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Race, Gender, and Social Status as Modifiers of the Effects of PM10 on Mortality
Abstract
Interest has recently been focused on which populations are most at risk of premature mortality induced by air pollution. This coincides with greater concern about environmental justice. We analyzed total mortality in the four largest US cities with daily measurements of particulate matter less than 10 microns (PM10) and combined the results to determine whether race, sex, and education are potential modifiers of the effects of PM10 on mortality. We computed daily counts of deaths stratified by sex, race, and education in each city and investigated their associations with PM10 in a Poisson regression model. We combined the results by using inverse variance weighted averages. We found evidence of effect modification by sex, with the slope in female deaths one third larger than in male deaths, whereas for social factors and race we found only weak evidence of effect modification. In general, the effect modification appeared modest compared with other reports of substantial effect modification by medical conditions.
... 12,21-23 Research conducted in Asia, Europe, and the Americas has explored a short-term association between meteorological factors and suicide. [10][11][12]18,[24][25][26][27] A time-series regression approach applying a generalized additive model (GAM) has typically been used in studies exploring the association between environmental factors and mortality 28,29 ; however, there are few studies about suicide. A study performed in Korea using the GAM, adjusted for confounding factors, observed a 1.4% increase in suicide with each 1 o C increase in daily mean temperature. ...
... These models use a smooth function that is a nonparametric tool allowing control for potential nonlinear dependence of the variable of interest (in this case, number of suicide) on covariates (in this case, weather). 29 In a GAM, the dependent variable belongs to exponential family and the predictors are smooth functions of each covariate. In this context, the expected number of suicides (a Poisson random variable) was estimated as the sum of smooth and linear functions of the weather predictor variables. ...
... Usually, PDL has been applied to social sciences studies and econometrics, and its use in epidemiology has been described in studies of the weather's effect on respiratory and cardiovascular deaths. 28,29,34 Weather can influence suicide deaths not only in the same week but also on subsequent weeks. 12 Hence, the number of suicides in a given week will depend not only on the same-weather week effect, but also on the lagged effect of the previous weeks. ...
Objective:
Considering the scarcity of reports from intertropical latitudes and the Southern Hemisphere, we aimed to examine the association between meteorological factors and suicide in São Paulo.
Method:
Weekly suicide records stratified by sex were gathered. Weekly averages for minimum, mean, and maximum temperature (°C), insolation (hours), irradiation (MJ/m²), relative humidity (%), atmospheric pressure (mmHg), and rainfall (mm) were computed. The time structures of explanatory variables were modeled by polynomial distributed lag applied to the generalized additive model. The model controlled for long-term trends and selected meteorological factors.
Results:
The total number of suicides was 6,600 (5,073 for men), an average of 6.7 suicides per week (8.7 for men and 2.0 for women). For overall suicides and among men, effects were predominantly acute and statistically significant only at lag 0. Weekly average minimum temperature had the greatest effect on suicide; there was a 2.28% increase (95%CI 0.90-3.69) in total suicides and a 2.37% increase (95%CI 0.82-3.96) among male suicides with each 1 °C increase.
Conclusion:
This study suggests that an increase in weekly average minimum temperature has a short-term effect on suicide in São Paulo.
... 12,21-23 Research conducted in Asia, Europe, and the Americas has explored a short-term association between meteorological factors and suicide. [10][11][12]18,[24][25][26][27] A time-series regression approach applying a generalized additive model (GAM) has typically been used in studies exploring the association between environmental factors and mortality 28,29 ; however, there are few studies about suicide. A study performed in Korea using the GAM, adjusted for confounding factors, observed a 1.4% increase in suicide with each 1 o C increase in daily mean temperature. ...
... These models use a smooth function that is a nonparametric tool allowing control for potential nonlinear dependence of the variable of interest (in this case, number of suicide) on covariates (in this case, weather). 29 In a GAM, the dependent variable belongs to exponential family and the predictors are smooth functions of each covariate. In this context, the expected number of suicides (a Poisson random variable) was estimated as the sum of smooth and linear functions of the weather predictor variables. ...
... Usually, PDL has been applied to social sciences studies and econometrics, and its use in epidemiology has been described in studies of the weather's effect on respiratory and cardiovascular deaths. 28,29,34 Weather can influence suicide deaths not only in the same week but also on subsequent weeks. 12 Hence, the number of suicides in a given week will depend not only on the same-weather week effect, but also on the lagged effect of the previous weeks. ...
Background
Smoking restriction laws have spread worldwide during the last decade. Previous studies have shown a decline in the community rates of myocardial infarction after enactment of these laws. However, data are scarce about the Latin American population. In the first phase of this study, we reported the successful implementation of the law in São Paulo city, with a decrease in carbon monoxide rates in hospitality venues.
Objective
To evaluate whether the 2009 implementation of a comprehensive smoking ban law in São Paulo city was associated with a reduction in rates of mortality and hospital admissions for myocardial infarction.
Methods
We performed a time-series study of monthly rates of mortality and hospital admissions for acute myocardial infarction from January 2005 to December 2010. The data were derived from DATASUS, the primary public health information system available in Brazil and from Mortality Information System (SIM). Adjustments and analyses were performed using the Autoregressive Integrated Moving Average with exogenous variables (ARIMAX) method modelled by environmental variables and atmospheric pollutants to evaluate the effect of smoking ban law in mortality and hospital admission rate. We also used Interrupted Time Series Analysis (ITSA) to make a comparison between the period pre and post smoking ban law.
Results
We observed a reduction in mortality rate (−11.9% in the first 17 months after the law) and in hospital admission rate (−5.4% in the first 3 months after the law) for myocardial infarction after the implementation of the smoking ban law.
Conclusions
Hospital admissions and mortality rate for myocardial infarction were reduced in the first months after the comprehensive smoking ban law was implemented.
... Throughout the last few decades, surface transportation funding has been majorly defined by federal appropriation acts, including the Intermodal Surface Transportation Efficiency Act (IS-TEA) (1991)(1992)(1993)(1994)(1995)(1996)(1997), the Transportation Equity Act for the 21 st Century (TEA-21) (1998)(1999)(2000)(2001)(2002)(2003), and the Safe, Accountable, Flexible, Efficient Transportation Equity Act: A Legacy for Users (SAFETEA-LU) (2005)(2006)(2007)(2008)(2009). The most recent transportation legislation, Moving Ahead for Progress in the 21 st Century Act (MAP-21) (2012)(2013)(2014), passed with provisions particularly relevant to freight transport: the number of federal surface transportation grant programs was consolidated by two-thirds, the environmental review process was altered to allow for more categorical exclusions and enforce four-year review timelines with penalties for agencies that conduct longer reviews, and a national freight plan is underway (Lang, 2012). These acts rely heavily on gas taxes, promoting oil dependence to maintain transportation infrastructure and, some argue, this source of funding will be unreliable if the nation continues to move towards development of alternative transportation modes (TRB, 2006). ...
... To validate digitization of land border crossings, I compared shapefiles to images in documents posted online by the General Services Administration, the independent U.S. agency responsible for acquisition, use, and disposal of government land property. As secondary references, I also referred to images in environmental assessment documents and Google Earth software (2012) to ensure boundaries were as accurate as possible. Digitized polygons likely provided conservative underestimates of exposed populations given that core infrastructure are frequently surrounded by expansive private transportation facilities. ...
... Drawing on methods used extensively in EJ research at hazardous sites (Mohai & Saha, 2006;Ringquist, 2005;Maantay, 2002;Taquino, Parisi, & Gill, 2002) and pollution exposure studies (Maantay, Maroko, & Porter-Morgan, 2008;Pastor, Sadd, Morellow-Frosch, 2002;Zanobetti & Schwartz, 2000), areal weights (Langford, Macguire, & Unwin, 1991) enable us to estimate characteristics of a geographic area based on information about the larger unit. In this study, this entailed creating 500-meter and 1-mile buffers around freight gateways and intersecting these with census tract shapefiles in ArcGIS10.0 ...
Transportation-related air and noise pollution from heavy-duty freight engines is associated with respiratory and cardiovascular illnesses, cancer, diabetes, nervous system and cognitive effects, hospital admissions, sleep disruption, and premature mortality. Research is needed to understand how residents in host communities nearby freight gateways (e.g., ports, borders) experience and counter these impacts. With an environmental justice framework, I used: 1) spatial analyses to quantitatively describe the demographic composition of U.S. freight host communities, and 2) institutional ethnography to qualitatively investigate public participation in freight land use deliberations.
Quantitatively, I derived demographic descriptions of host communities by overlaying American Community Survey (2005-2009) tract-level data with buffered digitized images of freight gateways. At the 50 largest U.S. freight gateways, results from areally weighted analyses show that populations within 500 meters of a freight gateway have significantly higher proportions of persons of color, Hispanic ethnicity, without a high school diploma, and below the federal poverty level. Logistic regression models also compare 500-meter and 1-mile host communities to non-host communities, and overall results suggest that communities of color are disproportionately compromised by both transportation and industrial air pollution sources.
Qualitatively, I synthesized data from interviews, content analysis, and participant observations at two distinct case sites: the proposed New International Trade Crossing in Detroit, Michigan and the Port of Long Beach in Long Beach, California. Interviewees identify catalysts, barriers, and opportunities for addressing freight???s local impacts through institutionally- and community-led strategies. Macroeconomic forces often override local concerns, whereby freight-related development decisions are made in advance or outside of public participation opportunities. Still, host communities may shift deliberations by exposing overlooked risks, legally challenging assessment procedures, proposing site or project alternatives, advocating adoption of sustainable technologies, equalizing mitigation opportunities, or codifying innovative governance structures.
This study defines freight transport as an environmental justice issue. Results from quantitative analyses demonstrate patterns of exposure to well-documented freight-related health risks with implications for health equity. Qualitative inquiry enables deconstruction of theories and practices related to public participation and environmental assessment in freight host communities. Collectively, these findings inform cross-sector interventions to address global freight transport???s local threats to public health.
... Compared with the results from the U.S. Agricultural Health Study, in this present study, the interaction between air quality, obesity and CVD was evident only in females. The mechanisms for this gender-specific interaction are unclear, although there is growing literature on the differing associations between air pollution and health for males and females (Clougherty, 2010;Kan et al., 2008;Zanobetti and Schwartz, 2000;Keitt et al., 2004). Kan et al. conducted a time-series analysis study in Shanghai, China and reported that women have been found to be more susceptible to the effects of exposure to air pollution (Kan et al., 2008). ...
... Kan et al. conducted a time-series analysis study in Shanghai, China and reported that women have been found to be more susceptible to the effects of exposure to air pollution (Kan et al., 2008). Another study of four US cities found a slightly higher risk of all deaths for females (Zanobetti and Schwartz, 2000). The different particle deposition characteristics in males and females might partially explain such discrepancies by gender (Kim and Hu, 1998;Kohlhäufl et al., 1999). ...
... high unemployment rate, low income, and low education level) compared to many other European countries. Many studies suggested that low socioeconomic status groups might be more susceptible toward a negative impact of ambient air pollution (Gouveia & Fletcher 2000;Zanobetti & Schwartz 2000;Fernández-Somoano et al. 2013). For this reason, it seems important to determine risk coefficients in the particular context of Wallonia. ...
... A possible explanation is that people of lower socioeconomic status has harmful behaviors like poorer nutrition or higher smoking prevalence. These negative behaviors make people with low socioeconomic status more susceptible to the adverse effects of air pollution than those in higher socioeconomic groups (Gouveia & Fletcher 2000;Zanobetti & Schwartz 2000;Fernández-Somoano et al. 2013). ...
The case-crossover design is frequently used for analyzing the acute health effects of air pollution. Nevertheless, only a few studies compared different methods for selecting control periods. In this study, the bidirectional method and three time-stratified methods were used to estimate the association between air pollution and acute myocardial infarction (AMI) in Charleroi, Belgium, during 1999-2008. The strongest associations between air pollution and AMI were observed for PM10 and NO2 during the warm period, OR = 1.095 (95 % CI: 1.003-1.169) and OR = 1.120 (95 % CI: 1.001-1.255), respectively. The results of this study reinforce the evidence of the acute effects of air pollution on AMI, especially during the warm season. This study suggests that the different methods of case-crossover study design are suitable to studying the association between acute events and air pollution. The temperature-stratified design is useful to exclude temperature as a potential confounder.
... Although the evidence regarding the adverse health impacts of household air pollution is growing, uncertainty remains as to the health improvements expected as a result of interventions introducing cleaner burning stoves. Evidence that certain characteristics confer increased susceptibility to the adverse effects associated with exposures to air pollution is mounting, especially for ambient air pollution [33][34][35][36][37][38][39][40][41]. Here, we define susceptibility as individual-and population-level characteristics that increase the risk of air pollution-related health effects in a population. ...
... Susceptibility may, therefore, indicate the presence of different exposure-response relationships among different populations (i.e., given the same level of air pollution exposure, some populations will experience greater health effects than others), or it may also refer to a characteristic of a population that increases the likelihood or opportunity for greater exposure to certain pollutants (sometimes referred to as vulnerability) [33]. Factors that have been observed to increase susceptibility to air pollution exposures include age, sex, genetics, underlying health, obesity, diet, smoking status, socioeconomic status, and psychosocial stressors [33][34][35][36][37][38][39][40][41]. ...
Household air pollution from solid fuel combustion in inefficient and poorly vented cookstoves is estimated to be responsible for 3.9 million premature deaths per year and 4.8 % of the global burden of disease, making it the third leading risk factor for morbidity and mortality worldwide. Despite increasing recognition surrounding this global environmental health problem, much remains to be elucidated regarding exposure response relationships, particularly among potentially susceptible population subgroups. Given that many of the communities most affected by household air pollution exposures also experience elevated exposures to poverty, psychosocial stressors, other environmental pollutants, and comorbid conditions, research needs to correctly specify risks due to these potentially interacting risk factors. Although suggestive evidence exists for differential improvements in health following reductions in ambient air pollution concentrations among specific subgroups, the question remains as to who will benefit and to what extent from efforts to reduce exposures to emissions from household solid fuel combustion. The ability to know what to expect from cookstove interventions and to accurately describe the presence of distinct subgroup responses is crucial to reduce uncertainty and to encourage policy makers to enact change.
... Air pollution is a serious worldwide public health problem. Recently, many studies have found that socio-economic disparities among cities are probably responsible for the differences in air pollution effects [1][2]. This inequity is one possible explanation for the disparities in health among areas of varying socio-economic status. ...
... Classification of socio-economic characteristics is the key step of exposure justice assessment to air pollutants. In most previous studies, socio-economic status measures were limited to education attainment and race [2,[9][10][11]. Only a few have investigated effect modification of other measures, such as occupation [5]. ...
Using general loglinear analysis and GIS spatial analysis, we evaluated the socio-economic inequities in exposure to SO2 in the urban and rural areas at census scale. The results show that differences of exposure inequities among socioeconomic groups exist in the urban and rural areas. Further studies are needed to analyze the impacts of scales and statistical methods on the accuracy of air pollution exposure justice assessment.
