05) and minimum (-9,203 ± 235 μl/s FA, -7,045 ± 189 μl/s PM2.5, P = 0.0005) in PM2.5-exposed mice. Isolated cardiomyocytes from the hearts of PM2.5-exposed mice had reduced peak shortening (%PS, 8.53 ± 2.82% FA, 6.82 ± 2.04% PM2.5, P = 0.003), slower calcium reuptake (τ, 0.22 ± 0.09 s FA, 0.26 ± 0.07 s PM2.5, P = 0.048), and reduced response to β-adrenergic stimulation compared with cardiomyocytes isolated from mice that were exposed to FA. Histological analyses revealed greater picro-sirius red-positive-stained areas in the PM2.5 vs. FA group, indicative of increased collagen deposition. We concluded that these data demonstrate the detrimental role of early life exposure to ambient particulate air pollution in programming of adult cardiovascular diseases and the potential for PM2.5 to induce persistent cardiac dysfunction at adulthood.
[Toxic Components of PM and Their Toxicity Mechanisms-On the Toxicity of Sulfate and Carbon Components].
Nihon eiseigaku zasshi. Japanese journal of hygiene
Recently, the main air pollutant has been fine particulate matter (PM), which is taken up by the whole body with severe adverse health effects. The main chemical components of PM are salts of sulfate (and nitrate) and carbons. However, it remains unknown which components are toxic. Here, the author reviewed the literatures to determine which components are toxic and the main mechanisms underlying their toxicity. Many epidemiological studies have shown that sulfate concentration is strongly related to mortality. However, there is no experimental evidence showing that sulfate at environmental concentrations of PM causes cardiovascular disease or other disease. On the other hand, carbon components such as elementary carbon (EC) produces high concentrations of reactive oxygen species (ROS) via its phagocytosis by macrophages, and organic carbon (OC) also produces high concentrations of ROS during its metabolic processes, and the ROS cause acute and chronic inflammation. They cause many diseases including cardiovascular disease, asthma and cancer. Furthermore, there are many lines of evidence showing that epigenetic changes such as DNA methylation or microRNA expression induced by particulate matters also induce the development of many diseases such as those mentioned above. It has been reported that carbon components are incorporated into the brain and produce ROS, and that the ROS cause damage to brain cells and Alzheimer's disease and cognitive disorders in the elderly.From these lines of evidence, the author would like to emphasize that the main toxicity of PM is due to carbon components, and it is important to take countermeasures to decrease the concentration of carbon components in ambient air.
Fine particulate matter constituents associated with cardiovascular hospitalizations and mortality in New York City.
Ito Kazuhiko,Mathes Robert,Ross Zev,Nádas Arthur,Thurston George,Matte Thomas
Environmental health perspectives
BACKGROUND:Recent time-series studies have indicated that both cardiovascular disease (CVD)mortality and hospitalizations are associated with particulate matter (PM). However, seasonal patterns of PM associations with these outcomes are not consistent, and PM components responsible for these associations have not been determined. We investigated this issue in New York City (NYC), where PM originates from regional and local combustion sources. OBJECTIVE:In this study, we examined the role of particulate matter with aerodynamic diameter ≤ 2.5 µm (PM(2.5)) and its key chemical components on both CVD hospitalizations and on mortality in NYC. METHODS:We analyzed daily deaths and emergency hospitalizations for CVDs among persons ≥ 40 years of age for associations with PM(2.5), its chemical components, nitrogen dioxide (NO(2)), carbon monoxide, and sulfur dioxide for the years 2000-2006 using a Poisson time-series model adjusting for temporal and seasonal trends, temperature effects, and day of the week. We estimated excess risks per interquartile-range increases at lags 0 through 3 days for warm (April through September) and cold (October through March) seasons. RESULTS:The CVD mortality series exhibit strong seasonal trends, whereas the CVD hospitalization series show a strong day-of-week pattern. These outcome series were not correlated with each other but were individually associated with a number of PM(2.5) chemical components from regional and local sources, each with different seasonal patterns and lags. Coal-combustion-related components (e.g., selenium) were associated with CVD mortality in summer and CVD hospitalizations in winter, whereas elemental carbon and NO(2) showed associations with these outcomes in both seasons. CONCLUSION:Local combustion sources, including traffic and residual oil burning, may play a year-round role in the associations between air pollution and CVD outcomes, but transported aerosols may explain the seasonal variation in associations shown by PM(2.5) mass.
Characterization of fine particulate matter and associations between particulate chemical constituents and mortality in Seoul, Korea.
Son Ji-Young,Lee Jong-Tae,Kim Ki-Hyun,Jung Kweon,Bell Michelle L
Environmental health perspectives
BACKGROUND:Numerous studies have linked fine particles [≤ 2.5 µm in aerodynamic diameter (PM(2.5))] and health. Most studies focused on the total mass of the particles, although the chemical composition of the particles varies substantially. Which chemical components of fine particles that are the most harmful is not well understood, and research on the chemical composition of PM(2.5) and the components that are the most harmful is particularly limited in Asia. OBJECTIVES:We characterized PM(2.5) chemical composition and estimated the effects of cause-specific mortality of PM(2.5) mass and constituents in Seoul, Korea. We compared the chemical composition of particles to those of the eastern and western United States. METHODS:We examined temporal variability of PM(2.5) mass and its composition using hourly data. We applied an overdispersed Poisson generalized linear model, adjusting for time, day of week, temperature, and relative humidity to investigate the association between risk of mortality and PM(2.5) mass and its constituents in Seoul, Korea, for August 2008 through October 2009. RESULTS:PM(2.5) and chemical components exhibited temporal patterns by time of day and season. The chemical characteristics of Seoul's PM(2.5) were more similar to PM(2.5) found in the western United States than in the eastern United States. Seoul's PM(2.5) had lower sulfate (SO(4)) contributions and higher nitrate (NO(3)) contributions than that of the eastern United States, although overall PM(2.5) levels in Seoul were higher than in the United States. An interquartile range (IQR) increase in magnesium (Mg) (0.05 μg/m³) was associated with a 1.4% increase (95% confidence interval: 0.2%, 2.6%) in total mortality on the following day. Several components that were among the largest contributors to PM(2.5) total mass--NO(3), SO(4), and ammonium (NH(4))--were moderately associated with same-day cardiovascular mortality at the p < 0.10 level. Other components with smaller mass contributions [Mg and chlorine (Cl)] exhibited moderate associations with respiratory mortality on the following day (p < 0.10). CONCLUSIONS:Our findings link PM(2.5) constituents with mortality and have implications for policy making on sources of PM(2.5) and on the relevance of PM(2.5) health studies from other areas to this region.
The role of metal components in the cardiovascular effects of PM2.5.
Niu Jingping,Liberda Eric N,Qu Song,Guo Xinbiao,Li Xiaomei,Zhang Jingjing,Meng Junliang,Yan Bing,Li Nairong,Zhong Mianhua,Ito Kazuhiko,Wildman Rachel,Liu Hong,Chen Lung Chi,Qu Qingshan
Exposure to ambient fine particulate matter (PM2.5) increases risks for cardiovascular disorders (CVD). However, the mechanisms and components responsible for the effects are poorly understood. Based on our previous murine exposure studies, a translational pilot study was conducted in female residents of Jinchang and Zhangye, China, to test the hypothesis that specific chemical component of PM2.5 is responsible for PM2.5 associated CVD. Daily ambient and personal exposures to PM2.5 and 35 elements were measured in the two cities. A total of 60 healthy nonsmoking adult women residents were recruited for measurements of inflammation biomarkers. In addition, circulating endothelial progenitor cells (CEPCs) were also measured in 20 subjects. The ambient levels of PM2.5 were comparable between Jinchang and Zhangye (47.4 and 54.5 µg/m(3), respectively). However, the levels of nickel, copper, arsenic, and selenium in Jinchang were 82, 26, 12, and 6 fold higher than Zhangye, respectively. The levels of C-reactive protein (3.44 ± 3.46 vs. 1.55 ± 1.13), interleukin-6 (1.65 ± 1.17 vs. 1.09 ± 0.60), and vascular endothelial growth factor (117.6 ± 217.0 vs. 22.7 ± 21.3) were significantly higher in Jinchang. Furthermore, all phenotypes of CEPCs were significantly lower in subjects recruited from Jinchang than those from Zhangye. These results suggest that specific metals may be important components responsible for PM2.5-induced cardiovascular effects and that the reduced capacity of endothelial repair may play a critical role.
Particle size and chemical constituents of ambient particulate pollution associated with cardiovascular mortality in Guangzhou, China.
Lin Hualiang,Tao Jun,Du Yaodong,Liu Tao,Qian Zhengmin,Tian Linwei,Di Qian,Rutherford Shannon,Guo Lingchuan,Zeng Weilin,Xiao Jianpeng,Li Xing,He Zhihui,Xu Yanjun,Ma Wenjun
Environmental pollution (Barking, Essex : 1987)
Though significant associations between particulate matter (PM) air pollution and cardiovascular diseases have been widely reported, it remains unclear what characteristics, such as particle size and chemical constituents, may be responsible for the effects. A time-series model was applied to examine the cardiovascular effects of particle size (for the period of 2009-2011) and chemical constituents (2007-2010) in Guangzhou, we controlled for potential confounders in the model, such as time trends, day of the week, public holidays, meteorological factors and influenza epidemic. We found significant associations of cardiovascular mortality with PM10, PM2.5 and PM1; the excess risk (ER) was 6.10% (95% CI: 1.76%, 10.64%), 6.11% (95% CI: 1.76%, 10.64%) and 6.48% (95% CI: 2.10%, 11.06%) for per IQR increase in PM10, PM2.5 and PM1 at moving averages for the current day and the previous 3 days (lag03), respectively. We did not find significant effects of PM2.5-10 and PM1-2.5. For PM2.5 constituents, we found that organic carbon, elemental carbon, sulfate, nitrate and ammonium were significantly associated with cardiovascular mortality, the corresponding ER for an IQR concentration increase at lag03 was 1.13% (95% CI: 0.10%, 2.17%), 2.77% (95% CI: 0.72%, 4.86%), 2.21% (95% CI: 1.05%, 3.38%), 1.98% (95% CI: 0.54%, 3.44%), and 3.38% (95% CI: 1.56%, 5.23%), respectively. These results were robust to adjustment of other air pollutants and they remained consistent in various sensitivity analyses by changing model parameters. Our study suggests that PM1 and constituents from combustion and secondary aerosols might be important characteristics of PM pollution associated with cardiovascular mortality in Guangzhou.
