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Case-Crossover Analysis of Air Pollution and Cardiorespiratory Hospitalizations: Using Routinely Collected Health and Environmental Data for Tracking: Science and Data
Abstract
From the early 1900s until its closure in February 1998, a Steel coke oven in Pittsburgh, Pennsylvania, was a key source of air pollution. A case-crossover study was performed to assess the associations between daily air pollution and cardiorespiratory (International Classification of Disease Ninth Revision [ICD-9]: 390-519) hospitalizations before and after plant closure and to evaluate how closure influenced these associations.
Air pollution data, climatic data, and cardiorespiratory hospitalizations among residents ages 65 years and older were obtained for the period of 1996 through 2000 for the study area. Data were analyzed using a case-crossover design and conditional logistical regression. Two distinct referent-sampling approaches were compared.
Significant associations were observed between the fourth quartile in PM10 and cardiorespiratory hospitalizations (odds ratio [OR]: 1.12; 95% CI: 1.02-1.23) and cardiovascular hospitalizations only (ICD-9: 390-459) (OR: 1.13; 95% CI: 1.01-1.26) before the plant closure. After closure of the plant, PM10 was not significantly associated with cardiorespiratory or cardiovascular disease hospitalizations. Moreover, the referent sampling approaches did not greatly alter the estimations in the case-crossover analysis.
Existing secondary data are an economical source to assess the impact of point source pollution on the environmental landscape. The findings suggest that closure of the steel coke plant was associated with a reduction risk of the cardiovascular hospitalizations.
... Overall, a majority of the articles focused on outdoor air pollution and accounted for 37% of publications in this category. The articles that demonstrated a specific adverse health outcome or health effect associated with outdoor air pollution is as follows: asthma (38%), 14,19,42,43,48,55,66,69 acute myocardial infarction (19%), 14,57,58,69 cancer (10%), 21,34 adverse birth or reproductive outcomes (10%), 68,75 other respiratory diseases (10%), 42,56 and other cardiovascular disease outcomes (10%). 61,68 Nine percent of the articles in the Science and Research category focused on water contaminants. ...
... 61,68 Nine percent of the articles in the Science and Research category focused on water contaminants. Two of these articles * References 8,9,11,[13][14][15][16][19][20][21][22][23][26][27][28][29]31,[33][34][35]39,[41][42][43][44][48][49][50][53][54][55][56][57][58][59][60][61][62][63][64][65][66][67][68][69]72,[74][75][76][77][78][79][80][81][82][83][84] discussed contaminants in water and the association with health effects. 33,35 One article associated nitrates in surface water with cardiovascular disease, 33 and the other associated trichloroethylene in ground water with cancer. ...
... Overall, a majority of the articles focused on outdoor air pollution and accounted for 37% of publications in this category. The articles that demonstrated a specific adverse health outcome or health effect associated with outdoor air pollution is as follows: asthma (38%), 14,19,42,43,48,55,66,69 acute myocardial infarction (19%), 14,57,58,69 cancer (10%), 21,34 adverse birth or reproductive outcomes (10%), 68,75 other respiratory diseases (10%), 42,56 and other cardiovascular disease outcomes (10%). 61,68 Nine percent of the articles in the Science and Research category focused on water contaminants. ...
... 61,68 Nine percent of the articles in the Science and Research category focused on water contaminants. Two of these articles * References 8,9,11,[13][14][15][16][19][20][21][22][23][26][27][28][29]31,[33][34][35]39,[41][42][43][44][48][49][50][53][54][55][56][57][58][59][60][61][62][63][64][65][66][67][68][69]72,[74][75][76][77][78][79][80][81][82][83][84] discussed contaminants in water and the association with health effects. 33,35 One article associated nitrates in surface water with cardiovascular disease, 33 and the other associated trichloroethylene in ground water with cancer. ...
The creation of the Centers for Disease Control and Prevention Environmental Public Health Tracking Program spawned an invigorating and challenging approach toward implementing the nation's first population-based, environmental disease tracking surveillance system. More than 10 years have passed since its creation and an abundance of peer-reviewed articles have been published spanning a broad variety of public health topics related primarily to the goal of reducing diseases of environmental origin.
To evaluate peer-reviewed literature related to Environmental Public Health Tracking during 2002-2012, recognize major milestones and challenges, and offer recommendations.
A narrative overview was conducted using titles and abstracts of peer-reviewed articles, key word searches, and science-based search engine databases.
Eighty published articles related to "health tracking" were identified and categorized according to 4 crossed-central themes. The Science and Research theme accounted for the majority of published articles, followed by Policy and Practice, Collaborations Among Health and Environmental Programs, and Network Development.
Overall, progress was reported in the areas of data linkage, data sharing, surveillance methods, and network development. Ongoing challenges included formulating better ways to establish the connections between health and the environment, such as using biomonitoring, public water systems, and private well water data. Recommendations for future efforts include use of data to inform policy and practice and use of electronic health records data for environmental health surveillance.
... Stroke might also be increasing, consequently causing extra demands and burdens on the current health care system; however, its etiology is still poorly understood [2,3] . Many epidemiological studies have shown deleterious effects of air pollution on health such as on cardiovascular morbidity and mortality [4][5][6][7] . More recently, the potential importance of ambient air pollution as a modifiable risk factor for stroke has been recognized [8] . ...
... Because we only examined the effect of air pollutants within a 4-day window, it is possible that we missed some stronger lag effects at later days. However, Xu 6 previous studies show that the effects of air pollution are relatively acute and occur within the first few days [8,18,21] . For the most part, our results revolved around 1.00 with very small confidence intervals, indicating that this may not be clinically significant. ...
Background:
Epidemiological studies have shown adverse short-term effects of air pollution on health including cardiovascular morbidity and mortality. However, air pollution-related stroke has received less attention.
Methods:
In this study, we performed a time-stratified case-crossover analysis to evaluate the relationships between stroke hospital admissions and O3, among patients aged 65 years and older in Allegheny County, Pa., USA, between 1994 and 2000. We also examined whether the effects of air pollutants differed across strata defined by patient demographic characteristics and ambient temperature.
Results:
Exposures to O3 on the current day increase the risk of total stroke hospitalization by 1.9% (95% CI: 0.01-3.8) per interquartile range increase in concentration. Furthermore, the results suggest that males were more sensitive to adverse health effects of O3 on stroke hospitalization than females.
Conclusion:
These results suggest that O3 has an adverse effect on stroke hospitalization. Specific patient subgroups, such as males, may be at increased risk.