... Air pollution is recognized as a priority global health issue, affecting millions in both the developed and developing world (Brauer et al., 2012). Early studies have found that socioeconomic disparities in air pollution exposure and related health effects are prevalent (Zanobetti and Schwartz, 2000;O'Neill et al., 2003). Identification of susceptible and disadvantaged socioeconomic status (SES) groups at the greatest risk of air pollution exposure is critical for accurately estimating the adverse outcomes of air pollution and may provide additional explanations for inconsistency in results between studies. ...
... Proper categorization of socio-demographic characteristics is a key step in the assessment of exposure justice to air pollutants. In line with previous studies (Zanobetti and Schwartz, 2000;Gwynn and Thurston, 2001;Pope et al., 2002;Ou et al., 2008), we selected age, race, educational attainment, and income as the socio-demographic characteristics of focus in this study. These characteristics were categorized into different levels for each of the three spatial scales based on the reference category for comparison based on previous studies in the environmental justice literature. ...
Recent studies examining racial and ethnic inequities in exposure to urban air pollution have led to advances in understanding the nature and extent of overall concentration exposures by pollutant, demarcated by disadvantaged groups. However, the stability of inequities at various spatial units and the exposure by air pollution sources are often neglected. In this case study from the Dallas-Fort Worth (Texas, USA) area, we used Geographic Information Systems (GIS) and an air dispersion model to estimate environmental justice impacts at different spatial scales (i.e., zip code, census tract, block group) and by source (i.e., industrial pollution sources, vehicle pollution sources, industry and vehicle pollution sources combined). Using whites as a reference, blacks and other races were more likely to be exposed to higher sulfur dioxide (SO2) concentrations although the Odds Ratio (OR) varied substantially by pollution source type [e.g., industrial pollution source based: (OR=1.80; 95% CI (Confidence Interval): 1.79-1.80) vs. vehicle pollution source based: (OR=2.70; 95% CI: 2.68-2.71)] and varied less between spatial scales [for vehicle pollution sources, (OR=2.70; 95% CI: 2.68-2.71) at the census tract level but was (OR=2.54; 95% CI: 2.53-2.55) at the block group scale]. Similar to the pattern of racial inequities, people with less education (i.e., less than 12 years of education) and low income (i.e., per capital income below $20 000) were more likely to be exposed to higher SO2 concentrations, and those ORs also varied greatly with the pollution sources and slightly with spatial scales. It is concluded that the type of pollution source plays an important role in SO2 pollution exposure inequity assessment, while spatial scale variations have limited influence. Future studies should incorporate source-specific exposure assessments when conducting studies on environmental justice.
... Our study suggested that women may suffer greater impacts of O 3 exposure on the risk of obesity, consistent with a prior study (36). There is growing evidence reporting the sex-specific difference between AP exposure and health, although some controversy still remains over their exact biological roles (37,38). One time-series study proposed that females were more vulnerable when exposed to AP (39). ...
Background
Previous animal studies have suggested that air pollution (AP) exposure may be a potential risk factor for obesity; however, there is limited epidemiological evidence available to describe the association of obesity with AP exposure.
Methods
A retrospective cross-sectional study was conducted on 11,766 participants across mainland China in 2015. Obesity was assessed using body mass index (BMI), waist circumference (WC), and visceral adiposity index (VAI). The space-time extremely randomized tree (STET) model was used to estimate the concentration of air pollutants, including SO 2 , NO 2 , O 3 , PM 1 , PM 2.5 , and PM 10 , matched to participants’ residential addresses. Logistic regression models were employed to estimate the associations of obesity with outdoor AP exposure. Further stratified analysis was conducted to evaluate whether sociodemographics or lifestyles modified the effects.
Results
Increased AP exposure was statistically associated with increased odds of obesity. The odds ratio (ORs) and 95% confidence interval (CI) of BMI-defined obesity were 1.21 (1.17, 1.26) for SO 2 , 1.33 (1.26, 1.40) for NO 2 , 1.15 (1.10, 1.21) for O 3 , 1.38 (1.29, 1.48) for PM 1 , 1.19 (1.15, 1.22) for PM 2.5 , and 1.11 (1.09, 1.13) for PM 10 per 10 μg/m ³ increase in concentration. Similar results were found for central obesity. Stratified analyses suggested that elderly participants experienced more adverse effects from all 6 air pollutants than middle-aged participants. Furthermore, notable multiplicative interactions were found between O 3 exposure and females as well as second-hand smokers in BMI-defined obesity.
Conclusions
This study suggested that outdoor AP exposure had a significant association with the risk of obesity in the middle-aged and elderly Chinese population. Elderly individuals and women may be more vulnerable to AP exposure.
... Knox [132] mentioned that suicide had always been a mental health problem and improved suicide prevention interventions. Zanobetti [133] found that among the three factors of gender, race, and social factors, the mortality rate of females to air pollution was higher than that of males only in terms of gender, and the other two factors had no significant impact. Wang [134] studied whether neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) were related to death through actual cases of COVID-19 infection and found that NLR was an effective biological indicator for predicting mortality. ...
Public health emergency management has been one of the main challenges of social sustainable development since the beginning of the 21st century. Research on public health emergency management is becoming a common focus of scholars. In recent years, the literature associated with public health emergency management has grown rapidly, but few studies have used a bibliometric analysis and visualization approach to conduct deep mining and explore the characteristics of the public health emergency management research field. To better understand the present status and development of public health emergency management research, and to explore the knowledge base and research hotspots, the bibliometric method and science mapping technology were adopted to visually evaluate the knowledge structure and research trends in the field of public health emergency management studies. From 2000 to 2020, a total of 3723 papers related to public health emergency management research were collected from the Web of Science Core Collection as research data. The five main research directions formed are child prevention, mortality from public health events, public health emergency preparedness, public health emergency management, and coronavirus disease 2019 (COVID-19). The current research hotspots and frontiers are climate change, COVID-19 and related coronaviruses. Further research is needed to focus on the COVID-19 and related coronaviruses. This study intends to contribute inclusive support to related academia and industry in the aspects of public health emergency management and public safety research, as well as research hotspots and future research directions.
... In our study, the disease was significantly more frequent in women than in men (25:4). It has been reported that women are more sensitive to polluted air and that they have a greater chance of dying from pollution than men (32). One of the explanations may be that women more often suffer from AITD (31). ...
Background: Endocrine disrupting air pollutants such as sulphur dioxide (SO2), carbon monoxide (CO), nitrogen dioxide (NO2), fine particle matter (PM2.5), and ozone (O3) can affect thyroid gland function on the level of synthesis, metabolism, and the action of its hormones.
Objective: The aim of this study was to establish whether increased air pollution could contribute to an increased incidence of autoimmune thyroid diseases (AITD).
Methods: A retrospective analysis was conducted of the medical records of 82000 patients at the University Clinical Centre in Tuzla, Bosnia and Herzegovina. The target group of this study comprised a total of 174 patients from the Lukavac area. Daily data on concentrations of air pollutants were collected from the air quality monitoring station located in Lukavac. The study covered the period from 2015 to 2020.
Results: The results of the monitoring confirmed the presence of air pollutants in concentrations above the permitted limits throughout the entire observed period. Concentrations of PM2.5, SO2, NO2, CO, and O3 were in the range of 1.90–431.40 µg/m3, 3.60-620.50 µg/m3, 3.40-66.20 µg/m3, 48.00-7002.00 µg/m3, and 0.70-89.40 µg/m3, with means of 64.08 µg/m3, 77.48 µg/m3, 22.57 µg/m3, 1657.15 µg/m3, and 31.49 µg/m3, respectively. During the six-year period, 174 cases of AITD were registered, of which 150 (86.21%) were women and 24 (13.79%) men. Hashimoto's thyroiditis was found in 33 patients (18.97%), whilst 141 patients (81.03%) were diagnosed with atrophic thyroiditis. The highest total incidence of autoimmune thyroiditis was recorded in 2017, when it reached 99.49, 95% CI.
Conclusion: The effects of chronic exposure to a mixture of air pollutants on the function of the thyroid gland are still not sufficiently well-known, but the numerical tendency towards a higher incidence of AITD in this study, albeit without statistical significance (p>0.05), still underlines the need for additional research.
... [3][4][5][6] Its harmful effects vary by specific subpopulations, for example by age, sex, genetics, behavior, and socioeconomic conditions, leading to a severe disproportionate disease burden. [6][7][8][9][10][11] Children's first years of life are a uniquely sensitive developmental epoch of rapid body and brain growth that establishes the foundation for future physical, socioemotional, and cognitive health. The rapid development that occurs in early childhood enhances children's vulnerability to social and environmental stressors, such as housing instability, 12 temperature extremes, 13 infections, 14 and air pollution exposure. ...
Background:
Inconsistent evidence has assessed the impact of air pollution exposure on children's growth trajectories. We investigated the role of 90-day average postnatal fine particulate matter (PM2.5) exposures by estimating the magnitude of effects at different ages, and the change in child weight trajectory by categories of exposure.
Methods:
We obtained weight values from electronic health records at each hospital visit (males = 1859, females = 1601) from birth to 6 years old children recruited into the Boston-based Children's HealthWatch cohort (2009-2014). We applied mixed models, adjusting for individual and maternal confounders using (1) varying-coefficient models allowing for smooth non-linear interaction between age and PM2.5, (2) factor-smooth interaction between age and PM2.5 quartiles. Additionally, we stratified by sex and low birthweight (LBW) status (≤2500 g).
Results:
Using varying-coefficient models, we found that PM2.5 significantly modified the association between age and weight in males, with a positive association in children younger than 3 years and a negative association afterwards. In boys, for each 10 µg/m3 increase in PM2.5 we found a 2.6% increase (95% confidence interval = 0.8, 4.6) in weight at 1 year of age and a -0.6% (95% confidence interval = -3.9, 2.9) at 5 years. We found similar but smaller changes in females, and no differences comparing growth trajectories across quartiles of PM2.5. Most of the effects were in LBW children and null for normal birthweight children.
Conclusions:
This study suggests that medium-term postnatal PM2.5 may modify weight trajectories nonlinearly in young children, and that LBW babies are more susceptible than normal-weight infants.
... Females have been reported to be more vulnerable to air pollution (PM 10 , SO 2 , NO 2 , and O 3 ), and to have a higher air pollution-related mortality than males in a few studies (30). However, this study with a large sample size demonstrated that ORs for each pollutant with TNs were consistently lower in participants who were women and/or elderly, which contradicts the sex-specific effect of air pollutant on other outcomes including thyroid function indexes and mortality. ...
Background
Thyroid nodules has become a significant public health issue worldwide with a rapidly increasing prevalence. However, its association with outdoor air pollution remains poorly understood. We aim to investigate the relationship between six outdoor air pollutants (PM2.5, PM10, NO2, SO2, CO, and O3) and the risk of thyroid nodules.
Methods
We utilized a database including 4,920,536 participants who attended the annual physical examinations in the Meinian HealthCare Screening Center in 157 Chinese cities in 2017. City-specific concentrations of six pollutants (PM2.5, PM10, NO2, SO2, CO, and O3) from 2015 to 2017 were estimated based on the China’s National Urban Air Quality Real Time Publishing Platform. Thyroid nodule was measured with ultrasound. Multivariable Logistic regression was used to examine the associations between air pollutants and thyroid nodules with adjustment for age, sex, education, smoking, body mass index, fasting blood glucose, triglyceride, low density lipoprotein cholesterol, high density lipoprotein cholesterol, urine iodine, gross domestic product, and thyroid stimulating hormone. We conducted stratified analyses to investigate potential effect modification by sex, age, and urine iodine groups.
Results
Approximately 38% of the participants (1,869,742) were diagnosed with thyroid nodules. Each of the six air pollutants was significantly and linearly associated with the risk for thyroid nodules. The adjusted odds ratios [95% CI] for every increase of 10 μg/m³ for PM2.5, PM10, NO2, SO2, and O3 were 1.062 [1.061, 1.064], 1.04 [1.03, 1.04], 1.10 [1.09, 1.10], 1.11 [1.11, 1.12], and 1.151 [1.149, 1.154], respectively; The odds ratio for each increase of 1 mg/m³ for CO was 1.50 [1.49 to 1.52]. Furthermore, these associations were significantly higher in the participants who were men, younger, or having lower urine iodine level (p <0.001).
Conclusion
The six air pollutants may contribute to the high prevalence of thyroid nodules in China.
... In the sex-stratified analysis, we found that females were more sensitive to PM 10 , although the association was not statistically significant. This finding is in agreement with the finding in a previous study (Zanobetti and Schwartz, 2000). In the age-stratified analysis, the elderly might be more vulnerable to PM, which might be a result of different physiological structures, exposure patterns, or individual social behaviors (Bell et al. 2013). ...
Epidemiological evidence has shown a significant association between short-term exposure to air pollution and mortality risk for circulatory system diseases (CSD). However, informative insights on the significance and magnitude of its relationship in the process of government interventions on abating air pollution are still lacking, particularly in a burgeoning Chinese city. In this study, we conducted a time series study in Lishui District, Nanjing, to examine the effect of ambient particulate matter (PM), e.g., PM2.5 and PM10, on daily death counts of CSD which included cardiovascular disease (CVD), cerebrovascular disease (CEVD), and arteriosclerotic heart disease (ASHD) mortality from January 1, 2015, to December 31, 2019. The results revealed that each 10 μg/m3 increase in PM2.5 and PM10 concentration at lag0 day was associated with an increase of 1.33% (95% confidence interval, 0.08%, 2.60%) and 1.12% (0.43%, 1.82%) in CSD mortality; 2.42% (0.44%, 4.43%) and 1.43% (0.32%, 2.55%) in CVD mortality; 1.20% (− 0.31%, 2.73%) and 1.21% (0.38%, 2.05%) in CEVD mortality; and 2.78% (0.00%, 5.62%) and 1.66% (0.14%, 3.21%) in ASHD mortality, respectively. For cumulative risk, the corresponding increase in daily mortality for the same change in PM2.5 concentration at lag03 day was significantly associated with 1.94% (0.23%, 3.68%), 3.17% (0.58%, 5.84%), 2.38% (0.17%, 4.63%), and 4.92% (1.18%, 8.81%) for CSD, CVD, CEVD, and ASHD, respectively. The exposure–response curves were approximately nonlinear over the entire exposure range of the PM concentrations. We also analyzed the effect modifications by season (warm or cold), age group (0–64 years, 65–74 years, or ≥ 75 years), and sex (male or female). Although not statistically significant, stratified analysis showed greater vulnerability to PM exposure for cold season, population over 65 years of age, and female group.
... The effect of socioeconomic status and PM 2.5 on CV mortality is not well understood. Prior limited studies have shown that socioeconomic status may modify the risk of PM on daily mortality in the US 25 and Hong Kong 26 , and asthma in Seoul, South Korea 27 . One study of carotid intimal media progression suggested the effect of PM 2.5 was greater among socially disadvantaged groups 28 . ...
Background
Air pollution and socioeconomic status have both been strongly associated with cardiovascular (CV) outcomes. We sought to determine if socioeconomic status modifies the risk association between fine particulate matter air pollution (PM2.5) and CV mortality.