Toxicological and epidemiological studies of cardiovascular effects of ambient air fine particulate matter (PM2.5) and its chemical components: coherence and public health implications.
Critical reviews in toxicology
Recent investigations on PM2.5 constituents' effects in community residents have substantially enhanced our knowledge on the impacts of specific components, especially the HEI-sponsored National Particle Toxicity Component (NPACT) studies at NYU and UW-LRRI that addressed the impact of long-term PM2.5 exposure on cardiovascular disease (CVD) effects. NYU's mouse inhalation studies at five sites showed substantial variations in aortic plaque progression by geographic region that was coherent with the regional variation in annual IHD mortality in the ACS-II cohort, with both the human and mouse responses being primarily attributable to the coal combustion source category. The UW regressions of associations of CVD events and mortality in the WHI cohort, and of CIMT and CAC progression in the MESA cohort, indicated that [Formula: see text] had stronger associations with CVD-related human responses than OC, EC, or Si. The LRRI's mice had CVD-related biomarker responses to [Formula: see text]. NYU also identified components most closely associated with daily hospital admissions (OC, EC, Cu from traffic and Ni and V from residual oil). For daily mortality, they were from coal combustion ([Formula: see text], Se, and As). While the recent NPACT research on PM2.5 components that affect CVD has clearly filled some major knowledge gaps, and helped to define remaining uncertainties, much more knowledge is needed on the effects in other organ systems if we are to identify and characterize the most effective and efficient means for reducing the still considerable adverse health impacts of ambient air PM. More comprehensive speciation data are needed for better definition of human responses.
Oxidant mechanisms in response to ambient air particles.
Molecular aspects of medicine
The toxic effects of air pollution are widely documented. In recent years, however, there has been an increasing interest in the study of the health effects of particulate matter (PM), a previously unexplored constituent of urban air pollution. Exposure to increased levels of PM of respirable size is strongly and consistently associated with increased cardiopulmonary morbidity and mortality. Conversely, improved air quality appears to correlate with decreased mortality. Particulate matter is a mixture of inorganic and organic components that vary in size, origin, and composition. The mechanisms of PM health effects are still poorly understood. However, studies in cellular and animal models suggest a variety of possible mechanisms including direct effects of particle components on the intracellular sources of reactive oxygen species (ROS), indirect effects due to pro-inflammatory mediators released from PM-stimulated macrophages, and neural stimulation after particle deposition in the lungs. The involvement of ROS in each one of these possible pathways is discussed.
Role of oxidative stress in arsenic-induced toxicity.
Lantz R Clark,Hays Allison M
Drug metabolism reviews
Arsenic is recognized as a carcinogen for human skin, bladder, and lung, following either ingestion or inhalation; however the exact mode of action of environmentally relevant exposure has not been determined. Because arsenic in the environment exists in several oxidative states and can interact with thiols, it is thought that arsenic toxicity is mediated through oxidative stress. Production of oxygen radicals following acute in vitro exposures has been demonstrated. However, our research has chosen to focus on the role of oxidative stress following whole animal exposure to environmentally relevant doses of arsenic. Following a 28-d inhalation of arsenic or cigarette smoke or both, there was a significant decrease in both the reduced and total glutathione levels in the combined arsenic and smoke group compared to groups exposed to arsenic or smoke alone. This correlated with a 5-fold increase in DNA oxidation. Lungs processed for immunohistochemistry localization of 8-oxo-dG showed increased staining in nuclei of airway epithelium and subadjacent interstitial cells. Increases in DNA oxidation were not due to increased inflammation. Although inhalation of arsenic is an important occupational exposure, the majority of human exposures occurs through ingestion of arsenic. Our recent work has been devoted to the identification of altered pulmonary gene and protein expression following ingestion of environmentally relevant levels of arsenic in drinking water. We have found that, following chronic exposure, arsenic leads to misregulation of a number of genes and proteins in the lung. A large percentage of the altered genes and proteins are known to be regulated by redox-sensitive transcription factors, (SP1, NF kappaB, AP-1), suggesting that, at environmentally relevant levels of chronic exposure, arsenic may be acting through alteration of cellular redox status. Validation of the alterations seen in animal models of exposure is being carried out in humans.
Exploration of the composition and sources of urban fine particulate matter associated with same-day cardiovascular health effects in Dearborn, Michigan.
Morishita Masako,Bard Robert L,Kaciroti Niko,Fitzner Craig A,Dvonch Timothy,Harkema Jack R,Rajagopalan Sanjay,Brook Robert D
Journal of exposure science & environmental epidemiology
The objective was to explore associations of chemical components and source factors of ambient fine particulate matter (aerodynamic diameter ≤ 2.5 μm; PM2.5) with cardiovascular (CV) changes following same-day exposure to ambient PM2.5. Twenty-five healthy adults living in rural Michigan were exposed to ambient air in an urban/industrial community for 4 to 5 h daily for five consecutive days. CV health outcomes were measured 1-2 h post exposure. Contributing emission sources were identified via positive matrix factorization. We examined associations between PM2.5 mass, composition and source factors, and same-day changes in CV outcomes using mixed-model analyses. PM2.5 mass (10.8 ± 6.8 μg/m(3)), even at low ambient levels, was significantly associated with increased heart rate (HR). Trace elements as well as secondary aerosol, diesel/urban dust and iron/steel manufacturing factors potentially explained the HR changes. However, trace element analysis demonstrated additional associations with other CV responses including changes in blood pressure (BP), arterial compliance, autonomic balance and trends toward reductions in endothelial function. Two factors were related to BP changes (diesel/urban dust, motor vehicle) and trends toward impaired endothelial function (diesel/urban dust). This study indicates composition of PM2.5 and its sources may contribute to CV health effects independently of PM2.5 mass.
Air pollution and lung function among susceptible adult subjects: a panel study.
Lagorio Susanna,Forastiere Francesco,Pistelli Riccardo,Iavarone Ivano,Michelozzi Paola,Fano Valeria,Marconi Achille,Ziemacki Giovanni,Ostro Bart D
Environmental health : a global access science source
BACKGROUND:Adverse health effects at relatively low levels of ambient air pollution have consistently been reported in the last years. We conducted a time-series panel study of subjects with chronic obstructive pulmonary disease (COPD), asthma, and ischemic heart disease (IHD) to evaluate whether daily levels of air pollutants have a measurable impact on the lung function of adult subjects with pre-existing lung or heart diseases. METHODS:Twenty-nine patients with COPD, asthma, or IHD underwent repeated lung function tests by supervised spirometry in two one-month surveys. Daily samples of coarse (PM10-2.5) and fine (PM2.5) particulate matter were collected by means of dichotomous samplers, and the dust was gravimetrically analyzed. The particulate content of selected metals (cadmium, chrome, iron, nickel, lead, platinum, vanadium, and zinc) was determined by atomic absorption spectrometry. Ambient concentrations of nitrogen dioxide (NO2), carbon monoxide (CO), ozone (O3), and sulphur dioxide (SO2) were obtained from the regional air-quality monitoring network. The relationships between concentrations of air pollutants and lung function parameters were analyzed by generalized estimating equations (GEE) for panel data. RESULTS:Decrements in lung function indices (FVC and/or FEV1) associated with increasing concentrations of PM2.5, NO2 and some metals (especially zinc and iron) were observed in COPD cases. Among the asthmatics, NO2 was associated with a decrease in FEV1. No association between average ambient concentrations of any air pollutant and lung function was observed among IHD cases. CONCLUSION:This study suggests that the short-term negative impact of exposure to air pollutants on respiratory volume and flow is limited to individuals with already impaired respiratory function. The fine fraction of ambient PM seems responsible for the observed effects among COPD cases, with zinc and iron having a potential role via oxidative stress. The respiratory function of the relatively young and mild asthmatics included in this study seems to worsen when ambient levels of NO2 increase.
Effects of airborne metals on lung function in inner Mongolian schoolchildren.
Madaniyazi Lina,Guo Yuming,Ye Xiaofang,Kim Daeseon,Zhang Yixiang,Pan Xiaochuan
Journal of occupational and environmental medicine
OBJECTIVES:To evaluate the effects of particles and their components on lung function. METHODS:A panel study was conducted on 107 primary schoolchildren. The peak expiratory flow rate (PEFR) for each subject was measured three times a day for 40 days continuously. Particulate air concentrations were measured every day. The concentrations of Pb, Ni, Fe, Mn, Cr, As, Cd, and Zn in particles were measured. Linear mixed-effect models were used to estimate the associations between particles, metal elements, and PEFR. RESULTS:We found that the increase in particles in air was associated with a significant reduction in PEFR. Its effects lasted 2 to 5 days. Pb, Ni, Fe, Mn, and Cr in particles also reduced PEFR. As and Cd increased PEFR. Zn showed inconstant effects on PEFR. CONCLUSION:This study suggested that most metal components in particles have negative effects on children's lung function.
Human arsenic exposure and lung function impairment in coal-burning areas in Guizhou, China.
Wang Wenjuan,Wang Qingling,Zou Zhonglan,Zheng Fanyan,Zhang Aihua
Ecotoxicology and environmental safety
To evaluate the effect of coal-burning arsenic (As) exposure on lung function and the potential underlying mechanisms, a total of 217 As-exposed subjects and 75 reference subjects were recruited into this study. Hair arsenic (H-As), pulmonary function tests, and serum inflammatory markers CC16, SP-A, MMP-9, and TIMP-1 were evaluated. Residents from As-exposed areas showed higher H-As concentrations (median 0.25 μg/g) than subjects from the reference area (median 0.14 μg/g). Large reductions in lung function parameters were noted in the As-exposed group. A significant negative correlation was observed between H-As concentrations and lung function. Specifically, monotonic negative dose-response relationships were observed between H-As and FEV1(%), FEV1/FVC (%) and FEF75 (%) (all P < 0.05), while the associations between H-As and FVC (%), FEF25 (%), and FEF50 (%) were nonlinear (P for nonlinearity = 0.03, 0.001, 0.01, respectively). In addition, there was a direct positive relationship between H-As and the inflammatory response. Alterations in inflammatory biomarkers (CC16, SP-A, MMP-9, and MMP-9/TIMP-1) were significantly associated with As-induced lung function impairment. Thus, this population-based study revealed that As exposure has significant toxic effects on lung function and increased inflammation may occur during this toxic process. We provide scientific evidence for an As-induced alteration in inflammatory biomarkers and pulmonary damage in an As-exposed population. The results of this study can inform risk assessment and risk control processes in relation to human As exposure in coal-burning arsenicosis areas.