... Figure 1 schematically depicts the results obtained in the bibliographic search. Of the total of 105 reports retrieved as a result of the bibliographic search, 24 addressed methodological aspects of CCO design Schwartz 1999, 2001;Figueiras et al. 2005;Fung et al. 2003;Hajat 2003;Jaakkola 2003;Janes et al. 2005aJanes et al. , 2005bSchindler 2005a, 2005b;Lee et al. 2000;Levy et al. 2001a;Lu et al. 2008;Lu and Zeger 2007;Lumley and Levy 2000;Maclure 1991;Maclure and Mittleman 2008;Marshall and Jackson 1993;Mittleman 2005, Navidi 1998Navidi et al. 1999;Navidi and Weinhandl 2002;Peters et al. 2006;Sheppard et al. 2001); the remaining studies applied CCO designs to study the relationship between different air pollutants and different outcome variables in terms of human health (Barnett et al. 2005(Barnett et al. , 2006Bateson and Schwartz 2004;Boutin-Forzano et al. 2004;Carracedo-Martinez et al. 2008;Chang et al. 2005;Checkoway et al. 2000;Cheng et al. 2007;D'ippoliti et al. 2003;Filleul et al. 2004;Forastiere et al. 2005Forastiere et al. , 2007Henrotin et al. 2007;Hinwood et al. 2006;Jalaludin et al. 2008;Johnston et al. 2007;Kan and Chen 2003;Karr et al. 2006;Kim et al. 2007;Kwon et al. 2001;Laurent et al. 2008;Lee and Schwartz 1999;Lee et al. 2007aLee et al. , 2007bLee et al. , 2008Levy et al. 2001b;Lin et al. 2002Lin et al. , 2003Lin et al. , 2005Ljungman et al. 2008;Luginaah et al. 2005;Maynard et al. 2007;Medina-Ramón et al. 2006;Neas et al. 1999;Peel et al. 2007;Perez et al. 2008;Peters et al. 2001Peters et al. , 2005Pope et al. 2006Pope et al. , 2008Rich et al. 2004Rich et al. , 2005Rich et al. , 2006aRich et al. , 2006bRomieu et al. 2004;Ruidavets et al. 2005;Schwartz 2004aSchwartz , 2004bSchwartz , 2005Ségala et al. 2008;Son et al. 2008;Stafoggia et al. 2008;Sullivan et al. 2003Sullivan et al. , 2005Sunyer and Basagana 2001;Sunyer et al. 2000Sunyer et al. , 2002Symons et al. 2006;Tecer et al. 2008;Tsai et al. 2003aTsai et al. , 2003bTsai et al. , 2006aTsai et al. , 2006bVilleneuve et al. 2006Villeneuve et al. , 2007Wellenius et al. 2005aWellenius et al. , 2005bWellenius et al. , 2006Xu et al. 2008;Yamakazi et al. 2007;Yang 2008;Yang et al. 2003Yang et al. , 2004aYang et al. , 2004bYang et al. , 2006Schwartz 2005, 2006;Zeka et al. 2005Zeka et al. , 2006. CCO design. ...
Case-crossover is one of the most used designs for analyzing the health-related effects of air pollution. Nevertheless, no one has reviewed its application and methodology in this context.
We conducted a systematic review of case-crossover (CCO) designs used to study the relationship between air pollution and morbidity and mortality, from the standpoint of methodology and application.
A search was made of the MEDLINE and EMBASE databases.Reports were classified as methodologic or applied. From the latter, the following information was extracted: author, study location, year, type of population (general or patients), dependent variable(s), independent variable(s), type of CCO design, and whether effect modification was analyzed for variables at the individual level.
The review covered 105 reports that fulfilled the inclusion criteria. Of these, 24 addressed methodological aspects, and the remainder involved the design's application. In the methodological reports, the designs that yielded the best results in simulation were symmetric bidirectional CCO and time-stratified CCO. Furthermore, we observed an increase across time in the use of certain CCO designs, mainly symmetric bidirectional and time-stratified CCO. The dependent variables most frequently analyzed were those relating to hospital morbidity; the pollutants most often studied were those linked to particulate matter. Among the CCO-application reports, 13.6% studied effect modification for variables at the individual level.
The use of CCO designs has undergone considerable growth; the most widely used designs were those that yielded better results in simulation studies: symmetric bidirectional and time-stratified CCO. However, the advantages of CCO as a method of analysis of variables at the individual level are put to little use.
... With this study design, we might explore if the C-R function varies over time, between sociodemographic groups or with proximity to specific sources of pollution. For example, Xu et al. (2008) conducted case-crossover analyses in an area near Pittsburgh, where a steel coke plant had operated for many years. The study revealed reductions in cardiorespiratory disease hospitalizations associated with reductions of ambient levels of coarse particulates (PM10) with the closing of the plant. ...
Environmental Public Health Tracking (EPHT) staff at the state and national levels are developing nationally consistent data and methods to estimate the impact of ozone and fine particulate matter on hospitalizations for asthma and myocardial infarction. Pilot projects have demonstrated the feasibility of pooling state hospitalization data and linking these data to The United States Environmental Protection Agency (EPA) statistically based ambient air estimates for ozone and fine particulates. Tools were developed to perform case-crossover analyses to estimate concentration-response (C-R) functions. A weakness of analyzing one state at a time is that the effects are relatively small compared to their confidence intervals. The EPHT program will explore ways to statistically combine the results of peer-reviewed analyses from across the country to provide more robust C-R functions and health impact estimates at the local level. One challenge will be to routinely share data for these types of analyses at fine geographic and temporal scales without disclosing confidential information. Another challenge will be to develop C-R estimates which take into account time, space, or other relevant effect modifiers.
The essential purpose of public health surveillance is to monitor important health outcomes and risk factors and provide actionable information to practitioners, policy makers, researchers, and the public to prevent or ameliorate exposure, disease, and death. Although separate 1970s-era acts of Congress made possible the creation of modern occupational health and environmental public health surveillance, these acts also led to fragmented responsibilities and unconnected data across federal agencies. Having a well-defined purpose for systematically collecting relevant data is key, and state and local programs play a crucial role in conducting meaningful surveillance and connecting it with evidence-based outreach and interventions. Congress has directed monies to environmental public health surveillance and capacity has improved, yet no analagous funding has occurred to address the fragmentation found within occupational health surveillance. This article provides a review of the advances and important themes within occupational health and environmental public health surveillance over the past decade.
Objective: To test the efficacy of a graded aerobic exercise programme in the chronic fatigue syndrome. Design: Randomised controlled trial with control treatment crossover after the first follow up examination. Setting: Chronic fatigue clinic in a general hospital department of psychiatry.
To determine whether there was excess ill health in people living near a coking works, and if so whether it was related to exposure to coking works' emissions.
Populations varying in proximity to the coking works were compared with control populations. Health data were correlated with available environmental data.
Analysis of routinely collected mortality, cancer registration, and birth statistics; community survey using self completed postal questionnaires; retrospective analysis of general practice (GP) records; tests of respiratory function; and analysis of available environmental data.
Study and control populations were comparable in terms of response rates, gender, and most socioeconomic indicators. For adults, age standardised mortality and cancer rates of the population closest to the coking works were comparable with those for the district as a whole. Gender ratios, birthweight, and stillbirth rates were comparable in the study and control populations. For several indicators of respiratory health including cough, sinus trouble, glue ear, and wheeze (but not for asthma and chronic bronchitis) there was a gradient of self reported ill health, with the highest prevalence in areas closest to the works. For example, sinus trouble was reported by 20% of adults and 13% of children in the area closest to the works compared with 13% and 6% respectively in the control area. GP consultations for respiratory disorders increased when pollution (measured by SO2 levels) was high: annual consultation rates per 1000 varied from 752 in the top group of daily pollution levels to 424 in the bottom group. Analysis of locally collected smoke and SO2 data indicated that SO2 concentrations were highest closest to the works and, after closure of the coking works, the number of days on which SO2 and smoke levels exceeded 100 micrograms/m3 and 90 micrograms/m3, respectively, fell steeply.
Routinely available indicators failed to provide convincing evidence that the coking works had harmed health. Self report and GP consultations indicated that respiratory ill health in the people living close to the works was worse than expected. Some of the excess probably resulted from exposure to coking works emissions. The health effects of relatively low level but intermittently high air pollution from a point source may be subtle, contributing to respiratory morbidity, but not apparent in analysis of routine health indicators.
To carry out a prospective combined quantitative analysis of the associations between all cause mortality and ambient particulate matter and sulphur dioxide.
Analysis of time series data on daily number of deaths from all causes and concentrations of sulphur dioxide and particulate matter (measured as black smoke or particles smaller than 10 microns in diameter (PM10)) and potential confounders.