Methods
We linked county-level age-adjusted CV mortality data from Multiple Cause of Death files (2000-2016, ICD10: I00-I99) with 2015 Social Deprivation Index (SDI), a validated estimate of socioeconomic status, and modelled spatial and temporal mean annual PM2.5 exposures (2012-2018). Higher SDI suggests greater deprivation and lower socioeconomic status. Associations between PM2.5 and age adjusted CV mortality were estimated using linear models.
Results
A total of 5,769,315 cardiovascular deaths from 2012-2018 across 3106 U.S. counties were analyzed. Both PM2.5 (β (SE) 7.584 (0.938), P<0.001) and SDI scores (β (SE) 0.591 (0.140), P<0.001) were independently associated with age-adjusted CV mortality (R²=0.341). The association between PM2.5 and CV mortality was stronger among counties with highest SDI, P value for interaction = 0.012.
Conclusion
Social deprivation and PM2.5 exposures were independently associated with county level age-adjusted CV mortality. The associations between PM2.5 and CV mortality were stronger in counties with high vs low social deprivation. SDI and PM2.5 represent potential targets to reduce CV mortality disparities and interventions to reduce PM2.5 exposure may be most impactful in communities of low socioeconomic status.
... In general, these are all lower exposure scenarios, and relationships may be nonlinear. Second, some studies have reported evidence of effect modification by age and sex (Clougherty, 2010;Yin et al., 2017;Zanobetti and Schwartz, 2000), but pooled estimates for gender-based effect modification have been weak and little is known in LMICs (Bell et al., 2013). Furthermore, not many studies on mortality have investigated the short-term associations beyond the window one week prior to death, and a few looked into lags of more than 30 days (Zanobetti et al., 2002;Zanobetti et al., 2003). ...
... Air pollution has also been associated with increase in mortality (Aga et al., 2003;Chung et al., 2015a;Schwartz, 2004;Stafoggia et al., 2008). This association has been found to be more pronounced in the elderly (Aga et al., 2003), and those who are made more vulnerable due to diabetes (Zeka et al., 2006), cardiovascular, or respiratory diseases (Zanobetti and Schwartz, 2000). Furthermore, recent studies in the US found causal associations between local air pollution and mortality (Schwartz et al., 2015(Schwartz et al., , 2017. ...
High temperature and air pollutants have been reported as potential risk factors of mortality. Previous studies investigated interaction between the two variables; however, the excess death risk due to the synergic effect (i.e. interaction on the additive scale) between the two variables has not been investigated adequately on a multi-country scale. This study aimed to assess the excess death risk due to the synergism between high temperature and air pollution on mortality using a multicity time-series analysis. We collected time-series data on mortality, weather variables, and four air pollutants (PM10, O3, NO2, and CO) for 16 metropolitan cities of three countries (Japan, Korea, and Taiwan) in Northeast Asia (1979-2015). Quasi-Poisson time-series regression and meta-analysis were used to estimate the additive interaction between high temperature and air pollution. The additive interaction was measured by relative excess risk due to interaction (RERI) index. We calculated RERI with relative risks (RR) of the 99th/10th, 90th/90th, and 99th/90th percentiles of temperature/air pollution metrics, where risk at the 90th/10th percentiles of temperature/air pollution metrics was the reference category. This study showed that there may exist positive and significant excess death risks due to the synergism between high temperature and air pollution in the total population for all pollutants (95% lower confidence intervals of all RERIs>0 or near 0). In final, we measured quantitatively the excess death risks due to synergic effect between high temperature and air pollution, and the synergism should be considered in public health interventions and a composite warning system.
... In general, these are all lower exposure scenarios, and relationships may be nonlinear. Second, some studies have reported evidence of effect modification by age and sex (Clougherty, 2010;Yin et al., 2017;Zanobetti and Schwartz, 2000), but pooled estimates for gender-based effect modification have been weak and little is known in LMICs (Bell et al., 2013). Furthermore, not many studies on mortality have investigated the short-term associations beyond the window one week prior to death, and a few looked into lags of more than 30 days (Zanobetti et al., 2002;Zanobetti et al., 2003). ...
There is limited evidence for short-term association between mortality and ambient air pollution in the Middle East and no study has evaluated exposure windows of about a month prior to death. We investigated all-cause non-accidental daily mortality and its association with fine particulate matter (PM2.5), nitrogen dioxide (NO2), and the Air Quality Index (AQI) from March 2011 through March 2014 in the megacity of Tehran, Iran. Generalized additive quasi-Poisson models were used within a distributed lag linear modeling framework to estimate the cumulative effects of PM2.5, NO2, and the AQI up to a lag of 45 days. We further conducted multi-pollutant models and also stratified the analyses by sex, age group, and season. The relative risk (95% confidence interval (CI)) for all seasons, both sexes and all ages at lag 0 for PM2.5, NO2, and AQI were 1.004 (1.001, 1.007), 1.003 (0.999, 1.007), and 1.004 (1.001, 1.007), respectively, per inter-quartile range (IQR) increment (18.8 µg/m3 for PM2.5, 12.6 ppb for NO2, and 31.5 for AQI). In multi-pollutant models, the PM2.5 associations were almost independent from NO2. However, the RRs for NO2 were slightly attenuated after adjustment for PM2.5 but they were still largely independent from PM2.5. The cumulative relative risks (95% CI) per IQR increment reached maximum during the cooler months, including: 1.13 (1.06, 1.20) for PM2.5 at lag 0-31 (for females, all ages); 1.17 (1.10, 1.25) for NO2 at lag 0-45 (for males, all ages); and 1.13 (1.07, 1.20) for the AQI at lag 0-30 (for females, all ages). Generally, the RRs were slightly larger for NO2 than PM2.5 and AQI. We found somewhat larger RRs in females, age group >65 years of age, and in cooler months. In summary, positive associations were found in most models. This is the first study to report short-term associations between all-cause non-accidental mortality and ambient PM2.5 and NO2 in Iran.
... Generalizability of our stove type results may be limited as other countries use different cleaner-burning stoves and/or fuels. Finally, factors that influence susceptibility to air pollution exposure include age, sex, genetics, underlying health, obesity, diet, smoking status, socioeconomic status, and psychosocial stressors.[40][41][42] Our results may, therefore, not apply to other populations with different underlying characteristics. ...
Household air pollution from biomass cookstoves is estimated to be responsible for more than two and a half million premature deaths annually, primarily in low and middle‐income countries where cardiometabolic disorders, such as Type II Diabetes, are increasing. Growing evidence supports a link between ambient air pollution and diabetes, but evidence for household air pollution is limited. This cross‐sectional study of 142 women (72 with traditional stoves and 70 with cleaner‐burning Justa stoves) in rural Honduras evaluated the association of exposure to household air pollution (stove type, 24‐hour average kitchen and personal fine particulate matter [PM2.5] mass and black carbon) with glycated hemoglobin (HbA1c) levels and diabetic status based on HbA1c levels. The prevalence ratio [PR] per interquartile range increase in pollution concentration indicated higher prevalence of prediabetes/diabetes (versus normal HbA1c) for all pollutant measures (e.g., PR per 84 μg/m³ increase in personal PM2.5, 1.49; 95% confidence interval [CI], 1.11 – 2.01). Results for HbA1c as a continuous variable were generally in the hypothesized direction. These results provide some evidence linking household air pollution with the prevalence of prediabetes/diabetes, and, if confirmed, suggest that the global public health impact of household air pollution may be broader than currently estimated.
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... Die eingeschlossenen Publikationen zeigten kaum weiterführende Ansätze zur Integration von Geschlecht in die Forschung. Beispielsweise wurde in einer Studie zur Wirkung von PM10 (Feinstaub) auf die Mortalität in den vier größten Städten der USA Geschlecht als Effektmodifikator identifiziert mit einer stärkeren Assoziation bei Frauen im Vergleich zu Männern [38]. Bildung und Ethnizität waren nicht von Bedeutung. ...
Die umfassende Berücksichtigung von Geschlecht (biologische und soziale Dimensionen) in der Gesundheitsforschung ist essenziell, um Relevanz und Validität der Forschungsergebnisse zu erhöhen. Im Unterschied zu anderen Bereichen der Gesundheitsforschung fehlt bislang eine systematische Aufarbeitung des Forschungsstandes zur Bedeutung von Geschlecht bei umweltbezogener Gesundheit. In dem interdisziplinären Forschungsnetzwerk Geschlecht – Umwelt – Gesundheit (GeUmGe-NET) wurde in ausgewählten Themenfeldern der Forschungsbereiche Umwelttoxikologie, Umweltmedizin, Umweltepidemiologie und Public-Health-Forschung zu Umwelt und Gesundheit der aktuelle Stand zur Integration von Geschlechteraspekten bzw. Genderkonzepten systematisch erhoben. In allen Bereichen wurden Wissenslücken und Forschungsbedarfe identifiziert sowie Potenziale für methodische Weiterentwicklungen durch Nutzung von Genderkonzepten aufgezeigt. Mit dem Forschungsnetzwerk GeUmGe-NET wurde ein Dialog zwischen biomedizinisch bzw. Public-Health-orientierter Gesundheitsforschung und sozialwissenschaftlicher Genderforschung begonnen. Dieser Dialog ist weiterzuführen, insbesondere hinsichtlich der gemeinsamen Erprobung methodischer Innovationen bei Datenerhebung und Datenanalyse. Erkenntnisse aus dieser interdisziplinären Forschung sind relevant für die Praxisfelder umweltbezogener Gesundheitsschutz, Gesundheitsförderung, Umweltgerechtigkeit und umweltbezogene Gesundheitsberichterstattung.
... The authors explain that this difference is due to the lower socioeconomic level of women in said country [37]. Other authors also show that women are more susceptible than men to air pollution [38]. These differences could be due, for example, to pulmonary absorption or a different hormonal status. ...
Many studies have shown a short-term association between NO2 and cardiovascular disease. However, few data are available on the delay between exposure and a health-related event. The aim of the present study is to determine the strength of association between NO2 and cardiovascular health in Wallonia for the period 2008–2011. This study also seeks to evaluate the effects of age, gender, season and temperature on this association. The effect of the delay between exposure and health-related event was also investigated. The daily numbers of hospital admissions for arrhythmia, acute myocardial infarction, ischemic and haemorrhagic stroke were taken from a register kept by Belgian hospitals. Analyses were performed using the quasi-Poisson regression model adjusted for seasonality, long-term trend, day of the week, and temperature.
Our study confirms the existence of an association between NO2 and cardiovascular disease. Apart from haemorrhagic stroke, the strongest association between NO2 concentrations and number of hospital admissions is observed at lag 0. For haemorrhagic stroke, the association is strongest with a delay of 2 days. All associations calculated without stratification are statistically significant and range from an excess relative risk of 2.8% for myocardial infarction to 4.9% for haemorrhagic strokes. The results of this study reinforce the evidence of the short-term effects of NO2 on hospital admissions for cardiovascular disease. The different delay between exposure and health-related event for haemorrhagic stroke compared to ischemic stroke suggests different mechanisms of action.
... Some authors have also reported that low socioeconomic populations may present higher residential exposure to traffic and air pollution 7,8 . In addition, factors such as age, gender, race, and medical conditions might also enhance the harmful air pollution effects related to human health [9][10][11] . RESUMO: Objetivo: Identificar áreas e fatores de risco para a mortalidade causada por doenças cardiovasculares (DC) associados à poluição do ar proveniente da alta exposição ao tráfego. ...
Objective:
To identify areas and risk factors in cardiovascular disease (CD) mortality associated with air pollution from high exposure to vehicular traffic.
Methods:
Cross-sectional study of CD mortality in 2,617 individuals aged 45-85 years living in the urban area of Cuiabá and Várzea Grande, Mato Grosso State, Brazil, between 2009 and 2011. We used the residential proximity of up to 150 meters to a roadway of great vehicle flow as a proxy of high exposure to air pollution from vehicular traffic. The association between age, gender, income, and traffic intensity with vehicular traffic exposure was assessed through the multiple logistic regression. We conducted stratified analyses to observe the influence of seasons and groups of causes. We used Bernoulli’s spatial model of probability to identify high-risk clusters.
Results:
Risk factors for CD mortality associated with high exposure to vehicular traffic were: living in census tracts with very unequal income (OR = 1.78; 95%CI 1.36 - 2.33), heavy traffic (OR = 1.20; 95%CI 1.01 - 1.43), and female gender (OR = 1.18; 95%CI 1.01 - 1.38). The CD mortality risk increases about 10% during the dry season period. We identified nine areas of risk.
Conclusion:
High exposure to traffic is associated with CD mortality in Cuiabá and Várzea Grande. Income inequality, traffic intensity, and female gender presented as the main determiners for this exposure. The dry season period enhances the effects of traffic exposure.
... Other supportive evidence of the synergistic adverse effects of air pollution and socioeconomic factors includes reports from the US, Canada, Italy, Switzerland, Hong Kong and Latin America [22][23][24][25][26][27][28]. On the other hand, a cross-sectional analysis of a large population-based US cohort of adults without a history of CVD (the Multi-Ethnic Study of Atherosclerosis) found little evidence that social disadvantage confers increased sensitivity to the hypertensive effects of PM 2.5 [29], which is consistent with several other previous studies [30][31][32][33]. These studies commonly reported multiplicative scale interactions (i.e. ...
Background:
Socioeconomically disadvantaged populations often have higher exposures to particulate air pollution, which can be expected to contribute to differentials in life expectancy. We examined socioeconomic differentials in exposure and air pollution-related mortality relating to larger scale (5 km resolution) variations in background concentrations of selected pollutants across England.
Methods:
Ozone and particulate matter (sub-divided into PM10, PM2.5, PM2.5-10, primary, nitrate and sulphate PM2.5) were simulated at 5 km horizontal resolution using an atmospheric chemistry transport model (EMEP4UK). Annual mean concentrations of these pollutants were assigned to all 1,202,578 residential postcodes in England, which were classified by urban-rural status and socioeconomic deprivation based on the income and employment domains of the 2010 English Index of Multiple Deprivation for the Lower-level Super Output Area of residence. We used life table methods to estimate PM2.5-attributable life years (LYs) lost in both relative and absolute terms.
Results:
Concentrations of the most particulate fractions, but not of nitrate PM2.5 or ozone, were modestly higher in areas of greater socioeconomic deprivation. Relationships between pollution level and socioeconomic deprivation were non-linear and varied by urban-rural status. The pattern of PM2.5 concentrations made only a small contribution to the steep socioeconomic gradient in LYs lost due to PM2.5 per 103 population, which primarily was driven by the steep socioeconomic gradient in underlying mortality rates. In rural areas, the absolute burden of air pollution-related LYs lost was lowest in the most deprived deciles.
Conclusions:
Air pollution shows modest socioeconomic patterning at 5 km resolution in England, but absolute attributable mortality burdens are strongly related to area-level deprivation because of underlying mortality rates. Measures that cause a general reduction in background concentrations of air pollution may modestly help narrow socioeconomic differences in health.