A Meta-analysis of Arsenic Exposure and Lung Function: Is There Evidence of Restrictive or Obstructive Lung Disease?
Sanchez Tiffany R,Powers Martha,Perzanowski Matthew,George Christine M,Graziano Joseph H,Navas-Acien Ana
Current environmental health reports
PURPOSE OF REVIEW:Hundreds of millions of people worldwide are exposed to arsenic via contaminated water. The goal of this study was to identify whether arsenic-associated lung function deficits resemble obstructive- or restrictive-like lung disease, in order to help illuminate a mechanistic pathway and identify at-risk populations. RECENT FINDINGS:We recently published a qualitative systematic review outlining the body of research on arsenic and non-malignant respiratory outcomes. Evidence from several populations, at different life stages, and at different levels of exposure showed consistent associations of arsenic exposure with chronic lung disease mortality, respiratory symptoms, and lower lung function levels. The published review, however, only conducted a broad qualitative description of the published studies without considering specific spirometry patterns, without conducting a meta-analysis, and without evaluating the dose-response relationship. We searched PubMed and Embase for studies on environmental arsenic exposure and lung function. We performed a meta-analysis using inverse-variance-weighted random effects models to summarize adjusted effect estimates for arsenic and forced expiratory volume in one second (FEV), forced vital capacity (FVC), and FEV/FVC ratio. Across nine studies, median water arsenic levels ranged from 23 to 860 μg/L. The pooled estimated mean difference (MD) comparing the highest category of arsenic exposure (ranging from > 11 to > 800 μg/L) versus the lowest (ranging from < 10 to < 100 μg/L) for each study for FEV was - 42 mL (95% confidence interval (CI) - 70, - 16) and for FVC was - 50 mL (95% CI - 63, - 37). Three studies reported effect estimates for FEV/FVC, for which there was no evidence of an association; the pooled estimated MD was 0.01 (95% CI - 0.005, 0.024). This review supports that arsenic is associated with restrictive impairments based on inverse associations between arsenic and FEV and FVC, but not with FEV/FVC. Future studies should confirm whether low-level arsenic exposure is a restrictive lung disease risk factor in order to identify at-risk populations in the USA.
Arsenic exposure alters lung function and airway inflammation in children: A cohort study in rural Bangladesh.
Ahmed Sultan,Akhtar Evana,Roy Adity,von Ehrenstein Ondine S,Vahter Marie,Wagatsuma Yukiko,Raqib Rubhana
Exposure to arsenic has been associated with increased risk of reduced lung function in adults, but the adverse impacts in early life are unclear. We aim to examine whether prenatal and childhood arsenic exposure is associated with reduced lung function and increased airway inflammation in school-aged children. Children born in the MINIMat cohort in rural Bangladesh were evaluated at 9years of age (n=540). Arsenic exposure was assessed in urine (U-As) that was collected from mothers during early pregnancy and their children aged 4.5 and 9years. In the 9-year-old children, lung function was assessed using spirometry and airway inflammation was assessed by the NIOX MINO system. C-reactive protein (CRP) and Clara cell secretory protein (CC16) concentrations were measured in plasma by immunoassays. The U-As concentrations in 9-year-old children were lower (median 53μg/l) compared to their mothers (median 76μg/l). Maternal U-As (log transformed) was inversely associated with forced vital capacity (FVC) and forced expiratory volume at 1s (FEV1) (β=-12; 95% CI: -22, -1.5; p=0.031 and β=-12; 95% CI: -22, -1.9; p=0.023, respectively) in all children, and the associations were stronger in boys and among children with adequate height and weight, as well as among those whose mothers had higher percentages of methylarsonic acid (MMA) and lower percentages of dimethylarsinic acid (DMA). U-As (log transformed) at 4.5 and 9years was positively associated with fractional exhaled nitric oxide (FE) concentrations in boys (β=0.89; 95% CI: 0.13, 1.66; p=0.022 and β=0.88; 95% CI: 0.16, 1.61; p=0.017, respectively) but not in girls. Increased CC16 concentrations were associated with higher lung function indices. In conclusion, our findings suggest that prenatal arsenic exposure is related to impaired lung function, while childhood exposure may increase airway inflammation, particularly in boys.
Associations of chemical composition and sources of PM with lung function of severe asthmatic adults in a low air pollution environment of urban Nagasaki, Japan.
Ng Chris Fook Sheng,Hashizume Masahiro,Obase Yasushi,Doi Masataka,Tamura Kei,Tomari Shinya,Kawano Tetsuya,Fukushima Chizu,Matsuse Hiroto,Chung Yeonseung,Kim Yoonhee,Kunimitsu Kenichi,Kohno Shigeru,Mukae Hiroshi
Environmental pollution (Barking, Essex : 1987)
Previous studies have linked ambient PM to decreased pulmonary function, but the influence of specific chemical elements and emission sources on the severe asthmatic is not well understood. We examined the mass, chemical constituents, and sources of PM for short-term associations with the pulmonary function of adults with severe asthma in a low air pollution environment in urban Nagasaki, Japan. We recruited 35 asthmatic adults and obtained the daily record of morning peak expiratory flow (PEF) in spring 2014-2016. PM filters were extracted from an air quality monitoring station (178 days) and measured for 27 chemical elements. Source apportionment was performed using Positive Matrix Factorization (PMF). We fitted generalized linear model with generalized estimating equation (GEE) method to estimate changes in PEF (from personal monthly maximum) and odds of severe respiratory deterioration (first ≥ 15% PEF reduction within a 1-week interval) associated with mass, constituents, and sources of PM, with adjustment for temperature and relative humidity. Constituent sulfate (SO) and PM from oil combustion and traffic were associated with reduced PEF. An interquartile range (IQR) increase in SO (3.7 μg/m, average lags 0-1) was associated with a decrease of 0.38% (95% confidence interval = -0.75% to -0.001%). An IQR increase in oil combustion and traffic-sourced PM (2.64 μg/m, lag 1) was associated with a decrease of 0.33% (-0.62% to -0.002%). We found a larger PEF decrease associated with PM from dust/soil on Asian Dust days. There was no evidence linking total mass and metals to reduced pulmonary function. The ventilatory capacity of adults with severe asthma is susceptible to specific constituents/sources of PM such as sulfate and oil combustion and traffic despite active self-management of asthma and low air pollution levels in the study location.
Chemical constituents of fine particulate air pollution and pulmonary function in healthy adults: the Healthy Volunteer Natural Relocation study.
Wu Shaowei,Deng Furong,Hao Yu,Shima Masayuki,Wang Xin,Zheng Chanjuan,Wei Hongying,Lv Haibo,Lu Xiuling,Huang Jing,Qin Yu,Guo Xinbiao
Journal of hazardous materials
The study examined the associations of 32 chemical constituents of particulate matter with an aerodynamic diameter ≤2.5 μm (PM₂.₅) with pulmonary function in a panel of 21 college students. Study subjects relocated from a suburban area to an urban area with changing ambient air pollution levels and contents in Beijing, China, and provided daily morning/evening peak expiratory flow (PEF) and forced expiratory volume in 1s (FEV₂₁) measurements over 6 months in three study periods. There were significant reductions in evening PEF and morning/evening FEV₂₁ associated with various air pollutants and PM₂.₅ constituents. Four PM₂.₅ constituents (copper, cadmium, arsenic and stannum) were found to be most consistently associated with the reductions in these pulmonary function measures. These findings provide clues for the respiratory effects of specific particulate chemical constituents in the context of urban air pollution.
Elemental composition of particulate matter and the association with lung function.
Eeftens Marloes,Hoek Gerard,Gruzieva Olena,Mölter Anna,Agius Raymond,Beelen Rob,Brunekreef Bert,Custovic Adnan,Cyrys Josef,Fuertes Elaine,Heinrich Joachim,Hoffmann Barbara,de Hoogh Kees,Jedynska Aleksandra,Keuken Menno,Klümper Claudia,Kooter Ingeborg,Krämer Ursula,Korek Michal,Koppelman Gerard H,Kuhlbusch Thomas A J,Simpson Angela,Smit Henriëtte A,Tsai Ming-Yi,Wang Meng,Wolf Kathrin,Pershagen Göran,Gehring Ulrike
Epidemiology (Cambridge, Mass.)
BACKGROUND:Negative effects of long-term exposure to particulate matter (PM) on lung function have been shown repeatedly. Spatial differences in the composition and toxicity of PM may explain differences in observed effect sizes between studies. METHODS:We conducted a multicenter study in 5 European birth cohorts-BAMSE (Sweden), GINIplus and LISAplus (Germany), MAAS (United Kingdom), and PIAMA (The Netherlands)-for which lung function measurements were available for study subjects at the age of 6 or 8 years. Individual annual average residential exposure to copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc within PM smaller than 2.5 μm (PM2.5) and smaller than 10 μm (PM10) was estimated using land-use regression models. Associations between air pollution and lung function were analyzed by linear regression within cohorts, adjusting for potential confounders, and then combined by random effects meta-analysis. RESULTS:We observed small reductions in forced expiratory volume in the first second, forced vital capacity, and peak expiratory flow related to exposure to most elemental pollutants, with the most substantial negative associations found for nickel and sulfur. PM10 nickel and PM10 sulfur were associated with decreases in forced expiratory volume in the first second of 1.6% (95% confidence interval = 0.4% to 2.7%) and 2.3% (-0.1% to 4.6%) per increase in exposure of 2 and 200 ng/m, respectively. Associations remained after adjusting for PM mass. However, associations with these elements were not evident in all cohorts, and heterogeneity of associations with exposure to various components was larger than for exposure to PM mass. CONCLUSIONS:Although we detected small adverse effects on lung function associated with annual average levels of some of the evaluated elements (particularly nickel and sulfur), lower lung function was more consistently associated with increased PM mass.