12 European cities in the APHEA project (Air Pollution and Health: a European Approach).
Relative risk of death.
In western European cities it was found that an increase of 50 micrograms/m3 in sulphur dioxide or black smoke was associated with a 3% (95% confidence interval 2% to 4%) increase in daily mortality and the corresponding figure for PM10 was 2% (1% to 3%). In central eastern European cities the increase in mortality associated with a 50 micrograms/m3 change in sulphur dioxide was 0.8% (-0.1% to 2.4%) and in black smoke 0.6% (0.1% to 1.1%). Cumulative effects of prolonged (two to four days) exposure to air pollutants resulted in estimates comparable with the one day effects. The effects of both pollutants were stronger during the summer and were mutually independent.
The internal consistency of the results in western European cities with wide differences in climate and environmental conditions suggest that these associations may be causal. The long term health impact of these effects is uncertain, but today's relatively low levels of sulphur dioxide and particles still have detectable short term effects on health and further reductions in air pollution are advisable.
To investigate whether residents near cokeworks have a higher standardised mortality than those further away, particularly from cardiovascular and respiratory causes, which may be associated with pollution from cokeworks.
Cross sectional small area study with routinely collected postcoded mortality data and small area census statistics. Populations within 7.5 km of 22 cokeworks in Great Britain, 1981-92. Expected numbers of deaths within 2 and 7.5 km of cokeworks, and in eight distance bands up to 7.5 km of cokeworks, were calculated by indirect standardisation from national rates stratified for age and sex and a small area deprivation index, and adjusted for region. Age groups examined were all ages, 1-14, 15-64, 65-74, > or = 75. Only the 1-14 and 15-44 age groups were examined for asthma mortality.
There was a 3% (95% confidence interval (95% CI) 1% to 4%) excess of all deaths within 2 km of cokeworks, and a significant decline in mortality with distance from cokeworks. The excess of deaths within 2 km was slightly higher for females and elderly people, but excesses within 2 km and declines in risk with distance were significant for all adult age groups and both sexes. The size of the excess within 2 km was 5% (95% CI 3% to 7%) for cardiovascular causes, 6% (95% CI 3% to 9%) for ischaemic heart disease, and 2% (95% CI -2% to 6%) for respiratory deaths, with significant declines in risk with distance for all these causes. There was a non-significant 15% (95% CI -1% to 101%) excess in asthma mortality in the 15-44 age group. There were no significant excesses in mortality among children but 95% CIs were wide. Within 2 km of cokeworks, the estimated additional excess all cause mortality for all ages combined related to region and mainly to the greater deprivation of the population over national levels was 12%.
A small excess mortality near cokeworks as found in this study is plausible in the light of current evidence about the health impact of air pollution. However, in this study the effects of pollution from cokeworks, if any, are outweighed by the effects of deprivation on weighed by the effects of deprivation on mortality near cokeworks. It is not possible to confidently exclude socioeconomic confounding or biases resulting from inexact population estimation as explanations for the excess found.
We used the case-crossover design to identify any increase in mortality in Seoul, Korea, when there were higher levels of ambient air pollution on case-days than would be expected solely as a result of chance. This empirical study showed that either unidirectional retrospective (selecting only control days prior to death) or prospective (selecting only control days after death) control sampling could cause risk estimates to be confounded by seasonal waves as well as time trends in air pollution levels. In bidirectional control sampling in which exposures at death were compared with exposures both before and after death, the estimated mortality was resistant to confounding by time patterns of air pollution. Using a bidirectional control sampling approach, the results from a conditional logistic regression model controlling for weather conditions showed that the nonaccidental mortality associated with a 50-ppb increment over a 3-day moving average of SO(2) concentrations, including the concurrent day and preceding 2 days, was 1.023 [95% confidence interval (CI), 1.016-1.084]. The relative risk of death was 1.023 (CI, 0.999-1.048) per 50 ppb for 1-hr maximum O(3) and 1.010 (CI, 0.988-1.032) per 100 microg/m(3 )or total suspended particulates. In conclusion, the findings of this study were 2-fold: given the consistency of the observed association between SO(2) and daily mortality across different analysis methods, the association reported here indicates that air pollution is a probable contributor to premature death; and bidirectional control sampling is needed in a case-crossover design applied to air pollution epidemiologic studies to control confounding by seasonal patterns of air pollution as well as time trends.
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This study reassessed Schwartz and Dockery's analysis of daily mortality from nonexternal causes among residents of Philadelphia, Pennsylvania, over 8 years, from 1973 to 1980 [American Review of Respiratory Disease 145:600-604 (1992)]. A Poisson regression analysis using the same model found that a 100-microg/m(3) increment in the 48-hr mean concentration of total suspended particulates (TSP) was associated with increased all-cause mortality [rate ratio = 1.069; 95% confidence interval (CI), 1.043-1.096) after adjustment for quadratic trend, season, year, previous day's mean temperature, dew point, winter temperature, and indicators of hot (temperature > 80 degrees F) and humid days (dew point > 66 degrees F). Critics suggested that time-varying factors such as season and day of week were not sufficiently controlled in this analysis and subsequent studies in other locations. We used a conditional logistic regression analysis with a case-crossover design to reanalyze the data, with air pollution in the prior and subsequent weeks to the day of death serving as referent periods. The case-crossover approach controls for season and day of week by design rather than modeling. We found that a 100-microg/m(3) increment in the 48-hr mean level of TSP was associated with increased all-cause mortality [odds ratio (OR) = 1.056; CI, 1.027-1.086) after adjustment for the same weather variables as above. Similar associations were observed for deaths in individuals over 65 years of age (OR = 1.074; CI, 1. 037-1.111) and for deaths due to cardiovascular disease (OR = 1.063; CI, 1.021-1.107). The current case-crossover analysis confirms the general conclusion of the previous Poisson regression analysis of an association of TSP with daily mortality in Philadelphia, Pennsylvania.
Particulate air pollution has been associated with excess deaths from, and increases in hospital admissions for, cardiovascular disease among older people. A study was undertaken to determine whether this may be a consequence of alterations in the blood, secondary to pulmonary inflammation caused by the action of fine particles on alveolar cells, by repeatedly measuring haematological factors in older people and relating them to measurements of exposure to airborne particles.
One hundred and twelve individuals aged 60+ years in two UK cities provided repeated blood samples over 18 months, 108 providing the maximum of 12 samples. Estimates of individual exposure to particles of less than 10 microm diameter (PM(10)), derived from a mathematical model based on activity diaries and comparative measurements of PM(10) at multiple sites and during a variety of activities, were made for each three day period prior to blood sampling. The relationships between blood values and estimates of both personal exposure and city centre measurements of PM(10) were investigated by analysis of covariance, adjusting for city, season, temperature, and repeated individual measurements.
Estimated personal exposure to PM(10) over the previous three days showed negative correlations with haemoglobin concentration, packed cell volume (PCV), and red blood cell count (p<0.001), and with platelets and factor VII levels (p<0.05). The changes in red cell indices persisted after adjustment for plasma albumin in a sample of 60 of the subjects. City centre PM(10) measurements over three days also showed negative correlations with haemoglobin and red cell count (p<0.001) and with PCV and fibrinogen (p<0.05), the relationship with haemoglobin persisting after adjustment for albumin. C reactive protein levels showed a positive association with city centre measurements of PM(10) (p<0.01). Based on a linear relationship, the estimated change in haemoglobin associated with an alteration in particle concentration of 100 microg/m(3) is estimated to have been 0.44 g/dl (95% CI 0.62 to 0.26) for personal PM(10) and 0.73 g/dl (95% CI 1.11 to 0.36) for city centre PM(10) measurements.