... However, the participants of this study differed by ethnicity (Latinos reporting the air quality as generally less of a problem) and gender (females view air quality as more of an issue). This is generally consistent with previous findings [24] that reported people from vulnerable communities, such as Latinos, tend to suffer disproportionally the burden of the impacts of air pollution [25][26][27]. This suggests a need for more communication efforts targeting Latinos [20][21][22]. ...
The San Joaquin Valley (SJV) of California has poor air quality, high rates of asthma, and high rates of obesity. Informational campaigns aimed at increasing awareness of the health impacts of poor air quality and promoting behavior change need to be tailored to the specific target audiences. The study examined perceptions of air quality, perceived health impacts, and methods of accessing information about air quality between Latinos and other groups in the SJV. Residents of the SJV (n = 744) where surveyed via one of three methods: community organizations (256), public locations (251), and an internet panel (237). The results suggest that people perceive the air quality in their region to be generally unhealthy, particularly for sensitive groups. The air quality is more likely to be reported as being unhealthy by people with health problems and less unhealthy by Latinos and people who report regularly exercising. Latinos are more likely to report working outdoors regularly, but also more likely to report being able to reduce their exposure if the air quality is unhealthy. The results report differences in informational sources about air quality, suggesting that informational campaigns should target high risk groups using a variety of media.
... We also did not find evidence that SeS or neighborhood segregation altered vulnerability. the empirical literature on the modifying role of neighborhood social disadvantage has yielded inconsistent results, with some reporting that socially disadvantaged neighborhoods show stronger, 37-39 weaker, 40 or no difference in 41,42 associations between air pollution and health. the lack of consistency may have to do with different neighborhood samples which would yield differences in the balance of factors that promote resiliency and vulnerability. ...
Background:
Social factors may enhance health effects of air pollution, yet empirical support is inconsistent. The interaction of social and environmental factors may only be evident with long-term exposures and outcomes that reflect long-term disease development.
Methods:
We used cardiac magnetic resonance imaging data from the Multi-Ethnic Study of Atherosclerosis to assess left-ventricular mass index (LVMI) and left-ventricular ejection fraction (LVEF). We assigned residential concentrations of fine particulate matter (PM2.5), oxides of nitrogen, and nitrogen dioxide in the year 2000 to each participant in 2000 using prediction models. We examined modifying roles of four measures of adversity: race/ethnicity, racial/ethnic residential segregation, and socioeconomic status and psychosocial adversity as composite indices on the association between air pollution and LVMI or LVEF.
Results:
Compared with whites, blacks showed a stronger adjusted association between air pollution and LVMI. For example, for each 5 µg/m greater PM2.5 level, whites showed a 1.0 g/m greater LVMI (95% confidence interval = -1.3, 3.1), while blacks showed an additional 4.0 g/m greater LVMI (95% confidence interval = 0.3, 8.2). Results were similar for oxides of nitrogen and nitrogen dioxide with regard to black race and LVMI. However, we found no evidence of a modifying role of other social factors or ethnic groups. Furthermore, we found no evidence of a modifying role for any social factors or racial/ethnic groups on the association between air pollution and LVEF.
Conclusions:
Our results suggest that racial group membership may modify the association between air pollution and cardiovascular disease.
... Some previous studies have found effect modification of PM-related health effects by, for example, age (Serinelli et al. 2010), gender (Chen et al. 2005), pre-existing disease (Pope et al. 2015) and socioeconomic class (Romieu et al. 2004;Serinelli et al. 2010). However, evidence remains inconclusive, as there are also studies which have not found a modifying effect of these factors (Anderson et al. 2003;Bateson and Schwartz 2004;Cakmak et al. 2006;Kan et al. 2008), or, for example, only weak evidence of a modification by race (Zanobetti and Schwartz 2000). Beijing has four clear seasons with hot, humid summers and generally cold, windy, dry winters. ...
Background:
The link between particulate matter (PM) and cardiovascular morbidity has been investigated in numerous studies. Less evidence exists, however, about how age, gender and season may modify this relationship. The aim of this study was to evaluate the association between ambient PM2.5 (PM ≤ 2.5 µm) and daily hospital emergency room visits (ERV) for cardiovascular diseases in Beijing, China. Moreover, potential effect modification by age, gender, season, air mass origin and the specific period with 2008 Beijing Olympic were investigated. Finally, the temporal lag structure of PM2.5 has also been explored.
Methods:
Daily counts of cardiovascular ERV were obtained from the Peking University Third Hospital from January 2007 to December 2008. Concurrently, data on PM2.5, PM10 (PM ≤ 10 µm), nitrogen dioxide and sulfur dioxide concentrations were obtained from monitoring networks and a fixed monitoring station. Poisson regression models adjusting for confounders were used to estimate immediate, delayed and cumulative air pollution effects. The temporal lag structure was also estimated using polynomial distributed lag (PDL) models. We calculated the relative risk (RR) for overall cardiovascular disease ERV as well as for specific causes of disease; and also investigated the potential modifying effect of age, gender, season, air mass origin and the period with 2008 Beijing Olympics.
Results:
We observed adverse effects of PM2.5 on cardiovascular ERV-an IQR increase (68 μg/m(3)) in PM2.5 was associated with an overall RR of 1.022 (95 % CI 0.990-1.057) obtained from PDL model. Strongest effects of PM2.5 on cardiovascular ERV were found for a lag of 7 days; the respective estimate was 1.012 (95 % CI 1.002-1.022). The effects were more pronounced in females and in spring. Arrhythmia and cerebrovascular diseases showed a stronger association with PM2.5. We also found stronger PM-effects for stagnant and southern air masses and the period of Olympics modified the air pollution effects.
Conclusions:
We observed a rather delayed effect of PM2.5 on cardiovascular ERV, which was modified by gender and season. Our findings provide new evidence about effect modifications and may have implications to improve policy making for particulate air pollution standards in Beijing, China.
... The current analysis showed that older (above the age of 65) females or Bedouin Arabs patients were at the highest risk for hospitalization due to ACS following OM exposure. These findings are consisted with several other studies [7,10,33] showing that female and older patients are at higher risk of death associated with PM 10 exposure. Chen et. ...
Background:
High concentrations of particulate matter (PM) air pollution have been associated with death and hospital admissions due to cardiovascular morbidity. However, it is not clear a) whether high levels of non-anthropogenic PM from dust storms constitute a health risk; and b) whether these health risks are exacerbated in a particular demographic.
Methods:
This study comprised all patients above 18 years old admitted to Soroka University Medical Center (1000 bed tertiary hospital, Be'er- Sheva, Israel, 2001-2010) with a primary diagnosis of acute coronary syndrome (ACS). Data on meteorological parameters and PM10 (particulate matter <10 μm in aerodiameter) were obtained from monitoring stations in the city of Be'er-Sheva. Data were analyzed using a case crossover analysis to examine the effect of dust exposure on hospitalization due to ACS and the interaction with co-morbidities and demographic factors.
Results:
There were 16,734 hospitalizations due to ACS during the study period. The estimated odds of hospitalization due to ACS was significantly associated with PM10 during non dust storm days at the same day of the exposure (lag0); OR = 1.014 (95%CI 1.001-1.027) for a 10 μg/m3 increase, while a delayed response (lag1) was found during the dust storm days; OR = 1.007 (95%CI 1.002-1.012). The effect size for the dust exposure association was larger for older (above the age of 65), female or Bedouin patients.
Conclusions:
Exposure to non-anthropogenic PM is associated with cardiovascular morbidity. Health risk associated dust exposure is gender and age specific with older women and Bedouin patients being the most vulnerable groups.
... In the review of Laurent et al. (2007) three studies reported short-term effects on health using socioeconomic variables at very coarse geographic resolutions, but none found differences according to socioeconomic variables, despite very large populations. The studies at finer geographic resolutions produced mixed results: five out of six studies which analysed individual socioeconomic variables reported stronger pollution-mortality associations for people with low SES, even adjusting for behavioural and occupational risk factors (Zanobetti and Schwartz, 2000;Wojtyniak et al., 2001;Filleul et al., 2004;Zeka et al., 2006, included in the Laurent's review). ...
Objective:
The Health in All Policies strategy aims to engage every policy domain in health promotion. The more socially disadvantaged groups are usually more affected by potential negative impacts of policies if they are not health oriented. The built environment represents an important policy domain and, apart from its housing component, its impact on health inequalities is seldom assessed.
Methods:
A scoping review of evidence on the built environment and its health equity impact was carried out, searching both urban and medical literature since 2000 analysing socio-economic inequalities in relation to different components of the built environment.
Results:
The proposed explanatory framework assumes that key features of built environment (identified as density, functional mix and public spaces and services), may influence individual health through their impact on both natural environment and social context, as well as behaviours, and that these effects may be unequally distributed according to the social position of individuals.
Conclusion:
In general, the expected links proposed by the framework are well documented in the literature; however, evidence of their impact on health inequalities remains uncertain due to confounding factors, heterogeneity in study design, and difficulty to generalize evidence that is still very embedded to local contexts.
... In agreement with our findings, Jerrett et al. (2010) also reported sex differences in that the traffic density near the homes of children was significantly associated with an elevated BMI in females, but not males. Although not fully understood, there is growing literature on the differing associations between air pollution and health for males and females (Clougherty, 2010;Keitt et al., 2004;Zanobetti and Schwartz, 2000). In the Public Health and Air Pollution in Asia (PAPA) study, Kan et al. (2008) found that women were more susceptible to the effects of exposure to air pollution. ...
... Our findings suggest a higher risk of short-term all-cause mortality among men than among women. A few studies have looked at gender as a potential effect-modifier for the association between NO 2 or PM and mortality, reaching partially inconsistent conclusions [13,20,23,49]. These results need further investigation, in particular to better understand whether the effect modification by gender could be explained by socially-derived gendered exposures and/ or by biological differences (e.g. ...
Background
While a great number of papers have been published on the short-term effects of air pollution on mortality, few have tried to assess whether this association varies according to the neighbourhood socioeconomic level and long-term ambient air concentrations measured at the place of residence. We explored the effect modification of 1) socioeconomic status, 2) long-term NO2 ambient air concentrations, and 3) both combined, on the association between short-term exposure to NO2 and all-cause mortality in Paris (France).
Methods
A time-stratified case-crossover analysis was performed to evaluate the effect of short-term NO2 variations on mortality, based on 79,107 deaths having occurred among subjects aged over 35 years, from 2004 to 2009, in the city of Paris. Simple and double interactions were statistically tested in order to analyse effect modification by neighbourhood characteristics on the association between mortality and short-term NO2 exposure. The data was estimated at the census block scale (n=866).
Results
The mean of the NO2 concentrations during the five days prior to deaths were associated with an increased risk of all-cause mortality: overall Excess Risk (ER) was 0.94% (95%CI=[0.08;1.80]. A higher risk was revealed for subjects living in the most deprived census blocks in comparison with higher socioeconomic level areas (ER=3.14% (95%CI=[1.41-4.90], p<0.001). Among these deprived census blocks, excess risk was even higher where long-term average NO2 concentrations were above 55.8 μg/m3 (the top tercile of distribution): ER=4.84% (95%CI=[1.56;8.24], p for interaction=0.02).
Conclusion
Our results show that people living in census blocks characterized by low socioeconomic status are more vulnerable to air pollution episodes. There is also an indication that people living in these disadvantaged census blocks might experience even higher risk following short-term air pollution episodes, when they are also chronically exposed to higher NO2 levels.
... These results confirm that people living in families with low socio-economic backgrounds experience poor general health. Socioeconomic inequalities in mortality and morbidity have already been found in Europe and Brazil (Martins et al., 2004; Zanobetti and Schwartz, 2000 ). However , further studies using a combination of individual and neighborhood-level indicators are required. ...
... Da questo punto di vista, è stata evidenziata l'importanza di pregresse sfavorevoli condizioni di salute [20], in particolare per i portatori di broncopneumopatie croniche [21][22][23], coronaropatie, malattie ischemiche del miocardio [22] e asma bronchiale [22]. Il sesso, l'etnia e lo stato socioeconomico non sembrano, invece, forti modificatori dell'effetto del materiale particellare atmosferico sulla mortalità giornaliera [24]. Non sono definitivamente chiari, infine, i meccanismi d'azione attraverso i quali l'esposizione acuta a livelli crescenti di materiale particellare atmosferico determina, in individui già affetti da forme più o meno gravi di patologia respiratoria o cardiaca, una caduta fatale dei meccanismi fisiologici di compensazione. ...
Negli ultimi anni la ricerca epidemiologica e tossicologica ha fatto notevoli passi in avanti nel dimostrare quali siano le conseguenze a lungo termine dell'esposizione alla miscela di polveri e gas che penetra quotidianamente nei polmoni di chi abita in città. Già negli anni Cinquanta si sospettava che l'inquinamento atmosferico potesse avere un effetto cancerogeno, ma solo nel 2002 se ne avuta la conferma grazie ai risultati di un grande studio [1], che ha coinvolto più di 500.000 persone negli Stati Uniti, in cui è risultata chiara l'associazione tra la concentrazione di polveri sottili nell'aria e l'aumento del rischio di cancro polmonare. Lo stesso studio dimostrava un aumento della mortalità per malattie cardiovascolari e respiratorie per effetto della esposizione a polveri aereodisperse. Accertato l'effetto, si tenta oggi di capire, tra le tante componenti dell'aria di città, quale sia quella realmente responsabile degli effetti nocivi: i metalli veicolati dalle polveri, le polveri stesse di dimensione molto piccola, i gas. Se l'epidemiologia non può certo fornire una risposta definitiva a riguardo, la ricerca tossicologica ha prodotto dati che sembrano propendere per un effetto autonomo delle polveri. Uno studio recente [2], per esempio, ha fornito informazioni utili su questo versante perché ha dimostrato che in topolini esposti ad aria inquinata si osservano segni precoci di aterosclerosi. Un dato, questo, che potrebbe spiegare gli eccessi di mortalità per cause cardiovascolari riscontrati negli studi americani. Ma gli effetti delle polveri non sono solo cronici e a lungo termine: si sono infatti osservati effetti acuti con una risposta di ore o di giorni ai picchi di inquinamento. Nei grandi centri urbani di molti paesi industrializzati di quasi tutti i continenti, in modo ripetuto e coerente, è stata osservata anche un'associazione tra fluttuazioni giornaliere della mortalità per cause cardiorespiratorie e concentrazioni atmosferiche di materiale particellare di granulometria inferiore ai 10 µm (PM10) [3] o ai 2.5 µm (PM2.5) [4]. Questi studi costituiscono una parte dell'evidenza scientifica sugli eccessi di rischio per la salute legati all'esposizione a concentrazioni di particolato atmosferico come quelli che si registrano nei centri urbani. Altri elementi che contribuiscono all'evidenza sono i risultati degli studi prospettici americani [1, 5-7] ed europei [8-13] e le serie temporali relative ai ricoveri ospedalieri per malattie respiratorie e cardiovascolari [14-15]. In questo senso, gli Stati Uniti hanno adottato standard di qualità dell'aria più restrittivi che in passato [16] mentre l'Organizzazione Mondiale della Sanità nella sua revisione delle linee guida per la qualità dell'aria in Europa non ha più indicato un valore unico per il materiale particellare in atmosfera, in quanto la relazione esposizione-effetto è di tipo lineare senza soglia, vale a dire che non è possibile individuare un limite per l'esposizione al di sotto del quale non vi sono conseguenze per la salute [17]. E' ovvio che molti temi sono ancora oggetto di ricerca [18-19]. Non è ancora ben chiaro, per esempio, quali siano i gruppi più suscettibili a tale effetto "letale" dell'inquinamento, né quali fattori di rischio (a livello di popolazione e di individuo) modifichino la relazione tra inquinamento e mortalità. Da questo punto di vista, è stata evidenziata l'importanza di pregresse sfavorevoli condizioni di salute [20], in particolare per i portatori di broncopneumopatie croniche [21-23], coronaropatie, malattie ischemiche del miocardio [22] e asma bronchiale [22]. Il sesso, l'etnia e lo stato socioeconomico non sembrano, invece, forti modificatori dell'effetto del materiale particellare atmosferico sulla mortalità giornaliera [24]. Non sono definitivamente chiari, infine, i meccanismi d'azione attraverso i quali l'esposizione acuta a livelli crescenti di materiale particellare atmosferico determina, in individui già affetti da forme più o meno gravi di patologia respiratoria o cardiaca, una caduta fatale dei meccanismi fisiologici di compensazione.