Fine particulate matter components and emergency department visits for cardiovascular and respiratory diseases in the St. Louis, Missouri-Illinois, metropolitan area.
Sarnat Stefanie Ebelt,Winquist Andrea,Schauer James J,Turner Jay R,Sarnat Jeremy A
Environmental health perspectives
BACKGROUND:Given that fine particulate matter (≤ 2.5 μm; PM2.5) is a mixture of multiple components, it has been of high interest to identify its specific health-relevant physical and/or chemical features. OBJECTIVES:We conducted a time-series study of PM2.5 and cardiorespiratory emergency department (ED) visits in the St. Louis, Missouri-Illinois metropolitan area, using 2 years of daily PM2.5 and PM2.5 component measurements (including ions, carbon, particle-phase organic compounds, and elements) made at the St. Louis-Midwest Supersite, a monitoring site of the U.S. Environmental Protection Agency Supersites ambient air monitoring research program. METHODS:Using Poisson generalized linear models, we assessed short-term associations between daily cardiorespiratory ED visit counts and daily levels of 24 selected pollutants. Associations were estimated for interquartile range changes in each pollutant. To allow comparison of relationships among multiple pollutants and outcomes with potentially different lag structures, we used 3-day unconstrained distributed lag models controlling for time trends and meteorology. RESULTS:Considering results of our primary models, as well as sensitivity analyses and models assessing co-pollutant confounding, we observed robust associations of cardiovascular disease visits with 17α(H),21β(H)-hopane and congestive heart failure visits with elemental carbon. We also observed a robust association of respiratory disease visits with ozone. For asthma/wheeze, associations were strongest with ozone and nitrogen dioxide; observed associations of asthma/wheeze with PM2.5 and its components were attenuated in two-pollutant models with these gases. Differential measurement error due to differential patterns of spatiotemporal variability may have influenced patterns of observed associations across pollutants. CONCLUSIONS:Our findings add to the growing field examining the health effects of PM2.5 components. Combustion-related components of the pollutant mix showed particularly strong associations with cardiorespiratory ED visit outcomes.
Chemical properties of air pollutants and cause-specific hospital admissions among the elderly in Atlanta, Georgia.
Suh Helen H,Zanobetti Antonella,Schwartz Joel,Coull Brent A
Environmental health perspectives
BACKGROUND:Health risks differ by fine particle (aerodynamic diameter ≤ 2.5 μm) component, although with substantial variability. Traditional methods to assess component-specific risks are limited, suggesting the need for alternative methods. OBJECTIVES:We examined whether the odds of daily hospital admissions differ by pollutant chemical properties. METHODS:We categorized pollutants by chemical properties and examined their impacts on the odds of daily hospital admissions among Medicare recipients > 64 years of age in counties in Atlanta, Georgia, for 1998-2006. We analyzed data in two stages. In the first stage we applied a case-crossover analysis to simultaneously estimate effects of 65 pollutants measured in the Aerosol Research and Inhalation Epidemiology Study on cause-specific hospital admissions, controlling for temperature and ozone. In the second stage, we regressed pollutant-specific slopes from the first stage on pollutant properties. We calculated uncertainty estimates using a bootstrap procedure. We repeated the two-stage analyses using coefficients from first-stage models that included single pollutants plus ozone and meteorological variables only. We based our primary analyses on exposures on day of admission. RESULTS:We found that 24-hr transition metals and alkanes were associated with increased odds [0.26%; 95% confidence interval (CI), 0.02-0.48; and 0.37%; 95% CI, 0.04-0.72, respectively] of hospital admissions for cardiovascular disease (CVD). Transition metals were significantly associated with increased hospital admissions for ischemic heart disease, congestive heart failure, and atrial fibrillation. Increased respiratory-related hospital admissions were significantly associated with alkanes. Aromatics and microcrystalline oxides were significantly associated with decreased CVD- and respiratory-related hospital admissions. CONCLUSIONS:The two-stage approach showed transition metals to be consistently associated with increased odds of CVD-related hospital admissions.
Assessing the association between fine particulate matter (PM) constituents and cardiovascular diseases in a mega-city of Pakistan.
Lu Yi,Lin Shao,Fatmi Zafar,Malashock Daniel,Hussain Mirza M,Siddique Azhar,Carpenter David O,Lin Ziqiang,Khwaja Haider A
Environmental pollution (Barking, Essex : 1987)
Concerning PM concentrations, rapid industrialization, along with increase in cardiovascular disease (CVD) were recorded in Pakistan, especially in urban areas. The degree to which air pollution contributes to the increase in the burden of CVD in Pakistan has not been assessed due to lack of data. This study aims to describe the characteristics of PM constituents and investigate the impact of individual PM constituent on cardiovascular morbidity in Karachi, a mega city in Pakistan. Daily levels of twenty-one constituents of PM were analyzed using samples collected at two sites from fall 2008 to summer 2009 in Karachi. Hospital admission and emergency room visits due to CVD were collected from two large hospitals. Negative Binominal Regression was used to estimate associations between pollutants and the risk of CVD. All PM constituents were assessed in single-pollutant models and selected constituents were assessed in multi-pollutant models adjusting for PM mass and gaseous pollutants. The most common CVD subtypes among our participants were ischemic heart disease, hypertension, heart failure, and cardiomyopathy. Extremely high levels of PM constituents from fossil-fuels combustion and industrial emissions were observed, with notable peaks in winter. The most consistent associations were found between exposure to nickel (5-14% increase per interquartile range) and cardiovascular hospital admissions. Suggestive evidence was also observed for associations between cardiovascular hospital admissions and Al, Fe, Ti, and nitrate. Our findings suggested that PM generated from fossil-fuels combustion and road dust resuspension were associated with the increased risk of CVD in Pakistan.
Inhaled environmental combustion particles cause myocardial injury in the Wistar Kyoto rat.
Kodavanti Urmila P,Moyer Carolyn F,Ledbetter Allen D,Schladweiler Mette C,Costa Daniel L,Hauser Russ,Christiani David C,Nyska Abraham
Toxicological sciences : an official journal of the Society of Toxicology
Epidemiologists have associated particulate matter (PM) air pollution with cardiovascular morbidity and premature mortality worldwide. However, experimental evidence demonstrating causality and pathogenesis of particulate matter (PM)-induced cardiovascular damage has been insufficient. We hypothesized that protracted, repeated inhalation by rats of oil combustion-derived, fugitive emission PM (EPM), similar in metal composition to selected sources of urban air PM, causes exposure duration- and dose-dependent myocardial injury in susceptible rat strains. Zinc was the only primary water-leachable/bioavailable element of this EPM. Male Sprague-Dawley (SD), Wistar Kyoto (WKY), and spontaneously hypertensive (SH) rats were exposed nose-only to EPM (2, 5, or 10 mg/m(3), 6 h/day for 4 consecutive days or 10 mg/m(3), 6 h/day, 1 day/week for 4 or 16 consecutive weeks). Two days following the last EPM exposure, cardiac and pulmonary tissues were examined histologically. The results showed that particle-laden alveolar macrophages were the only pulmonary lesions observed in all three rat strains. However, WKY rats exposed to EPM (10 mg/m(3) 6 h/day, 1 day/week for 16 weeks) demonstrated cardiac lesions with inflammation and degeneration. To further characterize the nature of EPM-associated lesions, more rigorous histopathological and histochemical techniques were employed for WKY and SD rats. We examined the hearts for myocardial degeneration, inflammation, fibrosis, calcium deposits, apoptosis, and the presence of mast cells. Decreased numbers of granulated mast cells, and multifocal myocardial degeneration, chronic-active inflammation, and fibrosis were present in 5 of 6 WKY rats exposed to EPM for 16 weeks. None of these lesions were present in WKY exposed to clean air. EPM-related cardiac lesions were indistinguishable from air-exposed controls in SD and SH rats. This study demonstrates that long-term inhalation exposures to environmentally relevant PM containing bioavailable zinc can cause myocardial injury in sensitive rats. These findings provide supportive evidence for the epidemiological associations of cardiovascular morbidity and ambient PM.
Systemic imbalance of essential metals and cardiac gene expression in rats following acute pulmonary zinc exposure.
Gilmour Peter S,Schladweiler Mette C,Nyska Abraham,McGee John K,Thomas Ronald,Jaskot Richard H,Schmid Judy,Kodavanti Urmila P
Journal of toxicology and environmental health. Part A
It was recently demonstrated that particulate matter (PM) containing water-soluble zinc produces cardiac injury following pulmonary exposure. To investigate whether pulmonary zinc exposure produces systemic metal imbalance and direct cardiac effects, male Wistar Kyoto (WKY) rats (12-14 wk age) were intratracheally (IT) instilled with saline or 2 micromol/kg zinc sulfate. Temporal analysis was performed for systemic levels of essential metals (zinc, copper, and selenium), and induction of zinc transporter-2 (ZT-2) and metallothionein-1 (MT-1) mRNA in the lung, heart, and liver. Additionally, cardiac gene expression profile was evaluated using Affymetrix GeneChips (rat 230A) arrays to identify zinc-specific effects. Pulmonary zinc instillation produced an increase in plasma zinc to approximately 20% at 1 and 4 h postexposure with concomitant decline in the lung levels. At 24 and 48 h postexposure, zinc levels rose significantly (approximately 35%) in the liver. At these time points, plasma and liver levels of copper and selenium also increased significantly, suggesting systemic disturbance in essential metals. Zinc exposure was associated with marked induction of MT-1 and ZT-2 mRNA in lung, heart, and liver, suggesting systemic metal sequestration response. Given the functional role of zinc in hundreds of proteins, the gene expression profiles demonstrated changes that are expected based on its physiological role. Zinc exposure produced an increase in expression of kinases and inhibition of expression of phosphatases; up- or downregulation of genes involved in mitochondrial function; changes in calcium regulatory proteins suggestive of elevated intracellular free calcium and increases in sulfotransferases; upregulation of potassium channel genes; and changes in free radical-sensitive proteins. Some of these expression changes are reflective of a direct effect of zinc on myocardium following pulmonary exposure, which may result in impaired mitochondrial respiration, stimulated cell signaling, altered Ca2+ homeostasis, and increased transcription of sulfotransferases. Cardiotoxicity may be an outcome of acute zinc toxicosis and occupational exposures to metal fumes containing soluble zinc. Imbalance of systemic metal homeostasis as a result of pulmonary zinc exposure may underlie the cause of extrapulmonary effects.