This investigation is the first to estimate personal exposures to PM(10) and to demonstrate associations between haematological indices and air pollution. The changes in haemoglobin adjusted for albumin suggest that inhalation of some component of PM(10) may cause sequestration of red cells in the circulation. We propose that an action of such particles either on lung endothelial cells or on erythrocytes themselves may be responsible for changing red cell adhesiveness. Peripheral sequestration of red cells offers an explanation for the observed cardiovascular effects of particulate air pollution.
The authors assessed the acute association between particulate air pollution and mortality among subjects suffering from chronic
obstructive pulmonary disease by using a case-crossover analysis. This design avoided the common concerns about the methods
used to assess the acute effects of air pollution. The 1, 845 men and the 460 women included were residents of Barcelona,
Spain, who were over age 35 years, had died during the period 1990–1995, and had visited emergency rooms because of a chronic
obstructive pulmonary disease exacerbation during the period 1985–1989. Particle levels (measured as black smoke at the city
monitoring stations) were associated with mortality for all causes (odds ratio (OR) for an increase of 20 μ/m3, the interquartile change, adjusted for temperature, humidity, and influenza = 1.112, 95 percent confidence interval (CI):
1.017, 1.215). The association was stronger for respiratory causes (OR = 1.182, 95 percent CI: 1.025, 1.365), but was not
significant for cardiovascular causes (OR = 1.077, 95 percent CI: 0.917, 1.264). Older women, patients admitted to intensive
care units, and patients with a higher rate of emergency room visits were at greater risk of dying associated with black smoke.
The results reinforced the deleterious role of urban pollution and provided information on factors possibly conferring susceptibility
to the acute role of air pollution.Am J Epidemiol 2000; 151:50-6.
Misclassification of exposure is a well-recognized inherent limitation of epidemiologic studies of disease and the environment. For many agents of interest, exposures take place over time and in multiple locations; accurately estimating the relevant exposures for an individual participant in epidemiologic studies is often daunting, particularly within the limits set by feasibility, participant burden, and cost. Researchers have taken steps to deal with the consequences of measurement error by limiting the degree of error through a study's design, estimating the degree of error using a nested validation study, and by adjusting for measurement error in statistical analyses. In this paper, we address measurement error in observational studies of air pollution and health. Because measurement error may have substantial implications for interpreting epidemiologic studies on air pollution, particularly the time-series analyses, we developed a systematic conceptual formulation of the problem of measurement error in epidemiologic studies of air pollution and then considered the consequences within this formulation. When possible, we used available relevant data to make simple estimates of measurement error effects. This paper provides an overview of measurement errors in linear regression, distinguishing two extremes of a continuum-Berkson from classical type errors, and the univariate from the multivariate predictor case. We then propose one conceptual framework for the evaluation of measurement errors in the log-linear regression used for time-series studies of particulate air pollution and mortality and identify three main components of error. We present new simple analyses of data on exposures of particulate matter < 10 μm in aerodynamic diameter from the Particle Total Exposure Assessment Methodology Study. Finally, we summarize open questions regarding measurement error and suggest the kind of additional data necessary to address them.
The case-crossover design compares exposures during the period of time of failure with one or more periods when failure did not occur and evaluates the potential excess risk using conditional logistic regression. In this simulation study, we applied several control sampling approaches to control for confounding by various temporal patterns of an exposure variable and evaluated the usefulness of symmetric bidirectional control strategies. We simulated true relative risks (RRs; true ss = 0.001) of deaths of 1.051 per 50-ppb increase of sulfur dioxide and included confounding by right- or left-skewed seasonal waves, linear long-term time trends, or a combination of both. The range of the estimated RRs from symmetric bidirectional control sampling approaches was 1.044 approximately 1. 056 at either a long-term trend or any skewed seasonal wave of SO(2) levels, which indicated the bidirectional control sampling methods would successfully control confounding by design. The simulations with bidirectional sampling, however, show that biases may occur if waves are incomplete (20-43% underestimated RRs). In conclusion, our simulations show that the symmetric bidirectional case-crossover design can substantially control for confounding by linear long-term trends and/or seasonality of an exposure variable by design as well. However, unidirectional control sampling would fail to control confounding by those variations of air pollution. Simulation results also show that even the bidirectional case-crossover design can be biased in a situation where the exposure variable shows incomplete cyclic waves, and therefore it cannot completely control for temporal confounding.
To confirm that arsenic (As) induces oxidative DNA damage in phytohemagglutinin (PHA)-stimulated and unstimulated human lymphocytes, we used the alkaline comet assay combined with specific enzyme [formamidopyrimidine-DNA glycosylase (FPG)] digestion to measure As-induced base damage. The results showed that the enzyme-sensitive sites were readily detected with the alkaline comet assay after the cells were treated with 10 microM As for 2 hr. The repair patterns observed for FPG-created DNA single strand breaks (SSBs) in As-treated cells were comparable to those in hydrogen peroxide (H(2)O(2))-treated cells. The enzyme-created SSBs, As-induced base damage, were more significant in PHA-stimulated lymphocytes. About 63% and 68% of SSBs induced by As and H(2)O(2), respectively, were repaired in PHA-stimulated lymphocytes by 2-hr repair incubation, but about 34% and 43%, respectively, were repaired in unstimulated cells. About 40% and 49% of base damage induced by As and H(2)O(2), respectively, were repaired in PHA-stimulated lymphocytes, but about 19% and 21%, respectively, were repaired in unstimulated cells. These results indicated that As induced oxidative DNA damage in human lymphocytes at micromolar concentrations. The damaged bases could be chiefly purines or formamidopyrimidines. Like the damage induced by H(2)O(2), As-induced DNA damage was repaired more slowly in unstimulated lymphocytes.
Airborne particles are associated with adverse health effects and contribute to excess mortality in epidemiological studies. A recent hypothesis proposes that the high numbers of ultrafine (<0.1 μm diameter) particles in ambient air might provoke alveolar inflammation and subsequently cause exacerbations in pre-existing cardiopulmonary diseases.
To test the hypothesis adult asthmatics were followed with daily peak expiratory flow (PEF) measurements and symptom and medication diaries for six months, while simultaneously monitoring particulate pollution in ambient air. The associations between daily health endpoints of 57 asthmatics and indicators of air pollution were examined by multivariate regression models.
Daily mean number concentration of particles, but not particle mass (PM 10 (particle mass <10 μm), PM 2.5–10 , PM 2.5 , PM 1 ), was negatively associated with daily PEF deviations. The strongest effects were seen for particles in the ultrafine range. However, the effect of ultrafine particles could not definitely be separated from other traffic generated pollutants, namely nitric oxide, nitrogen dioxide and carbon monoxide. No associations were observed with respiratory symptoms or medication use.
Particle mass measurements can be strongly influenced by mechanically produced, soil-derived particles, which may not be associated with adverse health effects. Therefore, air quality monitoring should include particle number concentrations, which mainly reflect ultrafine particles.