Even though industrial development has brought vast improvements to our daily lives, it carries with it negative effects such as adverse health outcomes caused by PM2.5 and other pollutants. The negative externalities and external costs might occur when property rights are not properly defined, which means that if no one holds a property right on the atmosphere and the quality of air, there is no appropriate mechanism to prevent a further expansion of negative effects. An economic burden of pollution related to premature morbidity and mortality in individual countries can account for 5–14% of GDP (World Bank, 2021). In 2019, the worldwide health cost of mortality and morbidity caused by exposure to PM2.5 concentration was $8.1 trillion, which is equivalent to 6.1 percent of the global gross domestic product (GDP) (World Bank estimate). Policymakers require evidence-based results that clearly show the impact that air pollution has on the economy and society, in order to be able to establish the proper regulations and ensure their successful implementation. The purpose of this long term study is to provide methods for assessing the negative effects of PM2.5 concentration on PM2.5 related mortality using panel data structure and demonstrate how socio-economic factors affect this relation. This study employed advanced econometric techniques to analyse the long-term impact of PM2.5 on human health, while controlling for socio economic indicators.
PurposeThe association between atmospheric particulate matter and emergency room visits for cerebrovascular disease were evaluated in Beijing.MethodsA generalized additive model was used to evaluate the associations between particulate matter and cerebrovascular disease, based on the daily data of meteorological elements, PM concentrations, and emergency room (ER) visits for cerebrovascular disease in Beijing from 2009 to 2012. Long-term trends and the effects of holidays, the day of the week, and confounding factors were controlled to determine the lag effect at 0–6 days. Single- and double-pollutant models were employed for different age and sex groups.ResultsThe effect of PM2.5 concentration on the number of daily ER visits for cerebrovascular disease was much stronger than that of PM10 concentration. PM2.5 and PM10 had maximum RR values of 1.096 and 1.054 at lag 6 for patients aged 61–75 years. For each inter-quartile range (IQR) increase in PM10 concentration, the maximum RR values for the total, males, females, aged 15–60 years, aged 61–75 years, and aged > 75 years were 1.024, 1.044, 1.043, 1.038, 1.054, and 1.032, respectively. For each IQR increase in PM2.5 concentration, the maximum RR values for the total, males, females, aged 15–60 years, aged 61–75 years, and aged > 75 years were 1.038, 1.064, 1.076, 1.054, 1.096, and 1.049, respectively. The RR values of the double-pollutant models were lower than those of the single-pollutant models.Conclusion
This study showed that the effects of PM pollution on cerebrovascular disease were different among different gender and age groups, and aged 61–75 years were mostly sensitive to particulate matters. The effects of PM2.5 on cerebrovascular disease were stronger than those of PM10. Our results can provide scientific evidence for the local government to take effective measures to improve air quality and the health of residents.
Understanding the environmental justice implications of the mortality impacts of air pollution exposure is a public health priority, as some subpopulations may face a disproportionate health burden. We examined which residential environmental and social factors may affect disparities in the air pollution-mortality relationship in North Carolina, US, using a time-stratified case-crossover design. Results indicate that air pollution poses a higher mortality risk for some persons (e.g., elderly) than others. Our findings have implications for environmental justice regarding protection of those who suffer the most from exposure to air pollution and policies to protect their health.
Introduction:
Epidemiologic studies have reported associations between short-term exposure to particulate matter <2.5 μm in aerodynamic diameter (PM2.5) and mortality, but the role of modifiers remains unclear with studies reporting inconsistent results. We evaluated the impact of individual (age, gender and education) and township (geographic area, socioeconomic status, background air pollution and road density) level factors on the relationship between short-term variation in PM2.5 with cause-specific mortality in Beijing (population: 21.7 million in 2016), China.
Methods:
Daily PM2.5 concentrations in each township (n = 327; township population: 2000-359,400; township area: 1-392 km2) within Beijing were estimated by kriging with external drift using measurements from 35 air quality monitoring stations and geographic variables. Time-stratified case-crossover analysis with township-level mortality data from Oct. 1st, 2012 to Dec. 31st, 2013 was then used to examine associations between PM2.5 exposure estimates and cause-specific mortality, stratified by the potential effect modifiers.
Results:
A 10-μg/m3 increase in PM2.5 concentration was associated with a 0.17% [95% confidence interval (CI): 0.05%-0.29%] and 0.27% (95%CI:0.01%-0.52%) increase in non-accidental and stroke mortality with no lag, a 0.81% (95%CI:0.39%-1.23%) and 0.96% (95%CI:0.35%-1.57%) increase in respiratory disease (RD) and chronic obstructive pulmonary disease (COPD) mortality at a lag of two-day moving average. For individual-level effect modifiers, the elderly showed higher effects for all the specific causes of mortality; those with lower education level showed higher effects for non-accidental, cardiovascular disease and stroke mortality; females showed higher effects for non-accidental and cause-specific cardiovascular diseases. For township-level effect modifiers, effect estimates tended to be larger for suburban areas, areas of lower road density, lower PM2.5 and lower socioeconomic status.
Conclusions:
Short-term exposure to township-level ambient PM2.5 was associated with increased mortality in Beijing, with indications of effect modification by both individual and township-level factors.
We analyzed racial differences in all-cause mortality rates associated with air pollution in a cohort of military veterans in which 37% of the 70,000 members identified as African-American (black). In this comprehensive analysis, spatial levels comprised individuals, zip-codes, and counties. Temporal levels comprised the 26-y follow-up period (1976–2001) and 4 subperiods.
Proportional hazard regression models were used, controlling for individual age, race (white, black), smoking (current, ever), education, height, body-mass index, and systolic and diastolic blood pressure; zipcode-average socioeconomic indicators; and county-average climate. County-level air quality measures included vehicular traffic density as a surrogate for all traffic-related pollutants including noise. The model accounted for nonlinear mortality relationships with age, body-mass index, blood pressure and zip-code racial composition.
Relative to whites, more of the black veterans smoked, had slightly higher blood pressure, and lived in predominately black zip-codes that had more poverty than whites. The black veterans lived in counties that had slightly worse ambient air quality and substantially higher levels of vehicular traffic density. We analyzed all-cause mortality associations with county-level average ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide for 1975–81, and subsequent data on particulates by particle size. We also considered sulfate and elemental carbon particles, benzene, SO2, and NOx based on nationwide modeling for 2002. We had no information on indoor air quality or personal exposures; our risk estimates should thus be regarded as characterizing the counties of residence rather than individual exposures of inhabitants.
In addition to age, the strongest predictors of veterans’ survival were residence in high-poverty zip-codes, smoking, and diastolic blood pressure, to all of which black veterans were less sensitive than whites. Black veterans had significantly lower mortality risks from aging, smoking, and elevated diastolic blood pressure, but larger risks from excessive body-mass index. They were less at risk from living a high-poverty zip-code than whites. We assumed these risk factors to be stable during follow-up and thus applicable to chronic health effects. After controlling for them, the all-cause mortality risk for black veterans was 10% lower than whites.
In an effort to reduce random scatter we computed mean risks associated with overlapping groups of similar pollutants. These means were statistically significant for both black and white veterans for traffic-related, gaseous, and NOx-O3 pollutants, for which the overall mean relative risk was 1.076 (1.057–1.090). Grouped mean risks for particulate pollutants, sulfur compounds, and non-traffic pollutants were not significant for either race. Black veterans carried more of the traffic-related risks than whites because of their greater exposures and risk coefficients. PM2.5 risk estimates were negative for black veterans (0.82 [0.75–0.89]) but positive for whites (1.05 [1.005–1.10]) which is consistent with regional differences in overall mortality.
The temporal analyses compared mortality rates by follow-up subperiod for the pollutants measured at enrollment. We expected increasing (cumulative) risks for chronic effects and decreasing risks for delayed acute effects, but found no significant trend for either race. We concluded that the higher exposures and mortality risks associated with vehicular traffic posed environmental injustice for the black veterans.
Background and objective
Aside from smoking, which is already recognized as a strong risk factor for COPD, interest in the impact of particulate matter (PM) on COPD is increasing. This study aimed to investigate the effect of PM, especially with an aerodynamic diameter ≤2.5 µm (PM2.5), and its chemical constituents on the exacerbation of COPD.
Methods
Data on hospital visits including admission and outpatient clinic visits for exacerbation of COPD in Chuncheon, Korea, between 2006 and 2012 were extracted from the National Health Insurance Service database. PM2.5 and its chemical constituents were measured on the roof of the four-story Kangwon National University Natural Sciences building once every 3 days. Meteorological data were provided by the Korean Meteorological Administration.
Results
During the study period, the mean level of PM2.5 was 35.0±25.2 µg/m³, and the number of daily hospital visits were 6.42±4.28 and 2.07±1.93 for males and females, respectively. The number of COPD-related hospital visits increased with increasing PM2.5 after adjusting for meteorological covariates and females tended to be more affected sooner than males. Among the PM2.5 constituents, Al, Si, and elemental carbon were associated with increased hospital visits and there was a difference according to sex. In males, some constituents of PM2.5 were related to an increased risk of a hospital visit, mainly on the first and second days of measurement (Lag1 and Lag2). In contrast, there was no significant increase in the risk of hospital visits due to any of the PM2.5 constituents in females.
Conclusion
Concentrations of PM2.5 mass and some of the PM2.5 constituents were associated with increased COPD-related hospital visits in Chuncheon.
The aim of the present study is to analyse the age effect on the lag patterns of relative risk of hospitalization for acute myocardial infarction and NO2, PM10 and O3. Daily hospitalizations for AMI during the period 2008–2011 were extracted from administrative data. Analyses were performed using the quasi-Poisson regression model adjusted for seasonality, long-term trend, day of the week and temperature. We observed very different patterns depending on age. For NO2 and PM10, the younger group (25–54 years) shows a more delayed effect in comparison with the two older age groups (55–64 and ≥ 65 years). Overall, the associations between NO2 and AMI are higher compared to PM10. There are no associations between O3 and AMI. This study indicates that age plays a major role in the lag pattern. Younger people have delayed effects, but they are nevertheless sensitive to air pollution.
There is growing interest in disentangling the health effects of spatially clustered social and physical environmental exposures and in exploring potential synergies among them, with particular attention directed to the combined effects of psychosocial stress and air pollution. Both exposures may be elevated in lower-income urban communities, and it has been hypothesized that stress, which can influence immune function and susceptibility, may potentiate the effects of air pollution in respiratory disease onset and exacerbation. In this paper, we review the existing epidemiologic and toxicologic evidence on synergistic effects of stress and pollution, and describe the physiologic effects of stress and key issues related to measuring and evaluating stress as it relates to physical environmental exposures and susceptibility. Finally, we identify some of the major methodologic challenges ahead as we work toward disentangling the health effects of clustered social and physical exposures and accurately describing the interplay among these exposures. As this research proceeds, we recommend careful attention to the relative temporalities of stress and pollution exposures, to nonlinearities in their independent and combined effects, to physiologic pathways not elucidated by epidemiologic methods, and to the relative spatial distributions of social and physical exposures at multiple geographic scales.
Background
Long-term exposure to air pollutants has been hypothesised as a factor in susceptibility to short-term exposure to particulate matter (PM), but results are not coherent. We studied the short-term effects of PM10 on mortality and assessed whether long-term exposure to nitrogen dioxide (NO2) modifies this association.
Methods
We used a case-crossover design to evaluate daily PM10-related mortality among 124 432 35+ year-old participants who died in Rome between 2001 and 2010 and maintained the same address for at least 5 years before death. Modification of PM10-related mortality by long-term NO2 exposure was determined by two-way interaction, while a three-way interaction was used to assess effect modification of high NO2 levels in population groups defined by sociodemographic position and pre-existing diseases.
Results
Mortality increased by 0.82% (0.23–1.41%) for each 10 µg/m3 increase in PM10. Mortality rose by 1.22% (0.17–2.38%) in participants exposed to NO2 levels ≥50 µg/m3 and by 0.69% (0.03–1.34%) in those exposed to levels <50 µg/m3 with no effect modification (p-interaction 0.378). A suggestion of effect modification was seen in 85+-year-olds (3.10%; p-interaction 0.043), as well as in those with a pre-existing arrhythmia (3.26%; p-interaction 0.014) and chronic obstructive pulmonary disease (3.52%; p-interaction 0.042).
Conclusions
Long-term exposure to NO2 is not likely to induce susceptibility to short-term PM10 exposure in the overall population. However, an effect modification of NO2 is probable in the elderly and in those suffering from arrhythmias and chronic obstructive pulmonary disease.
Older fossil-fueled power plants provide a significant portion of emissions of criteria air pollutants in the United States, in part because these facilities are not required to meet the same emission standards as new sources under the Clean Air Act. Pending regulations for older power plants need information about any potential public health benefits of emission reductions, which can be estimated by combining emissions information, dispersion modeling, and epidemiologic evidence. In this article, we develop an analytical modeling framework that can evaluate health benefits of emission controls, and we apply our model to two power plants in Massachusetts. Using the CALPUFF atmospheric dispersion model, we estimate that use of Best Available Control Technology (BACT) for NOx and SO2 would lead to maximum annual average secondary particulate matter (PM) concentration reductions of 0.2 mug/m(3). When we combine concentration reductions with current health evidence, our central estimate is that the secondary PM reductions from these two power plants would avert 70 deaths per year in a population of 33 million individuals. Although benefit estimates could differ substantially with different interpretations of the health literature, parametric perturbations within CALPUFF and other simple model changes have relatively small impacts from an aggregate risk perspective. While further analysis would be required to reduce uncertainties and expand on our analytical model, our framework can help decision-makers evaluate the magnitude and distribution of benefits under different control scenarios.