Long-term exposure to constituents of fine particulate air pollution and mortality: results from the California Teachers Study.
Ostro Bart,Lipsett Michael,Reynolds Peggy,Goldberg Debbie,Hertz Andrew,Garcia Cynthia,Henderson Katherine D,Bernstein Leslie
Environmental health perspectives
BACKGROUND:Several studies have reported associations between long-term exposure to ambient fine particulate matter (PM) and cardiovascular mortality. However, the health impacts of long-term exposure to specific constituents of PM(2.5) (PM with aerodynamic diameter < or = 2.5 microm) have not been explored. METHODS:We used data from the California Teachers Study, a prospective cohort of active and former female public school professionals. We developed estimates of long-term exposures to PM(2.5) and several of its constituents, including elemental carbon, organic carbon (OC), sulfates, nitrates, iron, potassium, silicon, and zinc. Monthly averages of exposure were created using pollution data from June 2002 through July 2007. We included participants whose residential addresses were within 8 and 30 km of a monitor collecting PM(2.5) constituent data. Hazard ratios (HRs) were estimated for long-term exposure for mortality from all nontraumatic causes, cardiopulmonary disease, ischemic heart disease (IHD), and pulmonary disease. RESULTS:Approximately 45,000 women with 2,600 deaths lived within 30 km of a monitor. We observed associations of all-cause, cardiopulmonary, and IHD mortality with PM(2.5) mass and each of its measured constituents, and between pulmonary mortality and several constituents. For example, for cardiopulmonary mortality, HRs for interquartile ranges of PM(2.5), OC, and sulfates were 1.55 [95% confidence interval (CI), 1.431.69], 1.80 (95% CI, 1.681.93), and 1.79 (95% CI, 1.582.03), respectively. Subsequent analyses indicated that, of the constituents analyzed, OC and sulfates had the strongest associations with all four outcomes. CONCLUSIONS:Long-term exposures to PM(2.5) and several of its constituents were associated with increased risks of all-cause and cardiopulmonary mortality in this cohort. Constituents derived from combustion of fossil fuel (including diesel), as well as those of crustal origin, were associated with some of the greatest risks. These results provide additional evidence that reduction of ambient PM(2.5) may provide significant public health benefits.
Systemic translocation of (70)zinc: kinetics following intratracheal instillation in rats.
Wallenborn J Grace,Kovalcik Kasey D,McGee John K,Landis Matthew S,Kodavanti Urmila P
Toxicology and applied pharmacology
Mechanisms of particulate matter (PM)-induced cardiotoxicity are not fully understood. Direct translocation of PM-associated metals, including zinc, may mediate this effect. We hypothesized that following a single intratracheal instillation (IT), zinc directly translocates outside of the lungs, reaching the heart. To test this, we used high resolution magnetic sector field inductively coupled plasma mass spectrometry to measure levels of five stable isotopes of zinc ((64)Zn, (66)Zn, (67)Zn, (68)Zn, (70)Zn), and copper in lungs, plasma, heart, liver, spleen, and kidney of male Wistar Kyoto rats (13 weeks old, 250-300 g), 1, 4, 24, and 48 h following a single IT or oral gavage of saline or 0.7 micromol/rat (70)Zn, using a solution enriched with 76.6% (70)Zn. Natural abundance of (70)Zn is 0.62%, making it an easily detectable tracer following exposure. In IT rats, lung (70)Zn was highest 1 h post IT and declined by 48 h. Liver endogenous zinc was increased 24 and 48 h post IT. (70)Zn was detected in all extrapulmonary organs, with levels higher following IT than following gavage. Heart (70)Zn was highest 48 h post IT. Liver, spleen and kidney (70)Zn peaked 4 h following gavage, and 24 h following IT. (70)Zn IT exposure elicited changes in copper homeostasis in all tissues. IT instilled (70)Zn translocates from lungs into systemic circulation. Route of exposure affects (70)Zn translocation kinetics. Our data suggests that following pulmonary exposure, zinc accumulation and subsequent changes in normal metal homeostasis in the heart and other organs could induce cardiovascular injury.
Differential pulmonary and cardiac effects of pulmonary exposure to a panel of particulate matter-associated metals.
Wallenborn J Grace,Schladweiler Mette J,Richards Judy H,Kodavanti Urmila P
Toxicology and applied pharmacology
Biological mechanisms underlying the association between particulate matter (PM) exposure and increased cardiovascular health effects are under investigation. Water-soluble metals reaching systemic circulation following pulmonary exposure are likely exerting a direct effect. However, it is unclear whether specific PM-associated metals may be driving this. We hypothesized that exposure to equimolar amounts of five individual PM-associated metals would cause differential pulmonary and cardiac effects. We exposed male WKY rats (14 weeks old) via a single intratracheal instillation (IT) to saline or 1 micromol/kg body weight of zinc, nickel, vanadium, copper, or iron in sulfate form. Responses were analyzed 4, 24, 48, or 96 h after exposure. Pulmonary effects were assessed by bronchoalveolar lavage fluid levels of total cells, macrophages, neutrophils, protein, albumin, and activities of lactate dehydrogenase, gamma-glutamyl transferase, and n-acetyl glucosaminidase. Copper induced earlier pulmonary injury/inflammation, while zinc and nickel produced later effects. Vanadium or iron exposure induced minimal pulmonary injury/inflammation. Zinc, nickel, or copper increased serum cholesterol, red blood cells, and white blood cells at different time points. IT of nickel and copper increased expression of metallothionein-1 (MT-1) in the lung. Zinc, nickel, vanadium, and iron increased hepatic MT-1 expression. No significant changes in zinc transporter-1 (ZnT-1) expression were noted in the lung or liver; however, zinc increased cardiac ZnT-1 at 24 h, indicating a possible zinc-specific cardiac effect. Nickel exposure induced an increase in cardiac ferritin 96 h after IT. This data set demonstrating metal-specific cardiotoxicity is important in linking metal-enriched anthropogenic PM sources with adverse health effects.
A Case-Crossover Study between Fine Particulate Matter Elemental Composition and Emergency Admission with Cardiovascular Disease.
Huang Zhijun,Zhou Yuqing,Lu Yao,Duan Yizhu,Tang Xiaohong,Deng Qihong,Yuan Hong
Acta Cardiologica Sinica
BACKGROUND:It is generally understood that Fine Particulate Matter (PM) can cause high blood pressure. However, it remains unclear whether there is a relationship between the elemental composition of PM and cardiovascular disease in emergency department patients. METHODS:Crossover design for time stratified cases and conditional logistic regression were used to analyze the correlation between emergency admissions for cerebral hemorrhage, cerebral infarction, TIA (Transient ischemic attack), coronary heart disease and PM, concentrations of chemical element compositions, and Particulate Matter 10 (PM) in Changsha city. RESULTS:When the temperature, atmosphere pressure, maximum wind speed, NO and SO were adjusted, the OR (Odd Ratio) of cerebral hemorrhage was 1.177 [95% confidence interval (CI): 1.006-1.376, p = 0.04] with every10 μg/m increase of PM. PM was unrelated to cardiovascular emergencies (p > 0.05). In addition, with each additional IQR (Interquartile Range) increase of Ni, Zn and Pb concentrations in PM, the values of OR were 1.826 (95% CI: 1.031-3.233), 1.568 (95% CI: 1.015-2.423) and 1.682 (95% CI: 1.010-2.800), respectively. CONCLUSIONS:Concentration rises of nickel, zinc and lead elements for PM in Changsha city were related to the increase of emergency admissions with cerebral hemorrhage.
Long-term Exposure to Particulate Matter Constituents and the Incidence of Coronary Events in 11 European Cohorts.
Wolf Kathrin,Stafoggia Massimo,Cesaroni Giulia,Andersen Zorana Jovanovic,Beelen Rob,Galassi Claudia,Hennig Frauke,Migliore Enrica,Penell Johanna,Ricceri Fulvio,Sørensen Mette,Turunen Anu W,Hampel Regina,Hoffmann Barbara,Kälsch Hagen,Laatikainen Tiina,Pershagen Göran,Raaschou-Nielsen Ole,Sacerdote Carlotta,Vineis Paolo,Badaloni Chiara,Cyrys Josef,de Hoogh Kees,Eriksen Kirsten T,Jedynska Aleksandra,Keuken Menno,Kooter Ingeborg,Lanki Timo,Ranzi Andrea,Sugiri Dorothea,Tsai Ming-Yi,Wang Meng,Hoek Gerard,Brunekreef Bert,Peters Annette,Forastiere Francesco
Epidemiology (Cambridge, Mass.)
BACKGROUND:Long-term exposure to particulate matter (PM) has been associated with increased cardiovascular morbidity and mortality but little is known about the role of the chemical composition of PM. This study examined the association of residential long-term exposure to PM components with incident coronary events. METHODS:Eleven cohorts from Finland, Sweden, Denmark, Germany, and Italy participated in this analysis. 5,157 incident coronary events were identified within 100,166 persons followed on average for 11.5 years. Long-term residential concentrations of PM < 10 μm (PM10), PM < 2.5 μm (PM2.5), and a priori selected constituents (copper, iron, nickel, potassium, silicon, sulfur, vanadium, and zinc) were estimated with land-use regression models. We used Cox proportional hazard models adjusted for a common set of confounders to estimate cohort-specific component effects with and without including PM mass, and random effects meta-analyses to pool cohort-specific results. RESULTS:A 100 ng/m³ increase in PM10 K and a 50 ng/m³ increase in PM2.5 K were associated with a 6% (hazard ratio and 95% confidence interval: 1.06 [1.01, 1.12]) and 18% (1.18 [1.06, 1.32]) increase in coronary events. Estimates for PM10 Si and PM2.5 Fe were also elevated. All other PM constituents indicated a positive association with coronary events. When additionally adjusting for PM mass, the estimates decreased except for K. CONCLUSIONS:This multicenter study of 11 European cohorts pointed to an association between long-term exposure to PM constituents and coronary events, especially for indicators of road dust.