Well-documented air pollution episodes throughout recent history have led to deaths among individuals with cardiovascular and respiratory disease. Although the components of air pollution that cause the adverse health effects in these individuals are unknown, a small proportion by mass but a large proportion by number of the ambient air particles are ultrafine, i.e., less than 100 nm in diameter. This ultrafine component of particulate matter with a mass median aerodynamic diameter less than 10 microm (PM(10) may mediate some of the adverse health effects reported in epidemiologic studies and for which there is toxicologic evidence to support this contention. The exact mechanism by which ultrafine particles have adverse effects is unknown, but these particles have recently been shown to enhance calcium influx on contact with macrophages. Oxidative stress is also to be anticipated at the huge particle surface; this can be augmented by oxidants generated by recruited inflammatory leukocytes. Atheromatous plaques form in the coronary arteries and are major causes of morbidity and death associated epidemiologically with particulate air pollution. In populations exposed to air pollution episodes, blood viscosity, fibrinogen, and C-reactive protein (CRP) were higher. More recently, increases in heart rate in response to rising air pollution have been described and are most marked in individuals who have high blood viscosity. In our study of elderly individuals, there were significant rises in CRP, an index of inflammation. In this present review, we consider the likely interactions between the ultrafine particles the acute phase response and cardiovascular disease.
Numerous studies show an association between particulate air pollution and adverse health effects. Particulate matter is a complex mixture of elemental carbon, ammonium, sulfates, nitrates, organic components, and metals. The mechanisms of action of particulate matter less than or equal to 2.5 micro m in mean aerodynamic diameter (PM(2.5)), as well as the constituents responsible for the observed cardiopulmonary health effects, have not been identified. In this study we focused on the association between the metallic component of PM(2.5) and cardiac autonomic function based on standard heart rate variability (HRV) measures in an epidemiologic study of boilermakers. Thirty-nine male boilermakers were monitored throughout a work shift. Each subject wore an ambulatory electrocardiogram (Holter) monitor and a personal monitor to measure PM(2.5). We used mixed-effects models to regress heart rate and SDNN index (standard deviation of the normal-to-normal) on PM(2.5) and six metals (vanadium, nickel, chromium, lead, copper, and manganese). There were statistically significant mean increases in the SDNN index of 11.30 msec and 3.98 msec for every 1 micro g/m(3) increase in the lead and vanadium concentrations, respectively, after adjusting for mean heart rate, age, and smoking status. Small changes in mean heart rate were seen with all exposure metrics. The results of this study suggest an association between exposure to airborne metals and significant alterations in cardiac autonomic function. These results extend our understanding of the adverse health effects of the metals component of ambient PM(2.5).
Four commercial quartz dusts (flours), two inflammogenic in vivo and activating macrophages in vitro (Qz 2/1-c and Qz 3/1-c) and two mostly inert (Qz 5/1-c and Qz 11/1-c), have been compared regarding their surface properties, in order to detect chemical differences which may account for their different biological behaviour. The following features have been examined: 1) extent of the amorphous fraction (heat associated α ↔ β transition of quartz) and its solubility in HF; 2) potential to cleave a carbon-hydrogen bond with consequent generation of carbon centred radicals (spin trapping technique, EPR); 3) evolution of surface functionalities upon heating (FTIR spectroscopy); 4) mechanisms of adsorption of water on dusts outgassed at 150° and at 800°C (adsorption calorimetry). HCl treated samples have also been examined. The two "less toxic" quartzes are more resistant to HF attack, coordinate irreversibly H2O molecules and exhibit strong adsorption sites, which are absent in the other two and in a very pure quartz dust. Conversely all samples show the same potential to release free radicals. The different behaviour of the two sets of dust is consistent with a different level of impurities, namely aluminium ex kaolin, carbon and alkaline ions. The less inflammogenic quartzes appear to be covered by aluminium ions (and possibly iron) which strongly holds molecular water or carbonates, thus reducing the silanol patches to a large extent and changing the surface properties of the particles. We hypothesize that cellular response, and particularly macrophage activation and death, is mediated by strong interactions between silanol patches and some cell membrane components, but inhibited when the surface of the particle is modified by the presence of aluminium ions, surface carbonates and other metal contaminants. This hypothesis suggests that grinding procedures with little appropriate additives, e.g. kaolin, alumina, can reduce the biological activity of quartz dusts.
In January 2001 the Pew Environmental Health Commission called for the creation of a coordinated public health system to prevent disease in the United States by tracking and combating environmental health threats. In response, the Centers for Disease Control and Prevention initiated the Environmental Public Health Tracking (EPHT) Program to integrate three distinct components of hazard monitoring and exposure and health effects surveillance into a cohesive tracking network. Uniform and acceptable data standards, easily understood case definitions, and improved communication between health and environmental agencies are just a few of the challenges that must be addressed for this network to be effective. The nascent EPHT program is attempting to respond to these challenges by drawing on a wide range of expertise from federal agencies, state health and environmental agencies, nongovernmental organizations, and the program's academic Centers of Excellence. In this mini-monograph, we present innovative strategies and methods that are being applied to the broad scope of important and complex environmental public health problems by developing EPHT programs. The data resulting from this program can be used to identify areas and populations most likely to be affected by environmental contamination and to provide important information on the health and environmental status of communities. EPHT will develop valuable data on possible associations between the environment and the risk of noninfectious health effects. These data can be used to reduce the burden of adverse health effects on the American public.
Epidemiologic studies report associations between particulate air pollution and cardiopulmonary morbidity and mortality. Although the underlying pathophysiologic mechanisms remain unclear, it has been hypothesized that altered autonomic function and pulmonary/systemic inflammation may play a role. In this study we explored the effects of air pollution on autonomic function measured by changes in heart rate variability (HRV) and blood markers of inflammation in a panel of 88 elderly subjects from three communities along the Wasatch Front in Utah. Subjects participated in multiple sessions of 24-hr ambulatory electrocardiographic monitoring and blood tests. Regression analysis was used to evaluate associations between fine particulate matter [aerodynamic diameter less than or equal to 2.5 microm (PM2.5)] and HRV, C-reactive protein (CRP), blood cell counts, and whole blood viscosity. A 100- microg/m3 increase in PM2.5 was associated with approximately a 35 (SE = 8)-msec decline in standard deviation of all normal R-R intervals (SDNN, a measure of overall HRV); a 42 (SE = 11)-msec decline in square root of the mean of the squared differences between adjacent normal R-R intervals (r-MSSD, an estimate of short-term components of HRV); and a 0.81 (SE = 0.17)-mg/dL increase in CRP. The PM2.5-HRV associations were reasonably consistent and statistically robust, but the CRP association dropped to 0.19 (SE = 0.10) after excluding the most influential subject. PM2.5 was not significantly associated with white or red blood cell counts, platelets, or whole-blood viscosity. Most short-term variability in temporal deviations of HRV and CRP was not explained by PM2.5; however, the small statistically significant associations that were observed suggest that exposure to PM2.5 may be one of multiple factors that influence HRV and CRP.
A systematic investigation of solid and gaseous atmospheric emissions from some coke-oven batteries of one of Europe's largest integrated steel factory (Taranto, Italy) has been carried out. In air monitoring samples, polycyclic aromatic hydrocarbons (PAHs) were consistently detected at concentrations largely exceeding threshold limit values. By means of PAHs speciation profile and benzo(a)pyrene (BaP) equivalent dispersion modeling from diffuse sources, the study indicated that serious health risks exist not only in working areas, but also in a densely populated residential district near the factory.
The goal of this study was to estimate the associations between outdoor air pollution and cardiovascular hospital admissions for the elderly.
Associations were assessed using the case-crossover method for seven cities: Auckland and Christchurch, New Zealand; and Brisbane, Canberra, Melbourne, Perth, and Sydney Australia. Results were combined across cities using a random-effects meta-analysis and stratified for two adult age groups: 15-64 years and >/= 65 years of age (elderly). Pollutants considered were nitrogen dioxide, carbon monoxide, daily measures of particulate matter (PM) and ozone. Where multiple pollutant associations were found, a matched case-control analysis was used to identify the most consistent association.