Solid evidence of social inequalities in health is today established in most industrialised countries. A part of these inequalities is likely to be explained by environmental exposures, especially air pollution exposures. Indeed, groups with lower socioeconomic status may simultaneously be more highly exposed to air pollution and more susceptible to its deleterious effects. This thesis aimed to explore the contribution of air pollution to social inequalities in health, while making progress in the understanding of involved mechanisms. In this context, we chose to be interested in the short-term association between air pollution and myocardial infarction onset and to investigate this relation using an ecological approach.
This study was carried out on the Strasbourg metropolitan area (SMA, Bas-Rhin) on a small-area scale (IRIS equivalent to a residential neighborhood). Myocardial infarction events occurred among population aged 35-74 years from January 1, 2000 to December 31, 2003 (n = 1193) were collected from the Bas-Rhin coronary heart disease registry. Hourly air pollution concentrations (NO2, PM10, O3 and CO) were modeled at neighborhood level using ADMS Urban model. Neighborhood socioeconomic status was estimated by a deprivation index, constructed by a principal component analysis from census data.
We first sought to assess the degree of environmental injustice which prevailed in our study area in order to check the assumption of an exposure differential to air pollution according to neighborhood socioeconomic status. Our spatial regression analysis demonstrated the existence of socioeconomic disparities in air pollution exposure; the midlevel deprivation neighborhoods, located in direct contact with the principal highway arteries that surround the urban centre, were most exposed to traffic-related air pollution.
We then addressed to examine the association between neighborhood socioeconomic status and myocardial infarction onset in order to check the assumption of social inequalities in health in our study area. Our Bayesian analysis showed that the existence of strong socioeconomic gradients in myocardial infarction risk among men and women and emphasized a singular susceptibility of women living in the most deprived neighborhoods.
We finally explored the contribution of air pollution to social inequalities in health while examining whether neighborhood socioeconomic status modified the effects of air pollution on myocardial infarction risk. Our case-crossover analysis highlighted a greater effect of particulate air pollution among subjects living in the most deprived neighborhoods, especially women aged 55-74 years. Depending on the results previously reported, these results may be more explained by a susceptibility differential than an exposure differential. Research into the mechanisms responsible for this increased sensitivity needs to continue so that appropriate public health actions can be taken to protect these susceptible populations.
This dissertation investigates theoretically and empirically the interrelationships among population's health, environmental degradation and economic development, its consequences for developing countries, and some effective policy responses. The first part explores the association between health, environment, and inequalities. It firstly analyzes whether environmental degradation could be considered as an additional channel through which income inequality affects infant and child mortality (chapter 2). Theoretical and empirical investigations show that income inequality affects negatively air and water quality, and this in turn worsens population's health. Therefore, environmental degradation is an important channel through which income inequality affects population health. Then, it is shown that sulphur dioxide emission (SO2) and particulate matter (PM10) are in part responsible for the large disparities in infant and child mortalities between and within developing countries (chapter 3). In addition, we found that democratic institutions play the role of social protection by mitigating this effect for the poorest income classes and reducing the health inequality it provokes. The second part is devoted to the link among health, environment, and economic growth. The effect of health (global burden of disease, communicable disease, and malaria) on economic growth is assessed in Chapter 4. This chapter shows that health indicators, when correctly measured by the gap between current health status and an ideal health situation where the entire population lives to an advanced age, free of disease and disability, and when accurately instrumented have significant impact on economic performance. The consequences of these interrelationships on the convergence of poor countries towards their steady state are theoretically and empirically investigated in the last Chapter (chapter 5). It is found that environment degradation reduces the ability of poor countries to reach their own steady state, reinforcing our argument according to which environment quality improvement plays a considerable role in economic convergence process. Moreover, the degradation of air and water quality affects negatively economic performance, and health status remains an important channel through which environment degradation affects economic growth even if it is not alone. The Environmental Kuznets Curve (EKC) hypothesis is also verified.
Résumé
Position du problème
De nombreuses études mettent en évidence un lien entre maladie cardiovasculaire et pollution atmosphérique. L’analyse cas-croisé est une méthode permettant d’étudier les effets à court terme de la pollution atmosphérique. Cette étude démontre son intérêt en évaluant l’effet modificateur des saisons ainsi que les effets confondants de différents paramètres environnementaux sur l’association entre pollution atmosphérique et infarctus du myocarde (IDM).
Méthodes
Les données sur l’IDM de 1999 à 2009 proviennent du registre de l’infarctus du myocarde de Charleroi. Charleroi est une zone géographique de Wallonie relativement polluée avec des niveaux élevés de PM10. Les principaux polluants (PM10, O3, NO2, CO) et la température ont été collectés à partir de cinq stations de mesure de la Région wallonne pour la même période. Une méthode cas-croisé stratifiée sur le temps avec ou sans ajustement sur d’autres paramètres a été utilisée. L’ajustement a été réalisé par appariement des cas et des témoins. Les analyses ont été effectuées pour l’ensemble de l’année ainsi que pour les périodes chaudes et les périodes froides de l’année.
Résultats
Un total de 3303 cas d’IDM pour la période allant de 1999 à 2009 ont été analysés. Il existe une association entre la concentration en O3 (pour une augmentation de 10 μg/m³) et l’IDM, OR = 1,028 (IC95 % : 1,003–1,054). Les associations les plus fortes sont observées pendant les mois chauds avec un OR = 1,086 (IC95 % : 1,020–1,151) pour les PM10 et un OR = 1,064 (IC95 % : 1,024–1,105) pour l’O3. L’ajustement sur la température diminue l’association entre O3 et l’IDM (OR = 1,003, IC95 % : 0,974–1,032). Par contre, cet ajustement est sans effet sur l’association entre PM10 et l’IDM. L’ajustement sur la concentration en NO2 diminue l’association entre PM10 et IDM.
Conclusion
Les résultats de cette étude renforcent les preuves des effets à court terme de la pollution atmosphérique sur l’IDM, en particulier pendant la saison chaude. La méthode cas-croisé est un outil approprié pour étudier l’association entre les événements aigus et la pollution atmosphérique. Cette méthode permet un ajustement sur les variables environnementales potentiellement confondantes.
We examined the association of particulate matter with an aerodynamic diameter (PM_{10}) with asthma-related hospitalization, stratified by socioeconomic status (SES), among children less than 15 years of age in Seoul, Korea, between 2003 and 2005. In addition, we estimated the reduction in the number of asthma-related hospitalizations that would result from implementing the World Health Organization (WHO) guideline. SES was defined based on data concerning health insurance premium grades, and grouped into two levels: lower-income group and control group. The lower-income group was classified as having an accumulated income which did not exceed the 50th percentile of the median income. Time-series analysis was performed to evaluate the association between PM_{10} and asthma-related hospitalization. The Environmental Benefits Mapping and Analysis Program was used to analyze the impact on children's health. Based upon an increase of 10\;?g/m^3 of PM_{10}, the asthma-related hospitalization risk for the lower-income group was increased by 1.78% (95% confidence intervals (CI) = 0.79-2.78%), while the risk for the control group was increased by 0.83% (95% CI = 0.34-1.32%). Attaining the WHO guideline, relative to the concentration in 2007, would result in a reduction in asthma-related hospitalizations of 18 cases per 100,000 of the children population in the lower-income group, and 7 cases in the control group. The health benefits of improved air quality for children in the lower-income group were thus 2.5 times greater than for children in the control group. Our results show that the lower-income group is disproportionately burdened with asthma-related hospitalization arising from air pollution. Therefore, biologically- and socioeconomically-disadvantaged populations should be considered in public health interventions in order to protect the children's health.
Although epidemiological studies have linked particulate air pollution with cardiopulmonary mortality, underlying biological mechanisms remain largely unknown. Unexplored pathophysiological pathways include transient declines in blood oxygenation and/or changes in cardiac rhythm following particulate exposure. In this study, blood oxygen saturation using pulse oximetry (SpO2) and pulse rate were measured daily on a panel of 90 elderly subjects during the winter of 1995–1996 in Utah Valley. Associations of SpO2 and pulse rate with respirable particulate pollution (particles with an aerodynamic diameter ⩽ a nominal 10 μ m [PM10]) were evaluated. SpO2 was not consistently associated with PM10. Pulse rate and the odds of the pulse rate being elevated by 5 or 10 beats per minute (beats/min) were associated with PM10 on the previous 1 to 5 d. A 100 μ g/m³ increase in previous-day PM10 was associated with an average increase of 0.8 beats/min and 29 and 95% increased odds of the pulse rate being elevated by 5 or 10 beats/min, respectively. Although there was little evidence of pollution-related hypoxia, alterations in pulse rate could reflect cardiac rhythm changes and may be part of the pathophysiology linking particles to cardiopulmonary mortality. The observed lag structure is consistent with particulate-induced pulmonary inflammation and cytokine release, but the biological relevance requires further study.
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 compare risk of myocardial infarction associated with smoking in men and women, taking into consideration differences in smoking behaviour and a number of potential confounding variables.
Prospective cohort study with follow up of myocardial infarction.
Pooled data from three population studies conducted in Copenhagen.
11,472 women and 13,191 men followed for a mean of 12.3 years.
First admission to hospital or death caused by myocardial infarction.
1251 men and 512 women had a myocardial infarction during follow up. Compared with non-smokers, female current smokers had a relative risk of myocardial infarction of 2.24 (range 1.85-2.71) and male smokers 1.43 (1.26-1.62); ratio 1.57 (1.25-1.97). Relative risk of myocardial infarction increased with tobacco consumption in both men and women and was higher in inhalers than in non-inhalers. The risks associated with smoking, measured by both current and accumulated tobacco exposure, were consistently higher in women than in men and did not depend on age. This sex difference was not affected by adjustment for arterial blood pressure, total and high density lipoprotein cholesterol concentrations, triglyceride concentrations, diabetes, body mass index, height, alcohol intake, physical activity, and level of education.
Women may be more sensitive than men to some of the harmful effects of smoking. Interactions between components of smoke and hormonal factors that may be involved in development of ischaemic heart disease should be examined further.
Cause-specific deaths by day for the years 1973 to 1980 in Philadelphia, Pennsylvania, were extracted from National Center for Health Statistics mortality tapes. Death from accidents (International Classification of Disease, Revision 9 greater than or equal to 800) and deaths outside of the city were excluded. Daily counts of deaths were regressed using Poisson regression on total suspended particulate (TSP) and/or SO2 on the same day and on the preceding day, controlling for year, season, temperature, and humidity. A significant positive association was found between total mortality (mean of 48 deaths/day) and both TSP (second highest daily mean, 222 micrograms/m3) and SO2 (second highest daily mean, 299 micrograms/m3). The strongest associations were found with the mean pollution of the current and the preceding days. Total mortality was estimated to increase by 7% (95% CI, 4 to 10%) with each 100-micrograms/m3 increase in TSP, and 5% (95% CI, 3 to 7%) with each 100-micrograms/m3 increase in SO2. When both pollutants were considered simultaneously, the SO2 association was no longer significant. Mortality increased monotonically with TSP. The effect of 100 micrograms/m3 TSP was stronger in subjects older than 65 yr of age (10% increase) compared with those younger than 65 yr of age (3% increase). Cause-specific mortality was also associated with a 100-micrograms/m3 increase in TSP: chronic obstructive pulmonary disease (ICD9 490-496), +19% (95% CI, 0 to 42%), pneumonia (ICD9 480-486 & 507), +11% (95% CI, -3 to +27%), and cardiovascular disease (ICD9 390-448), +10% (95% CI, 6 to 14%). These results are somewhat higher than previously reported associations, and they add to the body of evidence showing that particulate pollution is associated with increased daily mortality at current levels in the United States.
The association between daily mortality and respirable particulate pollution (PM10) in Utah County was assessed from April 1985 through December 1989. Poisson regression analysis was used to regress daily death counts on PM10 pollution levels, controlling for variability in the weather. A significant positive association between nonaccidental mortality and PM10 pollution was observed. The strongest association was with 5-d moving average PM10 levels, including the concurrent day and the preceding 4 d. An increase in 5-d moving average PM10 levels, equal to 100 micrograms/m3, was associated with an estimated increase in deaths per day equal to 16%. The association with mortality and PM10 was largest for respiratory disease deaths, next largest for cardiovascular deaths, and smallest for all other deaths. Mean PM10 concentrations during the study period equaled 47 micrograms/m3. The maximum 24-h and 5-d moving average PM10 levels equaled 365 and 297 micrograms/m3, respectively. Relatively low levels of sulfur dioxide, aerosol acidity, and ozone suggested an independent association between mortality and PM10. The relative risk of death increased monotonically with PM10, and the relationship was observed at PM10 levels that were well below the current National Ambient Air Quality Standard of 150 micrograms/m3.
This paper explores the relationship between daily mortality and suspended particulates in Santa Clara County, CA, for years 1980 to 1986. An association was found between high particulate concentrations and increased mortality. This association persists after adjustment for temperature, relative humidity, year, and seasonality. Contrary to expectation, the magnitude of the particulate effect appears the same or larger than that estimated for London, despite Santa Clara County's cleaner air. The persistence of an effect at these lower particulate concentrations suggests that the particulate variable may be acting as a surrogate for some constituent particles, such as acid aerosols.
Several recent studies have reported associations between short term changes in air pollution and respiratory hospital admissions. This relationship was examined in two cities with substantially different levels of sulphur dioxide (SO2) but similar levels of airborne particles in an attempt to separate the effects of the two pollutants. Significant differences in weather between the two cities allowed the evaluation of that potential confounder also.
Daily counts of admissions to all hospitals for respiratory disease (ICD 9 460-519) were constructed for persons aged 65 years and older in two cities - New Haven, Connecticut and Tacoma, Washington. Each city was analysed separately. Average daily concentrations of SO2, inhalable particles (PM10), and ozone were computed from all monitors in each city, and daily average temperature and humidity were obtained from the US weather service. Daily respiratory admission counts were regressed on temperature, humidity, day of the week indicators, and air pollution. A 19 day weighted moving regression filter was used to remove all seasonal and subseasonal patterns from the data. Possible U-shaped dependence of admissions on temperature was dealt with using indicator variables for eight categories each of temperature and humidity. Each pollutant was first examined individually and then multiple pollutant models were fitted.
All three pollutants were associated with respiratory hospital admissions of the elderly. The PM10 associations were little changed by control for either ozone or SO2. The ozone association was likewise independent of the other pollutants. The SO2 association was substantially attenuated by control for ozone in both cities, and by control for PM10 in Tacoma. The magnitude of the effect was small (relative risk 1.06 in New Haven and 1.10 in Tacoma for a 50 micrograms/m3 increase in PM10, for example) but, given the ubiquitous exposure, this has some public health significance.
Air pollution concentrations within current guidelines were associated with increased respiratory hospital admissions of the elderly. The strongest evidence for an independent association was for PM10, followed by ozone. These results are consistent with other studies and suggest that lowering air pollution concentrations would have some impact on public health.