The role of particulate matter-associated zinc in cardiac injury in rats.
Kodavanti Urmila P,Schladweiler Mette C,Gilmour Peter S,Wallenborn J Grace,Mandavilli Bhaskar S,Ledbetter Allen D,Christiani David C,Runge Marschall S,Karoly Edward D,Costa Daniel L,Peddada Shyamal,Jaskot Richard,Richards Judy H,Thomas Ronald,Madamanchi Nageswara R,Nyska Abraham
Environmental health perspectives
BACKGROUND:Exposure to particulate matter (PM) has been associated with increased cardiovascular morbidity; however, causative components are unknown. Zinc is a major element detected at high levels in urban air. OBJECTIVE:We investigated the role of PM-associated zinc in cardiac injury. METHODS:We repeatedly exposed 12- to 14-week-old male Wistar Kyoto rats intratracheally (1x/week for 8 or 16 weeks) to a) saline (control); b) PM having no soluble zinc (Mount St. Helens ash, MSH); or c) whole-combustion PM suspension containing 14.5 microg/mg of water-soluble zinc at high dose (PM-HD) and d ) low dose (PM-LD), e) the aqueous fraction of this suspension (14.5 microg/mg of soluble zinc) (PM-L), or f ) zinc sulfate (rats exposed for 8 weeks received double the concentration of all PM components of rats exposed for 16 weeks). RESULTS:Pulmonary inflammation was apparent in all exposure groups when compared with saline (8 weeks > 16 weeks). PM with or without zinc, or with zinc alone caused small increases in focal subepicardial inflammation, degeneration, and fibrosis. Lesions were not detected in controls at 8 weeks but were noted at 16 weeks. We analyzed mitochondrial DNA damage using quantitative polymerase chain reaction and found that all groups except MSH caused varying degrees of damage relative to control. Total cardiac aconitase activity was inhibited in rats receiving soluble zinc. Expression array analysis of heart tissue revealed modest changes in mRNA for genes involved in signaling, ion channels function, oxidative stress, mitochondrial fatty acid metabolism, and cell cycle regulation in zinc but not in MSH-exposed rats. CONCLUSION:These results suggest that water-soluble PM-associated zinc may be one of the causal components involved in PM cardiac effects.
Effects of long-term exposure to particulate matter and metal components on mortality in the Rome longitudinal study.
Badaloni Chiara,Cesaroni Giulia,Cerza Francesco,Davoli Marina,Brunekreef Bert,Forastiere Francesco
BACKGROUND:The effect of long-term exposure to metal components in particulate matter on mortality are still controversial. OBJECTIVES:To study the association between long-term exposure to PM, PM, PM absorbance, particulate matter components (copper, iron, zinc, sulfur, silicon, potassium, nickel, and vanadium) and non-accidental, cardiovascular (CVD), and ischemic heart disease (IHD) mortality. METHODS:All 30+ year olds from the Rome Longitudinal Study were followed for vital status from October 2001 until December 2010. We used land use regression models to estimate annual average concentrations at residences and Cox models to estimate the associations between pollutants and cause-specific mortality, adjusting for individual and contextual characteristics. Hazard ratios (HRs) were expressed per increments equal to the 5-95 percentile range of each pollutant distribution. RESULTS:We analyzed 1,249,108 residents and found strong associations between all exposure indicators and mortality. We observed higher mortality risk with increasing exposure to PM absorbance (HR=1.05; 95% CI: 1.03-1.06) and to tracers of non-tailpipe traffic emissions such as tire and brake wear (Cu, Fe, and Zn); for PMZn, we found HR=1.06 (95% CI: 1.04-1.08) for non-accidental mortality, HR=1.07 (95% CI: 1.04-1.10) for CVD, and HR=1.11 (95% CI: 1.06-1.16) for IHD mortality. With increasing levels of nickel in PM, we found HR=1.07 (95% CI: 1.05-1.09) for non-accidental mortality, HR=1.08 (95% CI: 1.05-1.11) for CVD, and HR=1.13 (95% CI: 1.08-1.18) for IHD mortality. Results were robust when we adjusted for PM mass and for cardiovascular mortality when we adjusted for NO. CONCLUSIONS:In addition to vehicular exhaust pollutants, PM related to non-tailpipe emissions and mixed oil burning/industry plays an important role in mortality.
Long-term effects of elemental composition of particulate matter on inflammatory blood markers in European cohorts.
Hampel Regina,Peters Annette,Beelen Rob,Brunekreef Bert,Cyrys Josef,de Faire Ulf,de Hoogh Kees,Fuks Kateryna,Hoffmann Barbara,Hüls Anke,Imboden Medea,Jedynska Aleksandra,Kooter Ingeborg,Koenig Wolfgang,Künzli Nino,Leander Karin,Magnusson Patrik,Männistö Satu,Penell Johanna,Pershagen Göran,Phuleria Harish,Probst-Hensch Nicole,Pundt Noreen,Schaffner Emmanuel,Schikowski Tamara,Sugiri Dorothea,Tiittanen Pekka,Tsai Ming-Yi,Wang Meng,Wolf Kathrin,Lanki Timo,
BACKGROUND:Epidemiological studies have associated long-term exposure to ambient particulate matter with increased mortality from cardiovascular and respiratory disorders. Systemic inflammation is a plausible biological mechanism behind this association. However, it is unclear how the chemical composition of PM affects inflammatory responses. OBJECTIVES:To investigate the association between long-term exposure to elemental components of PM and the inflammatory blood markers high-sensitivity C-reactive protein (hsCRP) and fibrinogen as part of the European ESCAPE and TRANSPHORM multi-center projects. METHODS:In total, 21,558 hsCRP measurements and 17,428 fibrinogen measurements from cross-sections of five and four cohort studies were available, respectively. Residential long-term concentrations of particulate matter <10μm (PM10) and <2.5μm (PM2.5) in diameter and selected elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium, zinc) were estimated based on land-use regression models. Associations between components and inflammatory markers were estimated using linear regression models for each cohort separately. Cohort-specific results were combined using random effects meta-analysis. As a sensitivity analysis the models were additionally adjusted for PM mass. RESULTS:A 5ng/m(3) increase in PM2.5 copper and a 500ng/m(3) increase in PM10 iron were associated with a 6.3% [0.7; 12.3%] and 3.6% [0.3; 7.1%] increase in hsCRP, respectively. These associations between components and fibrinogen were slightly weaker. A 10ng/m(3) increase in PM2.5 zinc was associated with a 1.2% [0.1; 2.4%] increase in fibrinogen; confidence intervals widened when additionally adjusting for PM2.5. CONCLUSIONS:Long-term exposure to transition metals within ambient particulate matter, originating from traffic and industry, may be related to chronic systemic inflammation providing a link to long-term health effects of particulate matter.
Oxidative potential and inflammatory impacts of source apportioned ambient air pollution in Beijing.
Liu Qingyang,Baumgartner Jill,Zhang Yuanxun,Liu Yanju,Sun Yongjun,Zhang Meigen
Environmental science & technology
Air pollution exposure is associated with a range of adverse health impacts. Knowledge of the chemical components and sources of air pollution most responsible for these health effects could lead to an improved understanding of the mechanisms of such effects and more targeted risk reduction strategies. We measured daily ambient fine particulate matter (<2.5 μm in aerodynamic diameter; PM2.5) for 2 months in peri-urban and central Beijing, and assessed the contribution of its chemical components to the oxidative potential of ambient air pollution using the dithiothreitol (DTT) assay. The composition data were applied to a multivariate source apportionment model to determine the PM contributions of six sources or factors: a zinc factor, an aluminum factor, a lead point factor, a secondary source (e.g., SO4(2-), NO3(2-)), an iron source, and a soil dust source. Finally, we assessed the relationship between reactive oxygen species (ROS) activity-related PM sources and inflammatory responses in human bronchial epithelial cells. In peri-urban Beijing, the soil dust source accounted for the largest fraction (47%) of measured ROS variability. In central Beijing, a secondary source explained the greatest fraction (29%) of measured ROS variability. The ROS activities of PM collected in central Beijing were exponentially associated with in vivo inflammatory responses in epithelial cells (R2=0.65-0.89). We also observed a high correlation between three ROS-related PM sources (a lead point factor, a zinc factor, and a secondary source) and expression of an inflammatory marker (r=0.45-0.80). Our results suggest large differences in the contribution of different PM sources to ROS variability at the central versus peri-urban study sites in Beijing and that secondary sources may play an important role in PM2.5-related oxidative potential and inflammatory health impacts.
Exposure to ambient and nonambient components of particulate matter: a comparison of health effects.
Ebelt Stefanie T,Wilson William E,Brauer Michael
Epidemiology (Cambridge, Mass.)
BACKGROUND:Numerous epidemiologic studies report associations between outdoor concentrations of particles and adverse health effects. Because personal exposure to particles is frequently dominated by exposure to nonambient particles (those originating from indoor sources), we present an approach to evaluate the relative impacts of ambient and nonambient exposures. METHODS:We developed separate estimates of exposures to ambient and nonambient particles of different size ranges (PM2.5, PM10-2.5 and PM10) based on time-activity data and the use of particle sulfate measurements as a tracer for indoor infiltration of ambient particles. To illustrate the application of these estimates, associations between cardiopulmonary health outcomes and the estimated exposures were compared with associations computed using measurements of personal exposures and outdoor concentrations for a repeated-measures panel study of 16 patients with chronic obstructive pulmonary disease conducted in the summer of 1998 in Vancouver. RESULTS:Total personal fine particle exposures were dominated by exposures to nonambient particles, which were not correlated with ambient fine particle exposures or ambient concentrations. Although total and nonambient particle exposures were not associated with any of the health outcomes, ambient exposures (and to a lesser extent ambient concentrations) were associated with decreased lung function, decreased systolic blood pressure, increased heart rate, and increased supraventricular ectopic heartbeats. Measures of heart rate variability showed less consistent relationships among the various exposure metrics. CONCLUSIONS:These results demonstrate the usefulness of separating total personal particle exposures into their ambient and nonambient components. The results support previous epidemiologic findings using ambient concentrations by demonstrating an association between health outcomes and ambient (outdoor origin) particle exposures but not with nonambient (indoor origin) particle exposures.