In the elderly, all pollutants except O3 were significantly associated with five categories of cardiovascular disease admissions. No associations were found for arrhythmia and stroke. For a 0.9-ppm increase in CO, there were significant increases in elderly hospital admissions for total cardiovascular disease (2.2%) , all cardiac disease (2.8%), cardiac failure (6.0%), ischemic heart disease (2.3%), and myocardial infarction (2.9%). There was some heterogeneity between cities, possibly due to differences in humidity and the percentage of elderly people. In matched analyses, CO had the most consistent association.
The results suggest that air pollution arising from common emission sources for CO, NO2, and PM (e.g., motor vehicle exhausts) has significant associations with adult cardiovascular hospital admissions, especially in the elderly, at air pollution concentrations below normal health guidelines. Relevance to clinical and professional practice: Elderly populations in Australia need to be protected from air pollution arising from outdoor sources to reduce cardiovascular disease.
A case-control design involving only cases may be used when brief exposure causes a transient change in risk of a rare acute-onset disease. The design resembles a retrospective nonrandomized crossover study but differs in having only a sample of the base population-time. The average incidence rate ratio for a hypothesized effect period following the exposure is estimable using the Mantel-Haenszel estimator. The duration of the effect period is assumed to be that which maximizes the rate ratio estimate. Self-matching of cases eliminates the threat of control-selection bias and increases efficiency. Pilot data from a study of myocardial infarction onset illustrate the control of within-individual confounding due to temporal association of exposures.
This study assessed the association between hospital admissions and fine particulate pollution (PM10) in Utah Valley during the period April 1985-February 1988. This time period included the closure and reopening of the local steel mill, the primary source of PM10. An association between elevated PM10 levels and hospital admissions for pneumonia, pleurisy, bronchitis, and asthma was observed. During months when 24-hour PM10 levels exceeded 150 micrograms/m3, average admissions for children nearly tripled; in adults, the increase in admissions was 44 per cent. During months with mean PM10 levels greater than or equal to 50 micrograms/m3 average admissions for children and adults increased by 89 and 47 per cent, respectively. During the winter months when the steel mill was open, PM10 levels were nearly double the levels experienced during the winter months when the mill was closed. This occurred even though relatively stagnant air was experienced during the winter the mill was closed. Children's admissions were two to three times higher during the winters when the mill was open compared to when it was closed. Regression analysis also revealed that PM10 levels were strongly correlated with hospital admissions. They were more strongly correlated with children's admissions than with adult admissions and were more strongly correlated with admissions for bronchitis and asthma than with admissions for pneumonia and pleurisy.
Time-series, cross-sectional, and prospective cohort studies have observed associations between mortality and particulate air pollution but have been limited by ecologic design or small number of subjects or study areas. The present study evaluates effects of particulate air pollution on mortality using data from a large cohort drawn from many study areas. We linked ambient air pollution data from 151 U.S. metropolitan areas in 1980 with individual risk factor on 552,138 adults who resided in these areas when enrolled in a prospective study in 1982. Deaths were ascertained through December, 1989. Exposure to sulfate and fine particulate air pollution, which is primarily from fossil fuel combustion, was estimated from national data bases. The relationships of air pollution to all-cause, lung cancer, and cardiopulmonary mortality was examined using multivariate analysis which controlled for smoking, education, and other risk factors. Although small compared with cigarette smoking, an association between mortality and particulate air pollution was observed. Adjusted relative risk ratios (and 95% confidence intervals) of all-cause mortality for the most polluted areas compared with the least polluted equaled 1.15 (1.09 to 1.22) and 1.17 (1.09 to 1.26) when using sulfate and fine particulate measures respectively. Particulate air pollution was associated with cardiopulmonary and lung cancer mortality but not with mortality due to other causes. Increased mortality is associated with sulfate and fine particulate air pollution at levels commonly found in U.S. cities. The increase in risk is not attributable to tobacco smoking, although other unmeasured correlates of pollution cannot be excluded with certainty.
This paper assesses whether air pollution increases resting heart rates in 2, 681 men and women aged 25–64 years who participated
in the MONICA (monitoring of trends and determinants in cardiovascular disease) Augsburg cohort. Increases in heart rate were
observed during the air pollution episode in January 1985 compared with non-episode days adjusted for cardiovascular risk
factors and meteorologic parameters. Consistently, heart rates were also elevated at high concentrations of sulfur dioxide,
total suspended particulates, or carbon monoxide. Acceleration in heart rates indicates an altered autonomic control of the
heart in association with air pollution, which may contribute to the observed health effects in association with air pollution.
Am J Epidemiol 1999; 150: 1094-8.
Numerous epidemiologic studies have reported increases in the daily incidence of cardiovascular mortality and morbidity associated with increases in daily levels of particulate matter air pollution. We studied the association between the incidence of primary cardiac arrest and two daily measures of particulate matter using a case-crossover study of 362 cases of out-of-hospital cardiac arrest. All cases were attended by paramedics and had no history of clinically recognized heart disease or life-threatening comorbidities. We compared particulate matter levels at index times with particulate matter levels from referent days matched on day of week within strata defined by month and year. The estimated relative risk at a lag of 1 day for an interquartile range (IQR) change in nephelometry (0.51 x 10(-1) km(-1)) was 0.893 (95% CI = 0.779-1.024). The estimated relative risk at a lag of 1 day for an IQR change in PM10 (19.3 microg m(-3)) was 0.868 (95% CI = 0.744-1.012). Other lag periods gave similar results. We did not find evidence of confounding by carbon monoxide or sulfur dioxide. Analysis of effect modification by individual-level variables did not reveal any susceptible subgroups. These findings do no support an association between particulate matter and increased risk of primary cardiac arrest among persons without clinically recognized heart disease. The null results of this study may result from several factors, including the highly selected nature of this case series and the relatively low particulate matter levels in the Seattle metropolitan area.
The case-crossover design was proposed for the study of a transient effect of an intermittent exposure on the subsequent occurrence of a rare acute-onset disease. This design can be an alternative to Poisson time series regression for studying the health effects of fine particulate matter air pollution. Characteristics of time-series of particulate matter, including long-term time trends, seasonal trends, and short-term autocorrelations, require that referent selection in the case-crossover design be considered carefully and adapted to minimize bias. We performed simulations to evaluate the bias associated with various referent selection strategies for a proposed case-crossover study of associations between particulate matter and primary cardiac arrest. Some a priori reasonable strategies were associated with a relative bias as large as 10%, but for most strategies the relative bias was less than 2% with confidence interval coverage within 1% of the nominal level. We show that referent selection for case-crossover designs raises the same issues as selection of smoothing method for time series analyses. In addition, conditional logistic regression analysis is not strictly valid for some case-crossover designs, introducing further bias.
A study was performed to assess the acute association between air pollution, pollen and spores, and mortality in a population based cohort of subjects with asthma recruited from emergency room admissions for an asthma exacerbation using a case crossover design.
Patients in Barcelona aged over 14 years who died during the period 1985-95 who had visited the emergency department of one of the four largest hospitals in the city for asthma during 1985-9 were included in the study (a total of 467 men and 611 women). Deaths were identified by record linkage of the cohort individuals with the Catalonia mortality registry. Causes of death were based on the underlying cause on the death certificate. Air pollution, pollen and spore levels were measured at the city monitoring stations which provide an average for the entire city.