The relationship between daily mortality of elderly (65+ y) persons and air pollution in the metropolitan area of Sao Paulo, Brazil, for the period May 1990 to April 1991 was evaluated by time series regression, controlling for season, weather, and other factors. Mortality was associated with respirable particles (PM10), nitrogen oxides (NOx), sulfur dioxide (SO2), and carbon monoxide (CO). The association with PM10 was most statistically significant, robust, and independent of other air pollutants. An increase in PM10 equal to 100 micrograms/m3 was associated with an increase in overall mortality equal to approximately 13%. This association was consistent across various model specifications and estimation techniques. The dose-response relationship between mortality and respirable particulate pollution was almost linear, with no evidence of a "safe" threshold level. The results were similar to those observed in London and several U.S. cities. The results were also supportive of recent animal studies that have observed adverse health outcomes in experimental animals exposed to air pollution in Sao Paulo.
In the December 1952 smog disaster in London, a substantial increase in mortality was closely associated with the increase in air pollution. Deaths from cardiovascular causes were elevated as well as respiratory deaths. The increase was greatest in the elderly. Hospital admissions were increased for both respiratory and cardiovascular diseases. Since then, many studies have reported associations between lower concentrations of air pollution and daily mortality. Little attention has been paid to the question of hospital admissions for cardiovascular illness, however. This study examined the association between air pollution and cardiovascular hospital admissions for persons aged 65 years and older in the Detroit, Michigan, metropolitan area during the years 1986-1989. After controlling for seasonal and other long-term temporal trends, temperature, and dew point temperature, the particulate matter with an aerodiameter of < or = 10 microns (PM10) was associated with daily admissions for ischemic heart disease (relative risk (RR) = 1.018, 95% confidence interval (CI) 1.005-1.032 for an interquartile range (32 micrograms/m3) increase in pollution). SO2, CO, and ozone made no independent contribution to ischemic heart disease admissions. Both PM10 (RR = 1.024, 95% CI 1.004-1.044) and CO (RR = 1.022, 95% CI 1.010-1.034 for an interquartile range (1.28 ppm) increase in pollution) showed independent associations with heart failure admissions. These results were robust to alternate methods of estimation and weather control.
Several recent studies have reported associations between airborne particles and/or ozone and hospital admissions for respiratory disease. PM10 has rarely been used as the particle exposure measure, however. This study examined whether such an association could be seen in Minneapolis-St. Paul, Minnesota, which has daily monitoring data for PM10. Data on hospital admissions in persons aged 65 y and older were obtained from Medicare records for the years 1986 through 1989. Daily counts of admissions, by admit date, were computed for pneumonia (ICD9 480-487) and chronic obstructive pulmonary disease (COPD) (ICD9 490-496). Classification was by discharge diagnosis. Daily air pollution data from all monitoring stations for ozone and PM10 in Minneapolis-St. Paul were obtained, and the daily average for each pollutant was computed. An average of approximately six pneumonia admissions and two admissions for chronic obstructive pulmonary disease occurred each day. Poisson regression analysis was used to control for time trends, seasonal fluctuations, and weather. PM10 was a risk factor for pneumonia admissions (relative risk [RR] = 1.17, 95% confidence interval [CI] = 1.33-1.02) and COPD admissions (RR = 1.57, 95% CI = 2.06-1.20). Ozone was also associated with pneumonia admissions (RR = 1.15, 95% CI = 1.36-0.97). The relative risks are for an increase of 100 micrograms/m3 in daily PM10 and 50 ppb in daily ozone concentration. Several alternative methods for controlling for seasonal patterns and weather were used, including nonparametric regression techniques. The results were not sensitive to the methods. When days exceeding the National Ambient Air Quality Standard for either pollutant were excluded, the association remained for both pneumonia (RR = 1.18, 95% CI = 1.34-1.03 for PM10, and RR = 1.18, 95% CI = 1.41-0.99 for ozone) and COPD (RR = 1.54, 95% CI = 2.06-1.16 for PM10).
Several studies in recent years have suggested that exposure to airborne particles and to ozone are associated with increases in respiratory hospital admissions. Few of those studies have used inhalable particles as their measure of exposure, and the studies did not always examine both particle and ozone exposure. This study examined the association between both PM10 and ozone and respiratory hospital admissions for persons 65 yr of age and older in the Detroit, Michigan, metropolitan area during the years 1986 to 1989. After controlling for seasonal and other long-term temporal trends, temperature, and dew point temperature, both PM10 (RR = 1.012, 95% CI = 1.019-1.004) and 24-h ozone concentrations (RR = 1.026, 95% CI = 1.040-1.013) were associated with daily admissions for pneumonia. The relative risks are for a 10-microgram/m3 increase in PM10 and a 5-ppb increase in 24-h ozone concentration and from models including both pollutants. Admissions for COPD other than asthma were associated with PM10 (RR = 1.020, 95% CI = 1.032-1.009) and ozone (RR = 1.028, 95% CI = 1.049-1.007) as well. Asthma admissions were not associated with either pollutant. Controlling for one pollutant did not effect the magnitude of the association with the other pollutant. The magnitude of these relative risks are very similar to those recently reported in Birmingham, Alabama, Ontario, and New York State. This suggests that the associations with both pollutants are likely to be causal.
In Erfurt, Germany, unfavorable geography and emissions from coal burning lead to very high ambient pollution (up to about 4000 micrograms/m3 SO2 in 1980-89). To assess possible health effects of these exposures, total daily mortality was obtained for this same period. A multivariate model was fitted, including corrections for long-term fluctuations, influenza epidemics, and meterology, before analyzing the effect of pollution. The best fit for pollution was obtained for log (SO2 daily mean) with a lag of 2 days. Daily mortality increased by 10% for an increase in SO2 from 23 to 929 micrograms/m3 (5% quantile to 95% quantile). A harvesting effect (fewer people die on a given day if more deaths occurred in the last 15 days) may modify this by +/- 2%. The effect for particulates (SP, 1988-89 only) was stronger than the effect of SO2. Log SP (daily mean) increasing from 15 micrograms/m3 to 331 micrograms/m3 (5% quantile to 95% quantile) was associated with a 22% increase in mortality. Depending on harvesting, the observable effect may lie between 14% and 27%. There is no indication of a threshold or synergism. The effects of air pollution are smaller than the effects of influenza epidemics and are of the same size as meterologic effects. The results for the lower end of the dose range are in agreement with linear models fitted in studies of moderate air pollution and episode studies.
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Several studies have reported associations between airborne particles and/or ozone and hospital admissions for respiratory disease. This study examined whether such an association could be seen in Birmingham, Alabama, one of the few cities in the United States with daily monitoring of inhalable particles. Daily counts of hospital admissions were computed by date of admission from Medicare records for pneumonia and chronic obstructive pulmonary disease for the years 1986-1989. Classification was by discharge diagnosis. The daily average of ozone and particulate matter with an aerodiameter of < or = 10 microns (PM10) from all monitoring stations in Birmingham was computed. Approximately six admissions for pneumonia and two for chronic obstructive pulmonary disease were observed each day. In Poisson regression analysis controlling for time trends, seasonal fluctuations, and weather, inhalable particles were a risk factor for admission for pneumonia (for an increase of 100 micrograms/m3 in daily concentration, relative risk (RR) = 1.19, 95% confidence interval (CI) 1.07-1.32) and chronic obstructive pulmonary disease (RR = 1.27, 95% CI 1.08-1.50). The results were not sensitive to alternative methods for controlling for seasonal patterns and weather, nor to the exclusion of very hot or cold days. Ozone was more weakly associated with admissions for pneumonia, with a 2-day lag (RR = 1.14, 95% CI 0.94-1.38), and for chronic obstructive pulmonary disease, with a 1-day lag (RR = 1.17, 95% CI 0.86-1.60). The risks are for an increase in ozone exposure of 50 parts per billion. Tests for nonlinearity in the relation between inhalable particles and admissions were not significant, and nonparametric smoothing found no evidence of a threshold in the relation.
Several recent studies have reported associations between common levels of particulate air pollution and small increases in daily mortality. This study examined whether a similar association could be found in the southern United States, with different weather patterns than the previous studies, and examined the sensitivity of the results to different methods of analysis and covariate control. Data were available in Birmingham, Alabama, from August 1985 through 1988. Regression analyses controlled for weather, time trends, day of the week, and year of study and removed any long-term patterns (such as seasonal and monthly fluctuations) from the data by trigonometric filtering. A significant association was found between inhalable particles and daily mortality in Poisson regression analysis (relative risk = 1.11, 95% confidence interval 1.02-1.20). The relative risk was estimated for a 100-micrograms/m3 increase in inhalable particles. Results were unchanged when least squares regression was used, when robust regression was used, and under an alternative filtering scheme. Diagnostic plots showed that the filtering successfully removed long wavelength patterns from the data. The generalized additive model, which models the expected number of deaths as nonparametric smoothed functions of the covariates, was then used to ensure adequate control for any nonlinearities in the weather dependence. Essentially identical results for inhalable particles were seen, with no evidence of a threshold down to the lowest observed exposure levels. The association also was unchanged when all days with particulate air pollution levels in excess of the National Ambient Air Quality Standards were deleted. The magnitude of the effect is consistent with recent estimates from Philadelphia, Steubenville, Detroit, Minneapolis, St. Louis, and Utah Valley.
Recent studies have associated short-term exposure to respirable particulate matter (PM10) exposure with peak flow decrements, increased symptoms of respiratory irritation, increased use of asthma medications, and increased hospitalization for asthma. Increased mortality from chronic respiratory disease has also been reported. To help confirm whether PM10 exposure is a risk factor for the exacerbation of asthma, we compiled daily records of asthma emergency room visits from eight hospitals in the Seattle area. In Poisson regressions controlling for weather, season, time trends, age, hospital, and day of the week, the daily counts of emergency room visits for persons under age 65 were significantly associated with PM10 exposure on the previous day. The mean of the previous 4 days' PM10 was a better predictor (p < 0.005). The relative risk for a 30 micrograms/m3 increase in PM10 was 1.12 (95% confidence interval 1.20 to 1.04). Daily PM10 concentrations never exceeded 70% of the current ambient air quality standards during the period. The consistency of investigations of the health effects of PM10 suggest that increased attention should be given to the control of particulate matter air pollution.
Recent epidemiologic studies have consistently reported increased daily mortality associated with exposures to particulate air pollution. Currently, particulate mass is measured as particles smaller than 10 microns (PM10). Fine (PM2.5) and coarse (PM10-PM2.5) mass and sulfate particle concentrations were measured in six eastern U.S. cities for eight years, and aerosol acidity concentrations were measured for approximately one year. Daily mortality for these metropolitan areas was combined with particulate air pollution and weather measurements. City-specific associations with each measure of particle pollution were estimated by Poisson regression, adjusting for time trends and weather by nonparametric methods. Combined effect estimates were calculated as the inverse variance weighted mean of the city-specific estimates. PM10, PM2.5, and SO4= were each significantly associated with increased daily mortality, while no associations were found with coarse mass nor with aerosol acidity (H+) concentrations. The strongest association was found with PM2.5. A 10 micrograms/m3 increase in two-day mean PM2.5 was associated with a 1.5% (95% CI 1.1% to 1.9%) increase in total daily mortality. Somewhat larger increases were found for deaths caused by chronic obstructive pulmonary disease (+3.3%) and by ischemic heart disease (+2.1%). These data suggest that increased daily mortality is specifically associated with particle mass constituents found in the aerodynamic diameter size range under 2.5 microns, that is, with combustion-related particles.
The authors conducted a survival analysis to determine the effect of poverty on mortality in a national sample of blacks and whites, 25 to 74 years of age (the first National Health and Nutrition Examination Survey (NHANES-1) and NHANES-1 Epidemiologic Follow up Study). They estimated the proportion of mortality associated with poverty during 1971-1984 and in 1991 by calculating population attributable risk and assessed confounding by major known risk factors (e.g., smoking, cholesterol levels, and physical inactivity). In 1973, 6.0 percent of U.S. mortality among black and white persons 25 to 74 years of age was attributable to poverty; in 1991, the proportion was 5.9 percent. In 1991, rates of mortality attributable to poverty were lowest for white women, 2.2 times as high for white men, 8.6 times as high for black men, and 3.6 times as high for black women. Adjustment for all these potential confounders combined had little effect on the hazard ratio among men, but reduced the effect of poverty on mortality among women by 42 percent. The proportion of mortality attributable to poverty among U.S. black and white adults has changed only minimally in recent decades. The effect of poverty on mortality must be largely explained by conditions other than commonly recognized risk factors.
Recent studies have shown that an increased concentration of ambient particulate matter (PM10) is related to decreased pulmonary function and respiratory and cardiovascular mortality. The mechanisms responsible for this excess mortality are unknown and the relationship between the level of PM10 and the circulating leukocyte counts has not been previously investigated. We postulated that the deposition of PM10 in the peripheral lung stimulates alveolar macrophages (AM), which results in polymorphonuclear leukocyte (PMN) release from bone marrow (BM). To test this hypothesis, either colloidal carbon (CC) (n = 3) or saline (n = 4) was instilled into the lungs of rabbits and PMN release from BM was evaluated by using 5'-bromo-2'-deoxyuridine (BrdU). CC instillation in the lung shortened the transit time of PMN through the BM to 71.0 +/- 6.9 h compared with the saline controls (85.5 +/- 2.8 h, p < 0.01). The role of AM in this response was further investigated by incubating isolated AM in tissue culture medium either with or without the presence of CC, and measuring the effect of the supernatants on the release of PMN from the BM. The supernatant of AM incubated with CC shortened the PMN transit time through the BM to 74.9 +/- 3.7 h (p < 0.05) compared with the supernatant from the unstimulated AM (98.6 +/- 1.9 h) and medium alone (94.3 +/- 3.7 h). We conclude that the phagocytosis of CC by AM releases mediators (cytokines) that stimulate the BM to release PMN. We speculate that these newly released PMN may play an important role in the decline in lung function and high mortality seen in populations exposed to high concentrations of atmospheric PM10.
Recent findings suggest that females may be more susceptible than males to the deleterious influence of tobacco smoking in developing chronic obstructive pulmonary disease (COPD). This paper studies the interaction of gender and smoking on development of COPD as assessed by lung function and hospital admission. A total of 13,897 subjects, born after 1920, from two population studies, 9,083 from the Copenhagen City Heart Study (CCHS) and 4,814 from the Glostrup Population Studies (GPS), were followed for 7-16 yrs. Data were linked with information on hospital admissions caused by COPD. Based on cross-sectional data, in the CCHS the estimated excess loss of forced expiratory volume in one second (FEV1) per pack-year of smoking was 7.4 mL in female smokers who inhaled and 6.3 mL in male smokers who inhaled. In the GPS, the corresponding excess loss of FEV1 was 10.5 and 8.4 mL in females and males, respectively. Two hundred and eighteen subjects in the CCHS and 23 in the GPS were hospitalized during follow-up. Risk associated with pack-years was higher in females than in males (relative risks (RRs) for 1-20, 20-40 and >40 pack-years were 7.0 (3.5-14.1), 9.8 (4.9-19.6) and 23.3 (10.7-50.9) in females, and 3.2 (1.1-9.1), 5.7 (2.2-14.3) and 8.4 (3.3-21.6) in males) but the interaction term gender x pack-years did not reach significance (p=0.08). Results were similar in the GPS. After adjusting for smoking in more detail, females in both cohorts had an increased risk of hospitalization for COPD compared to males with a RR of 1.5 (1.2-2.1) in the CCHS and 3.6 (1.4-9.0) in the GPS. This was not likely to be caused by a generally increased rate of hospital admission for females. Results were similar when including deaths from COPD as endpoint. In two independent population samples, smoking had greater impact on the lung function of females than males, and after adjusting for smoking females subsequently suffered a higher risk of being admitted to hospital for COPD. Results suggest that adverse effects of smoking on lung function may be greater in females than in males.