Pulmonary retention of particulate matter is associated with airway inflammation in allergic rats exposed to air pollution in urban Detroit.
Morishita Masako,Keeler Gerald,Wagner James,Marsik Frank,Timm Edward,Dvonch J,Harkema Jack
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.
Summer-winter differences of PM toxicity to human alveolar epithelial cells (A549) and the roles of transition metals.
Chen Yan,Luo Xiao-San,Zhao Zhen,Chen Qi,Wu Di,Sun Xue,Wu Lichun,Jin Ling
Ecotoxicology and environmental safety
Atmospheric fine particulate matters (PM) induce adverse human health effects through inhalation, and the harmful effects of PM are determined not only by its air concentrations, but also by the particle components varied temporally. To investigate seasonal differences of the aerosol toxicity effects including cell viability and membrane damage, cell oxidative stress and responses of inflammatory cytokines, the human lung epithelial cells (A549) were exposed to PM samples collected in both summer and winter by the in vitro toxicity bioassays. Toxicological results showed that, the PM led to the cell viability decrease, cell membrane injury, oxidative stress level increase and inflammatory responses in a dose-dependent manner. Temporally, the cytotoxicity of winter PM was higher than summer of this studied industrial area of Nanjing, China. According to the different contents of heavy metals accumulated in PM, the transition metals such as Cu might be an important contributor to the aerosol cell toxicity.
PM-bound metal metabolic distribution and coupled lipid abnormality at different developmental windows.
Ku Tingting,Zhang Yingying,Ji Xiaotong,Li Guangke,Sang Nan
Environmental pollution (Barking, Essex : 1987)
Atmospheric fine particulate matter (PM) is a serious threat to human health. As a toxicant constituent, metal leads to significant health risks in a population, but exposure to PM-bound metals and their biological impacts are not fully understood. In this study, we determined the metal contents of PM samples collected from a typical coal-burning city and then investigated the metabolic distributions of six metals (Zn, Pb, Mn, As, Cu, and Cd) following PM inhalation in mice in different developmental windows. The results indicate that fine particles were mainly deposited in the lung, but PM-bound metals could reach and gather in secondary off-target tissues (the lung, liver, heart and brain) with a developmental window-dependent property. Furthermore, elevations in triglycerides and cholesterol levels in sensitive developmental windows (the young and elderly stages) occurred, and significant associations between metals (Pb, Mn, As and Cd) and cholesterol in the heart, brain, liver and lung were observed. These findings suggest that PM inhalation caused selective metal metabolic distribution in tissues with a developmental window-dependent property and that the effects were associated with lipid alterations. This provides a foundation for the underlying systemic toxicity following PM exposure based on metal components.
Seasonal variations in chemical composition and in vitro biological effects of fine PM from Milan.
Perrone Maria Grazia,Gualtieri Maurizio,Ferrero Luca,Lo Porto Claudia,Udisti Roberto,Bolzacchini Ezio,Camatini Marina
Fine particulate matter (PM1 and PM2.5) was collected in Milan over the summer (August-September) and winter (January-March) seasons of 2007/2008. Particles were analyzed for their chemical composition (inorganic ions, elements and PAHs) and the effects produced on the human lung carcinoma epithelial cell line A549. In vitro tests were performed to assess cell viability with MTT assay, cytokine release (IL-6 and IL-8) with ELISA, and DNA damage with COMET assay. Results were investigated by bivariate analysis and multivariate data analysis (Principal Component Analysis, PCA) to investigate the relationship between PM chemical composition and the biological effects produced by cell exposure to 12 microg cm(-2). The different seasonal chemical composition of PM showed to influence some biological properties. Summer PM samples had a high mass contribution of SO(4)(=) (13+/-2%) and were enriched in some elements, like Al, As, Cr, Cu, and Zn, compared to winter PM samples. Cell viability reduction was two times higher for summer PM samples in comparison with winter ones (27+/-5% and 14+/-5%, respectively), and the highest correlation coefficients between cell viability reduction and single chemical components were with As (R(2)=0.57) and SO(4)(=) (R(2)=0.47). PM1 affected cell viability reduction and induced IL-8 release, and these events were interrelated (R(2)=0.95), and apparently connected with the same chemical compounds. PM2.5 fraction, which was enriched in Ca(++) and Mg(++) (from soil dust), and Al, Fe, Zn, Ba Mn, produced cell viability reduction and DNA damage (R(2)=0.73).
[Fine particulate matter - a health hazard for lungs and other organs?].
Pneumologie (Stuttgart, Germany)
BACKGROUND:Epidemiological studies provide evidence that particulate air pollution (PM10) increases pulmonary as well as cardiovascular mortality. This review summarises current hypotheses on the mechanisms of entry of inhaled fine particles into the systemic circulation and the mechanisms of action on the cardiovascular system. PARTICLE ENTRY:Following particle deposition in the lungs, soluble components like metal salts or soluble organics are taken up into the pulmonary capillary blood. Ultrafine particles can pass the lung-blood barrier by endocytosis, transcytosis, or stochastic transport, depending on their physicochemical properties, and a fraction (0.1 - 1 %) is thus dislocated into the systemic circulation. MECHANISMS OF ACTION:Direct actions of translocated particles, soluble compounds and/or inflammatory mediators have been shown to alter cardiovascular homeostasis. Effects associated with high PM10 are arrhythmias, myocardial infarction, and cardiac failure. Cardiovascular regulation may be impaired by autonomic imbalances such as those caused by inflammatory or stress-related processes. Local or systemic inflammatory responses may cause endothelial dysfunction, a procoagulatory state with the risk of enhanced atherosclerosis. Cardiac function may be impaired by alterations in ion channel functions leading to electrophysiological instability. OUTLOOK:Systemic actions of inhaled particles are an important issue in environmental health, and there is evidence that they are in no way limited to the cardiovascular system, but also affect other organs like the brain. Details on particle translocation mechanisms and pathophysiological pathways of action remain to be elucidated.
Toxicity of coarse and fine particulate matter from sites with contrasting traffic profiles.
Gerlofs-Nijland Miriam E,Dormans Jan A M A,Bloemen Henk J T,Leseman Daan L A C,John A,Boere F,Kelly Frank J,Mudway Ian S,Jimenez Al A,Donaldson Ken,Guastadisegni Cecilia,Janssen Nicole A H,Brunekreef Bert,Sandström Thomas,van Bree Leendert,Cassee Flemming R
Residence in urban areas with much traffic has been associated with various negative health effects. However, the contribution of traffic emissions to these adverse health effects has not been fully determined. Therefore, the objective of this in vivo study is to compare the pulmonary and systemic responses of rats exposed to particulate matter (PM) obtained from various locations with contrasting traffic profiles. Samples of coarse (2.5 microm-10 microm) and fine (0.1 microm-2.5 microm) PM were simultaneously collected at nine sites across Europe with a high-volume cascade impactor. Six PM samples from various locations were selected on the basis of contrast in in vitro analysis, chemical composition, and traffic profiles. We exposed spontaneously hypertensive (SH) rats to a single dose (3 mg PM/kg body weight or 10 mg PM/kg body weight) of either coarse or fine PM by intratracheal instillation. We assessed changes in biochemical markers, cell differentials, and histopathological changes in the lungs and blood 24 h postexposure. The dose-related adverse effects that both coarse and fine PM induced in the lungs and vascular system were mainly related to cytotoxicity, inflammation, and blood viscosity. We observed clear differences in the extent of these responses to PM from the various locations at equivalent dose levels. There was a trend that suggests that samples from high-traffic sites were the most toxic. It is likely that the toxicological responses of SH rats were associated with specific PM components derived from brake wear (copper and barium), tire wear (zinc), and wood smoke (potassium).
Metal composition of fine particulate air pollution and acute changes in cardiorespiratory physiology.
Cakmak Sabit,Dales Robert,Kauri Lisa Marie,Mahmud Mamun,Van Ryswyk Keith,Vanos Jennifer,Liu Ling,Kumarathasan Premkumari,Thomson Errol,Vincent Renaud,Weichenthal Scott
Environmental pollution (Barking, Essex : 1987)
BACKGROUND:Studying the physiologic effects of components of fine particulate mass (PM2.5) could contribute to a better understanding of the nature of toxicity of air pollution. OBJECTIVES:We examined the relation between acute changes in cardiovascular and respiratory function, and PM2.5-associated-metals. METHODS:Using generalized linear mixed models, daily changes in ambient PM2.5-associated metals were compared to daily changes in physiologic measures in 59 healthy subjects who spent 5-days near a steel plant and 5-days on a college campus. RESULTS:Interquartile increases in calcium, cadmium, lead, strontium, tin, vanadium and zinc were associated with statistically significant increases in heart rate of 1-3 beats per minute, increases of 1-3 mmHg in blood pressure and/or lung function decreases of up to 4% for total lung capacity. CONCLUSION:Metals contained in PM2.5 were found to be associated with acute changes in cardiovascular and respiratory physiology.
Effects of thoracic and fine PM and their components on heart rate and pulmonary function in COPD patients.
Hsu Sha O-I,Ito Kazuhiko,Lippmann Morton
Journal of exposure science & environmental epidemiology
Population-based personal exposures to particulate matter (PM) and personal-ambient relationships of PM and component concentrations for outpatients with COPD and/or asthma were investigated in New York City (NYC) and Seattle for thoracic PM (PM(10)) and fine PM (PM(2.5)). Measurements of outdoor, indoor, and personal PM(10) and PM(2.5) concentrations were made concurrently for 12-consecutive days at 24 patients' residences. Filters were analyzed for elemental components, using XRF and black carbon (BC), by reflectance. Daily morning and evening measurements of heart rate (HR) and blood oxygen saturation (SpO(2)) by pulse oximeter, and forced expiratory volume in 1 s (FEV(1)) and peak expiratory flowrate (PEF) by spirometry were also measured, and symptom data were collected. Central monitoring site, outdoor, indoor, and personal concentration-response relationships of PM(2.5), PM(10-2.5), and their components were examined using mixed-effect models. The relatively small sample size of the study limited the interpretation of results, but of the PM chemical components examined, only nickel concentrations showed consistent associations, and only with HR in the NYC COPD patients.