Nitrogen dioxide was associated with mortality for all causes of death (adjusted odds ratio (OR) for an increase of the interquartile range = 1.50, 95% confidence interval (CI) 1.09 to 2.64) in asthmatic patients with more than one emergency room admission for asthma. The association was particularly strong for respiratory causes (OR 1.63, 95% CI 0.93 to 2.86). Ozone also increased the risk of death in asthmatic patients (OR 1.90, 95% CI 1.09 to 3.30) during spring and summer. The association with particles, pollen, and spores was not significant, and no interactions between air pollutants and pollen and spores were found.
Nitrogen dioxide and ozone may exacerbate severe asthma and even cause death among asthmatic subjects.
A recent document of the American Thoracic Society and two previous reports of the International Union Against Tuberculosis and Lung Disease have summarized the negative health effects due to air pollution in a list ranging from the increase of mortality to the perception of bad odors. A significant attempt to estimate, on an annual basis, the negative effects of air pollution from particulate matter less than 10 microns in aerodynamic diameter (PM10) has been carried out on data from Austria, France, and Switzerland: e.g. in France, air pollution from PM10 is responsible annually for 31,700 deaths, 36,700 new cases of chronic bronchitis and 577,000 attacks of asthma in adults, 450,000 cases of acute bronchitis and 243,000 attacks of asthma in children. Recently, a study on the long-term effects of air pollution on about 500,000 residents in metropolitan US areas evidenced that each 10 micrograms/m3 elevation in fine particulate air pollution is associated with approximately a 4%, 6% and 8% increased risk of all-cause, cardiopulmonary and lung cancer mortality, respectively. Some Italian experiences have also confirmed respiratory health damages from air pollution, namely the prospective epidemiologic studies on general population samples of the Po Delta and Pisa areas; the cross-sectional study on schoolchildren of the 'Italian study on respiratory disorders in childhood and environment' (SIDRIA); and a meta-analysis of the Italian studies on short-term effects of air pollution. In conclusion, epidemiologic studies suggest that air pollution plays an important role in the exacerbation and in the pathogenesis of chronic respiratory diseases. Thus, respiratory physicians, as well as public health professionals, should advocate for a cleaner environment.
12 PAHs in air of different production sector in coking plant were measured with the result showing that, the total PAHs concentrations ranged from 11.75 to 46.66 micrograms/m3, among which, BaP was 0.050-1.054 micrograms/m3 descending following the order: the outlet of coke oven, the top of coke oven, the gate, the point of flaming out coke. BaP pollution in air of the top and the outlet of coke oven were much heavier than in the soot and in air of arterial road. The toxic equivalency factors (TEF) adjusted concentrations of total PAHs were 0.3875-1.714 micrograms/m3, and in this way, workers' daily exposure to PAHs were 3.100-13.71 micrograms/m3.
Daily air pollution is associated with increased hospital admissions for cardiovascular diseases, but there are few observations on the link with acute myocardial infarction. To evaluate the relation between various urban air pollutants (total suspended particulate, SO2, CO, NO2) and hospital admissions for acute myocardial infarction in Rome, Italy, we performed a case-crossover analysis and studied whether individual characteristics act as effect modifiers.
We studied 6531 subjects residing in Rome and hospitalized for a first episode of acute myocardial infarction (International Classification of Diseases, 9th edition: 410) from January 1995 to June 1997. The following individual information was available: sex, age, date of hospitalization, coexisting illnesses (hypertension, 25%; diabetes, 15%), and cardiac severity (conduction disorders, 6%; cardiac dysrhythmias, 20%; heart failure, 11%). Daily air pollution data were taken from 5 city monitors. We used a time-stratified case-crossover design; control days were the same day of the week as the myocardial infarction occurred, in other weeks of the month.
Positive associations were found for total suspended particulate, NO2 and CO. The strongest and most consistent effect was found for total suspended particulate. The odds ratio (OR) associated with 10 micro g/m3 of total suspended particulate over the 0- to 2-day lag was 1.028 (95% confidence interval [CI] = 1.005-1.052). The association with total suspended particulate tended to be stronger among people older than 74 years of age (OR = 1.046; CI = 1.005-1.089), in the warm period of the year (OR = 1.046; CI = 1.008-1.087), and among subjects who had heart conduction disorders (OR = 1.080; CI = 0.987-1.181).
The results suggest that air pollution increases the risk of myocardial infarction, especially during the warm season. There was a tendency for a stronger effect among the elderly and people with heart conduction disturbances.
Many studies have reported increases in daily cardiovascular mortality and hospital admissions associated with increases in levels of air pollutants. However, little is known about the relationship between hospital admissions for stroke and air pollution. This study was undertaken to determine whether there is an association between air pollution and hospital admissions for stroke in Kaohsiung, Taiwan.
Data on a total of 23 179 stroke admissions were obtained for the period 1997 through 2000. The relative risk of hospital admissions was estimated with a case-crossover approach.
In the single-pollutant models, on warm days (> or =20 degrees C), significant positive associations were found between levels of PM10, NO2, SO2, CO, and O3 and both primary intracerebral hemorrhage and ischemic stroke admissions. On cool days (<20 degrees C), only CO levels and ischemic stroke admissions were significantly associated. For the 2-pollutant models, PM10 and NO2 remained consistently and significantly associated with admissions for both types of stroke on warm days. We observed estimated relative risks of 1.54 (95% confidence interval [95%], 1.31 to 1.81) and 1.56 (95% CI, 1.32 to 1.84) for primary intracerebral hemorrhage for each interquartile range increase in PM10 and NO2. The values for ischemic stroke were 1.46 (95% CI, 1.32 to 1.61) and 1.55 (95% CI, 1.40 to 1.71), respectively. The effects of CO, SO2, and O3 were mostly nonsignificant when either NO2 or PM10 was controlled for.
This study provides an association between exposure to air pollution and hospital admissions for stroke.
There is conflicting evidence in the literature as to the predominant mechanism and also the compositional element(s) that drives the pulmonary inflammatory response of ambient particulate matter (PM). We have investigated the inflammogenic potential of coarse (2.5-10 microm) and fine (<2.5 microm) PM from both a rural and an industrial location in Germany, using bronchoalveolar lavage (BAL) of rat lungs 18 h post intratracheal instillation with PM. Irrespective of the sampling location, the coarse fraction of PM(10) but not its fine counterpart caused neutrophilic inflammation in rat lungs, in the absence of any severe pulmonary toxicity as indicated by the lack of an increase in lavage protein and lactate dehydrogenase levels. The rural sample of coarse PM also caused a significant increase in the tumor necrosis factor alpha (TNFalpha) content as well as glutathione depletion in the BAL fluid. The contrasting inflammatory responses of the different samples could not be explained by differences in the concentrations of soluble Fe, Cu, V, Ni, Cr, or Al or by the.OH generating capacities of the PM suspensions. However, the effects of the different PM samples were clearly associated with their endotoxin content, as well as their ability to induce interleukin (IL)-8 and TNFalpha from whole blood in vitro. In conclusion, on an equal mass basis, coarse but not fine PM samples from our sampling campaign induced an inflammatory reaction in the lung in the absence of gross cellular lung damage, following intratracheal instillation. Our data also indicate, in accordance with previous independent in vitro observations, that endotoxin or related contaminants may play a role in these in vivo effects.