The characteristics of coarse particulate matter air pollution associated with alterations in blood pressure and heart rate during controlled exposures.
Morishita Masako,Bard Robert L,Wang Lu,Das Ritabrata,Dvonch J Timothy,Spino Catherine,Mukherjee Bhramar,Sun Qinghua,Harkema Jack R,Rajagopalan Sanjay,Brook Robert D
Journal of exposure science & environmental epidemiology
Although fine particulate matter (PM) air pollution <2.5 μm in aerodynamic diameter (PM2.5) is a leading cause of global morbidity and mortality, the potential health effects of coarse PM (2.5-10 μm in aerodynamic diameter; PM10-2.5) remain less clearly understood. We aimed to elucidate the components within coarse PM most likely responsible for mediating these hemodynamic alterations. Thirty-two healthy adults (25.9 ± 6.6 years) were exposed to concentrated ambient coarse PM (CAP) (76.2 ± 51.5 μg/m(3)) and filtered air (FA) for 2 h in a rural location in a randomized double-blind crossover study. The particle constituents (24 individual elements, organic and elemental carbon) were analyzed from filter samples and associated with the blood pressure (BP) and heart rate (HR) changes occurring throughout CAP and FA exposures in mixed model analyses. Total coarse PM mass along with most of the measured elements were positively associated with similar degrees of elevations in both systolic BP and HR. Conversely, total PM mass was unrelated, whereas only two elements (Cu and Mo) were positively associated with and Zn was inversely related to diastolic BP changes during exposures. Inhalation of coarse PM from a rural location rapidly elevates systolic BP and HR in a concentration-responsive manner, whereas the particulate composition does not appear to be an important determinant of these responses. Conversely, exposure to certain PM elements may be necessary to trigger a concomitant increase in diastolic BP. These findings suggest that particulate mass may be an adequate metric of exposure to predict some, but not all, hemodynamic alterations induced by coarse PM mass.
Reduced in vitro toxicity of fine particulate matter collected during the 2008 Summer Olympic Games in Beijing: the roles of chemical and biological components.
Shang Yu,Zhu Tong,Lenz Anke-Gabriele,Frankenberger Birgit,Tian Feng,Chen Chenyong,Stoeger Tobias
Toxicology in vitro : an international journal published in association with BIBRA
Beijing has implemented systematic air pollution control legislation to reduce particulate emissions and improve air quality during the 2008 Summer Olympics, but whether the toxicity of fine fraction of particles (PM(2.5)) would be changed remains unclear. In present study we compared in vitro biological responses of PM(2.5) collected before and during the Olympics and tried to reveal possible correlations between its chemical components and toxicological mechanism(s). We measured cytotoxicity, cytokines/chemokines, and related gene expressions in murine alveolar macrophages, MH-S, after treated with 20 PM(2.5) samples. Significant, dose-dependent effects on cell viability, cytokine/chemokine release and mRNA expressions were observed. The cytotoxicity caused at equal mass concentration of PM(2.5) was notably reduced (p<0.05) by control measures, and significant association was found for viability and elemental zinc in PM(2.5). Endotoxin content in PM(2.5) correlated with all of the eight detected cytokines/chemokines; elemental and organic carbon correlated with four; arsenic and chromium correlated with six and three, respectively; iron and barium showed associations with two; nickel, magnesium, potassium, and calcium showed associations with one. PM(2.5) toxicity in Beijing was substantially dependent on its chemical components, and lowering the levels of specific components in PM(2.5) during the 2008 Olympics resulted in reduced biological responses.
Short-Term Effects of Carbonaceous Components in PM on Pulmonary Function: A Panel Study of 37 Chinese Healthy Adults.
Huang Shichun,Feng Huan,Zuo Shanshan,Liao Jingling,He Mingquan,Shima Masayuki,Tamura Kenji,Li Yang,Ma Lu
International journal of environmental research and public health
OBJECTIVES:To explore the health effects of indoor/outdoor carbonaceous compositions in PM on pulmonary function among healthy students living in the local university campus. METHODS:Daily peak expiratory flow (PEF) and forced expiratory volume in 1 second (FEV) were measured among 37 healthy students in the morning and evening for four two-week periods. Concurrent concentrations of indoor and outdoor PM (particulate matter with an aerodynamic diameter ≤ 2.5μm), carbonaceous components in PM, ambient temperature, and relative humidity in the study area were also obtained. Mixed-effects model was applied to evaluate the associations between carbonaceous components and lung function. Different lags for the carbonaceous components were investigated. RESULTS:In single-pollutant model, a 10 μg/m increase of indoor and outdoor EC (elemental carbon) associated with -3.93 (95%: -6.89, -0.97) L/min and -3.21 (95%: -5.67, -0.75) L/min change in evening PEF at lag 0 day, respectively. Also, a 10 μg/m increase of indoor and outdoor POC (primary organic carbon) concentration was significantly associated with -5.82 (95%: -10.82, -0.81) L/min and -7.32 (95%: -12.93, -1.71) L/min change of evening PEF at lag 0 day. After adjusting total mass of PM, indoor EC consistently had a significant adverse impact on evening PEF and FEV at lag3 day and a cumulative effect at lag0-3 day. CONCLUSIONS:This study suggests that carbonaceous components in PM indeed have impacts on pulmonary function among healthy young adults especially on evening PEF. Thus, the local mitigation strategies on pollution are needed.
In vitro particulate matter exposure causes direct and lung-mediated indirect effects on cardiomyocyte function.
Gorr Matthew W,Youtz Dane J,Eichenseer Clayton M,Smith Korbin E,Nelin Timothy D,Cormet-Boyaka Estelle,Wold Loren E
American journal of physiology. Heart and circulatory physiology
Particulate matter (PM) exposure induces a pathological response from both the lungs and the cardiovascular system. PM is capable of both manifestation into the lung epithelium and entrance into the bloodstream. Therefore, PM has the capacity for both direct and lung-mediated indirect effects on the heart. In the present studies, we exposed isolated rat cardiomyocytes to ultrafine particulate matter (diesel exhaust particles, DEP) and examined their contractile function and calcium handling ability. In another set of experiments, lung epithelial cells (16HBE14o- or Calu-3) were cultured on permeable supports that allowed access to both the basal (serosal) and apical (mucosal) media; the basal media was used to culture cardiomyocytes to model the indirect, lung-mediated effects of PM on the heart. Both the direct and indirect treatments caused a reduction in contractility as evidenced by reduced percent sarcomere shortening and reduced calcium handling ability measured in field-stimulated cardiomyocytes. Treatment of cardiomyocytes with various anti-oxidants before culture with DEP was able to partially prevent the contractile dysfunction. The basal media from lung epithelial cells treated with PM contained several inflammatory cytokines, and we found that monocyte chemotactic protein-1 was a key trigger for cardiomyocyte dysfunction. These results indicate the presence of both direct and indirect effects of PM on cardiomyocyte function in vitro. Future work will focus on elucidating the mechanisms involved in these separate pathways using in vivo models of air pollution exposure.
Panel studies of air pollution in patients with COPD: Systematic review and meta-analysis.
Bloemsma Lizan D,Hoek Gerard,Smit Lidwien A M
BACKGROUND:Epidemiological studies have shown an increase in morbidity and mortality rates in patients with chronic obstructive pulmonary disease (COPD) following exposure to elevated levels of air pollution. Panel studies have been used to assess short-term effects of air pollution which are not detected by registry studies, specifically lung function and symptoms. The aim of this systematic review was to assess the evidence of panel studies on acute effects of air pollution among patients with COPD. METHODS:We searched the PubMed database, and identified additional studies by inspecting reference lists and literature reviews. We identified and summarized 25 panel studies that were published between 1993 and February 2016. Results were presented in forest plots and effect estimates of sufficiently comparable outcomes and pollutants were summarized by a random-effects meta-analysis. RESULTS:Meta-analysis showed that a 10µg/m increase in ambient levels of particles less than 10µm in diameter (PM) had a small, but statistically significant impact on FEV (-3.38mL, 95% CI -6.39 to -0.37) and PEF (-0.61L/min, -1.20 to -0.01). There was significant heterogeneity across the included studies. A forest plot showing associations between PM and respiratory symptoms was also suggestive of an adverse effect of particulate air pollution, but this was not formally tested in a meta-analysis due to the heterogeneity of outcomes. Results for gaseous pollutants were inconsistent for lung function or symptoms. CONCLUSIONS:Evidence from the identified panel studies indicated statistically significant associations of particulate matter air pollution with lung function in patients with COPD.
COPD Patients as Vulnerable Subpopulation for Exposure to Ambient Air Pollution.
Heinrich Joachim,Schikowski Tamara
Current environmental health reports
PURPOSE OF REVIEW:The prevalence of chronic obstructive pulmonary disease (COPD) is increasing worldwide with no known cure and an increasing number of triggers that exacerbate symptoms and speed up progression. This review aims to summarize the evidence for COPD patients being more vulnerable to air pollution exposure assessed as acute effects. RECENT FINDINGS:Several recent systematic reviews show consistently increased risks for COPD mortality and COPD hospital admission, ranging between 2 and 3% with increasing PM or PM. Similar adverse impacts were shown for NO Also adverse health effects among COPD patients were also found for other gaseous pollutants such as ozone and SO; most of these studies could not be included in the meta-analysis we reviewed. Data from ten panel studies of COPD patients reported a small but statistically significant decline of FEV1 [- 3.38 mL (95% CI - 6.39 to - 0.37)] per increment of 10 μg/m PM, supporting an impact on respiratory health with increasing PM exposure. The combined information from systematic reviews and more recent findings lead us to conclude that COPD patients are more vulnerable to ambient air pollution than healthier people.