Both occupational and environmental exposure to particles is associated with an increased risk of lung cancer. Particles are thought to impact on genotoxicity as well as on cell proliferation via their ability to generate oxidants such as reactive oxygen species (ROS) and reactive nitrogen species (RNS). For mechanistic purposes, one should discriminate between a) the oxidant-generating properties of particles themselves (i.e., acellular), which are mostly determined by the physicochemical characteristics of the particle surface, and b) the ability of particles to stimulate cellular oxidant generation. Cellular ROS/RNS can be generated by various mechanisms, including particle-related mitochondrial activation or NAD(P)H-oxidase enzymes. In addition, since particles can induce an inflammatory response, a further subdivision needs to be made between primary (i.e., particle-driven) and secondary (i.e., inflammation-driven) formation of oxidants. Particles may also affect genotoxicity by their ability to carry surface-adsorbed carcinogenic components into the lung. Each of these pathways can impact on genotoxicity and proliferation, as well as on feedback mechanisms involving DNA repair or apoptosis. Although abundant evidence suggests that ROS/RNS mediate particle-induced genotoxicity and mutagenesis, little information is available towards the subsequent steps leading to neoplastic changes. Additionally, since most of the proposed molecular mechanisms underlying particle-related carcinogenesis have been derived from in vitro studies, there is a need for future studies that evaluate the implication of these mechanisms for in vivo lung cancer development. In this respect, transgenic and gene knockout animal models may provide a useful tool. Such studies should also include further assessment of the relative contributions of primary (inflammation-independent) and secondary (inflammation-driven) pathways.
Numerous recent epidemiologic studies report increases in the daily incidence of cardiovascular disease mortality and morbidity related to increases in daily levels of fine particulate matter (PM)* air pollution. This study sought to evaluate the possible association between the occurrence of out-of-hospital sudden cardiac arrest (SCA) and daily PM levels in the Seattle metropolitan area. The underlying hypothesis was that PM exposure may act as a cardiovascular trigger for SCA. A case-crossover study was conducted among 362 SCA cases identified by paramedics from October 1988 through June 1994. Cases were King County WA residents who were married, aged 25 to 74 years at the time of their SCA, with no prior history of clinically recognized heart disease or other life-threatening comorbid conditions. Daily averages of regional PM monitoring data for nephelometry measures of PM (reported in units of bsp, referred to as coefficient of light scattering) and PM10 (particulate matter 10 microm or smaller in aerodynamic diameter) from three monitoring sites were used as indicators of exposure. In the case-crossover analysis, PM levels during index times of cases within the five days preceding an SCA were compared with PM levels at referent days, defined as the same days of the week during the month of SCA occurrence. Lag periods for index days of 0 to 5 days were investigated. The estimated relative risk (RR) at a lag of 1 day for an interquartile range (IQR) change in nephelometry (0.51 bsp) was 0.893 (95% confidence interval [CI] 0.779-1.024). Varying the lag period had only minimal change on the observed association. The estimated relative risk at a lag of 1 day for an IQR change of PM10 (19.3 microg/m3) was 0.868 (95% CI 0.744-1.012). There was no evidence of confounding by ambient daily exposures to carbon monoxide or sulfur dioxide. Analysis of effect modification by individual-level variables, including age, cigarette smoke exposure, physical activity, and other risk or protective factors for cardiovascular disease did not reveal any susceptible subgroups. The null results of this study may be due to several factors; these include: the highly selected nature of this SCA case series; the fact that cases were free of prior clinically recognized heart disease or major life-threatening comorbidity; and the possibility that PM exposures at the relatively low levels seen in the Seattle metropolitan area do not trigger cardiovascular toxic mechanisms that culminate in SCA.
Exposure to ambient air particulate matter (PM) is associated with pulmonary and cardiovascular diseases and cancer. The mechanisms of PM-induced health effects are believed to involve inflammation and oxidative stress. The oxidative stress mediated by PM may arise from direct generation of reactive oxygen species from the surface of particles, soluble compounds such as transition metals or organic compounds, altered function of mitochondria or NADPH-oxidase, and activation of inflammatory cells capable of generating ROS and reactive nitrogen species. Resulting oxidative DNA damage may be implicated in cancer risk and may serve as marker for oxidative stress relevant for other ailments caused by particulate air pollution.
The objectives of this study were to determine whether differences in the size and composition of coarse (2.5-10 micro m), fine (< 2.5 microm), and ultrafine (< 0.1 microm) particulate matter (PM) are related to their uptake in macrophages and epithelial cells and their ability to induce oxidative stress. The premise for this study is the increasing awareness that various PM components induce pulmonary inflammation through the generation of oxidative stress. Coarse, fine, and ultrafine particles (UFPs) were collected by ambient particle concentrators in the Los Angeles basin in California and used to study their chemical composition in parallel with assays for generation of reactive oxygen species (ROS) and ability to induce oxidative stress in macrophages and epithelial cells. UFPs were most potent toward inducing cellular heme oxygenase-1 (HO-1) expression and depleting intracellular glutathione. HO-1 expression, a sensitive marker for oxidative stress, is directly correlated with the high organic carbon and polycyclic aromatic hydrocarbon (PAH) content of UFPs. The dithiothreitol (DTT) assay, a quantitative measure of in vitro ROS formation, was correlated with PAH content and HO-1 expression. UFPs also had the highest ROS activity in the DTT assay. Because the small size of UFPs allows better tissue penetration, we used electron microscopy to study subcellular localization. UFPs and, to a lesser extent, fine particles, localize in mitochondria, where they induce major structural damage. This may contribute to oxidative stress. Our studies demonstrate that the increased biological potency of UFPs is related to the content of redox cycling organic chemicals and their ability to damage mitochondria.
Exposure to particulate matter (PM) air pollution increases the risk for myocardial infarctions, strokes, and cardiovascular mortality. A variety of responsible mechanisms have been described, including PM-induced elevations in blood pressure. Observational studies and controlled experiments have provided evidence that PM is capable of acutely increasing blood pressure in certain scenarios. Enhanced sympathetic tone and vascular dysfunction due to PM-induced systemic oxidative stress/inflammation are leading explanations. The hemodynamic responses to air pollution may be altered by underlying cardiovascular risk factors and the chemical composition of the PM. However, even the small elevations in blood pressure observed following certain exposures to PM have tremendous public health implications, due to the ubiquitous nature of air pollution.
The concentration of suspended particulate matter (SPM), nitrogen dioxide (NO,) and sulphur dioxide (SO2) were measured at 13 important traffic intersections in Pune city. In order to study the contribution of these pollutants from motor vehicles, attention was focused on the roadside, street-level concentration. The statistical analysis of the sampling results indicates that there is not only high correlation between SPM and NO2 but the levels of these pollutants are above the National Ambient Air Quality Standards (NAAQS) laid down by the Central Pollution Control Board (CPCB), India. The SO, concentrations are found to be well below the NAAQS.
Evidence for an associationbetweenairpollutionanddailystrokeadmissions in Kaohsiung
- Ss Tsai
- Wb Goggins
- Hf Chiu
- Yang
Tsai SS, Goggins WB, Chiu HF, Yang CY. Evidence for an associationbetweenairpollutionanddailystrokeadmissions in Kaohsiung, Taiwan. Stroke. 2003;34:2612–2616
The effects of airpollutiononhospitalizationsforcardiovasculardiseasein elderlypeopleinAustralianandNewZealandcities
- Ag Barnett
- Gm Williams
- J Schwartz
Barnett AG, Williams GM, Schwartz J, et al. The effects of airpollutiononhospitalizationsforcardiovasculardiseasein elderlypeopleinAustralianandNewZealandcities.Environ Health Perspect. 2006;114:1018–1023
Committee of the Environmental and Occupational Health Assembly of the Health effects of outdoor air pollution
Committee of the Environmental and Occupational Health
Assembly of the American Thoracic Society. Health effects of
outdoor air pollution. Am J Respir Crit Care Med. 1996;153:3–
50.