The relation between air pollution and mortality in London was examined for the winters of 1958–1972. The data exhibited a high degree of autocorrelation, requiring analyses using autoregressive models. There was a highly significant relation between mortality and either particulate matter or sulfur dioxide (after controlling for temperature and humidity), both overall and in each individual year. Graphic analysis revealed a nonlinear relation with no threshold, and a steeper exposure-response curve at lower air pollution levels. in models with both pollutants, particulate matter remained a significant predictor with about a 10% reduction in its estimated coefficients, while sulfur dioxide was insignificant, with a large drop in its estimated coefficient The authors conclude that particulates are strongly associated with mortality rates in London, and the relation is likely causal.
Environmental epidemiologists often encounter time series data in the form of discrete or other nonnormal outcomes; for example, in modeling the relationship between air pollution and hospital admissions or mortality rates. We present a case study examining the association between pollen counts and meteorologic covariates. Although such time series data are inadequately described by standard methods for Gaussian time series, they are often autocorrelated, and warrant an analysis beyond those provided by ordinary generalized linear models (GLMs). Transitional regression models (TRMs), signifying nonlinear regression models expressed in terms of conditional means and variances given past observations, provide a unifying framework for two mainstream approaches to extending the GLM for autocorrelated data. The first approach models current outcomes with a GLM that incorporates past outcomes as covariates, whereas the second models individual outcomes with marginal GLMs and then couples the error terms with an autoregressive covariance matrix. Although the two approaches coincide for the Gaussian GLM, which serves as a helpful introductory example, in general they yield fundamentally different models. We analyze the pollen study using TRM's of both types and present parameter estimates together with asymptotic and bootstrap standard errors. In several cases we find evidence of residual autocorrelation; however, when we relax the TRM to allow for a nonparametric smooth trend, the autocorrelation disappears. This kind of trade-off between autocorrelation and flexibility is to be expected, and has a natural interpretation in terms of the covariance function for a nonparametric smoother. We provide an algorithm for fitting these flexible TRM's that is relatively easy to program with the generalized additive model software in S-PLUS.
We present an analytical investigation of the propagation and the switching of fundamental solitons in a three-core nonlinear fiber coupler with a variational method using the Lagrangian density formulation. The analytical solutions were obtained directly from the coupled nonlinear Schrödinger equations. The transmission characteristics of first order solitons obtained by the analytical procedure agree well with the results from numerical analysis. Three different geometries for the nonlinear three-core directional coupler were studied. Taking into account the length of the coupler and the critical power a comparative study between these geometries was done. © 1998 American Institute of Physics.
To examine the biological plausibility of the adverse health effects of ambient particulate matter (PM), we have studied the cardio-pulmonary effects of PM in an animal model of pulmonary hypertension. Normal and monocrotaline-treated rats were exposed, nose-only, for 3 h to filtered air or concentrated ambient PM. At 3 h—but not 24 h—post-exposure, the percentage of neutrophils in peripheral blood was significantly elevated in PM-exposed animals while the percentage of lymphocytes was decreased with no change in white blood cell counts. These changes in white blood cell differential occurred in both normal and monocrotaline-treated animals. Small, but consistent changes in heart rate, but not core temperature, were observed after exposure to concentrated ambient PM. Pulmonary injury, as evidenced by increased protein levels in lavage fluid, occurred only in monocrotaline-treated animals exposed to >360 μg/m3 PM. The observed pattern of hematological and cardiac changes suggests an activation of the sympathetic stress response.
This article describes flexible statistical methods that may be used to identify and characterize nonlinear regression effects. These methods are called "generalized additive models". For example, a commonly used statistical model in medical research is the logistic regression model for binary data. Here we relate the mean of the binary response ¯ = P (y = 1) to the predictors via a linear regression model and the logit link function: log
The visual information on a scatterplot can be greatly enhanced, with little additional cost, by computing and plotting smoothed points. Robust locally weighted regression is a method for smoothing a scatterplot, (x i , y i ), i = 1, …, n, in which the fitted value at z k is the value of a polynomial fit to the data using weighted least squares, where the weight for (x i , y i ) is large if x i is close to x k and small if it is not. A robust fitting procedure is used that guards against deviant points distorting the smoothed points. Visual, computational, and statistical issues of robust locally weighted regression are discussed. Several examples, including data on lead intoxication, are used to illustrate the methodology.
Population-based studies of hospital usage have been used to identify the ongoing adverse impacts of photochemical air pollutants on respiratory health. In this study we examined the relationship between the number of daily emergency room (ER) visits for respiratory illnesses (25 hospitals) and outdoor air pollution in Montreal, Quebec (June-August, 1989-1990). Air pollutants measured included 1- and 8-h maximum ozone (O3) and estimated particulate matter < 2.5 microns in aerometric diameter (PM2.5). Seasonal and day-of-week trends, autocorrelation, temperature, and relative humidity were controlled for in-time series regressions. Although O3 levels never exceeded the U.S. National Ambient Air Quality Standard (NAAQS) of 120 ppb (maximum day, 106 ppb), statistically significant (P < 0.01) relationships were found between respiratory ER visits for patients over the age of 64 and both 1- and 8-h maximum O3 measured 1 day prior to the ER visit day during the 1989 summer: ER visits were 18.7% higher than average (95% Cl, 6.5-30.9%) for a mean increase of 44 ppb O3 (1-h maximum), and 21.8% higher than average (95% Cl, 9.7-33.8%) for a mean increase of 38 ppb O3 (8-h maximum). There was an association between respiratory ER visits for the elderly and estimated PM2.5 lagged 1 day (0.1 visit/microgram/m3 PM2.5, P < 0.07), but this was confounded by both temperature and O3. The only finding for a reference group of nonrespiratory conditions was an inverse association between ER visits for infants and O3, but this was confounded by weather. These findings confirm the impression that while air quality standards may protect the respiratory health of the general population, this is not the case for susceptible subgroups such as the elderly.
Differential mortality exists in the United States both between racial/ethnic groups and along gradients of socioeconomic status. The specification of statistical models for processes underlying these observed disparities has been hindered by the fact that social and economic quantities are distributed in a highly nonrandom manner throughout the population. We sought to provide a substantive foundation for model development by representing the shape of the income-mortality relation by racial/ethnic group. We used data on black and white men and women from the longitudinal component of the National Health Interview Survey (NHIS), 1986-1990, which provided 1,191,824 person-years of follow-up and 12,165 mortal events. To account for family size when considering income, we used the ratio of annual family income to the federal poverty line for a family of similar composition. To avoid unnecessary categorizations and prior assumptions about model form, we employed kernel smoothing techniques and calculated the continuous mortality surface across dimensions of adjusted income and age for each of the gender and racial/ethnic groups. Representing regions of equal mortality density with contour plots, we observed interactions that need to be accommodated by any subsequent statistical models. We propose two general theories that provide a foundation for more elaborate and testable hypotheses in the future.
Public health data do not simply exist: the variables included or excluded from any given data set reflect the choices of individuals and institutions with the power to make these decisions. Their judgement typically is guided by prevailing theories of disease causation, which in turn usually resonate with their society's predominant political, economic, and ideological characteristics. This essay examines the making of public health data as a social process, both historically and in the present, and critiques the routine omission of social class data from US public health data bases, the treatment of "race" and "sex" as primarily biological variables, and their conflation with ethnicity and gender. Overcoming these problems will require developing social theories of disease causation and ending the pervasive silence about the health consequences of class, race, and gender inequalities.
Particulate air pollution has been associated with increased mortality during episodes of high pollution concentrations. The relationship at lower concentrations has been more controversial, as has the relative role of particles and sulfur dioxide. Replication has been difficult because suspended particle concentrations are usually measured only every sixth day in the U.S. This study used concurrent measurements of total suspended particulates (TSP) and airport visibility from every sixth day sampling for 10 years to fit a predictive model for TSP. Predicted daily TSP concentrations were then correlated with daily mortality counts in Poisson regression models controlling for season, weather, time trends, overdispersion, and serial correlation. A significant correlation (P less than 0.0001) was found between predicted TSP and daily mortality. This correlation was independent of sulfur dioxide, but not vice versa. The magnitude of the effect was very similar to results recently reported from Steubenville, Ohio (using actual TSP measurements), with each 100 micrograms/m3 increase in TSP resulting in a 6% increase in mortality. Graphical analysis indicated a dose-response relationship with no evidence of a threshold down to concentrations below half of the National Ambient Air Quality Standards for particulate matter.
This study evaluated changes in respiratory health associated with daily changes in fine particulate pollution (PM10). Participants included a relatively healthy school-based sample of fourth and fifth grade elementary students, and a sample of patients with asthma 8 to 72 yr of age. Elevated PM10 pollution levels of 150 micrograms/m3 were associated with an approximately 3 to 6% decline in lung function as measured by peak expiratory flow (PEF). Current day and daily lagged associations between PM10 levels and PEF were observed. Elevated levels of PM10 pollution also were associated with increases in reported symptoms of respiratory disease and use of asthma medication. Associations between compromised respiratory health and elevated PM10 pollution were observed even when PM10 levels were well below the 24-h national ambient air quality standard of 150 micrograms/m3. Associations between elevated PM10 levels, reductions in PEF, and increases in symptoms of respiratory disease and asthma medication use remained statistically significant even when the only pollution episode that exceeded the standard was excluded. Concurrent measurements indicated that little or no strong particle acidity was present.
The interaction between sex and smoking habits on pulmonary function was examined among 1,149 adults 25 to 59 yr of age in a rural community in Saskatchewan. Pulmonary function tests included FVC, FEV1, maximal midexpiratory flow rate (MMFR), the slope of phase III of the single-breath nitrogen test (delta N2/L), and closing volume as a percent of vital capacity (CV/VC). The data show that after fixing the effects of age, height, and weight by analysis of covariance, the adjusted means of delta N2/L in nonsmokers, ex-smokers, and current smokers were 0.92, 1.10, and 1.60% in women and 0.97, 1.05, and 1.23% in men, respectively. The difference in the adjusted means for delta N2/L between smokers and nonsmokers was larger in women than in men, 0.67% versus 0.26%, respectively. Multiple multivariate analyses show that the regression slopes for the residuals of FEV1, MMFR, and delta N2/L versus pack-years were significantly different between men and women. The regressions of FEV1 and MMFR decreased and the regression of delta N2/L increased with increasing pack-years more rapidly in women than in men. The combined effect of sex and pack-years on pulmonary function was not significant for ex-smokers. These data suggest that cigarette smoking may be more detrimental in its effects on lung function in women than in men.
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.
Air pollution in the huge conurbation of São Paulo, Brazil (13 million inhabitants) has been mapped from air quality monitoring stations. In three contrasted sample areas, children's respiratory health parameters were collected to assess the roles of poverty and poor housing against those of air pollution. Respiratory ill-health is clearly shown to vary with pollution levels and there is evidence that socio-economic conditions aggravate the problem.
Air pollution data from 17 sampling stations between Windsor and Peterborough in Southern Ontario, for January, February, July, and August in 1974 and 1976 to 1983, have been analyzed. Each station reported O3, NO3, SO2, and the coefficient of haze (COH) every hour and aerosol sulfates for a 24-hr period every sixth day using glass-fiber filters. Data on mean daily temperature and relative humidity for the region were also recorded. It is shown that there are high correlations between different pollutants and between these and temperature in the summer. In the summer, sulfate levels were significantly correlated with relative humidity. In winter, the highest correlation was between COH and NO2. Over the 9-year period, SO2 levels in both winter and summer have fallen considerably; there have been no significant trends in O3, NO3, or COH data. Aerosol sulfates increased between 1976 and 1980 in both summer and winter and have since declined slightly. Hospital admission data for the 79 acute care hospitals serving the region, which contains about 5.9 million people, have been analyzed on a daily basis for the same months of the same years. Total admissions and total respiratory admissions have declined about 15% over the period, but asthma admissions appear to have risen. The asthma category of admissions is complicated by the effects of a change in ICD coding in 1979. It has been shown that significant correlations exist between O3, SO4, SO2, and temperature, on the one hand, and deviations from the mean respiratory admissions for that day of the week, for that season, for that year, on the other. These correlations exist if asthma is excluded from the diagnoses. In winter, asthma admissions are correlated with temperature only. A group of nonrespiratory conditions showed no correlations with air pollutants in winter or summer. Stepwise multiple regression analysis based on each year considered individually indicates that in summer SO4 and temperature account for about 5% of the variance in respiratory or asthma admissions. It is shown that the mean of the hourly ozone maxima has a high correlation with the maximal 8-hr average for ozone, and that using this index instead of the mean of the hourly maxima does not increase the correlation coefficient with respiratory disease. Another analysis has been performed by grouping the hospitals and sampling stations into nine separate regions.(ABSTRACT TRUNCATED AT 400 WORDS)
This paper analyzes and systematizes the race and class differentials in exposure to toxic hazards and actual health outcomes. Research is categorized into the following: Proximity to known hazards includes (1) presence of hazardous waste sites and facilities (landfills, incinerators, Superfund sites), (2) exposure to air pollution, (3) exposure to various environmental hazards, e.g., toxic releases and hazards in pesticides and foods; Regulation, amelioration and cleanup includes (4) record of decisions (RODs) and cleanups at NPL sites, (5) regulatory action, as measured by assessed fines for environmental pollution; Health effects includes (6) specific health outcomes which are related to environmental burden (e.g., blood lead levels). Proximity to prospective hazards includes (7) sitting decisions for incinerators, hazardous waste sites, and nuclear storage sites. The overwhelming bulk of evidence supports the "environmental justice" belief that environmental hazards are inequitably distributed by class, and especially race.
Athens has a serious air pollution problem which became evident in the early 1970s. Studies for the years 1975-1982 have indicated a positive association of sulphur dioxide (SO2) with total daily mortality. Since 1983 the pollution profile in Athens has gradually changed but the levels of smoke, SO2 and carbon monoxide (CO) remain relatively high.
The association of air pollution with daily all-cause mortality in Athens for the years 1984-1988 was investigated using daily values of SO2, smoke and CO. Autoregressive models with log-transformed daily mortality as the dependent variable, were used to adjust for temperature and relative humidity (both lagged by 1 day), year, season and day of week, as well as for serial correlations in mortality.
Graphic analysis revealed non-linear monotonically increasing relationships between total mortality and SO2, smoke and CO, with steeper exposure-response slopes at lower air pollution levels. Air pollution data lagged by 1 day had the strongest association with daily mortality. In three separate autoregression models for log(SO2), log(smoke) and log(CO) the regression coefficients for each were highly statistically significant (P < 0.001). Further multiple regression modelling showed that SO2 and smoke are both independent predictors of daily mortality, though to a lesser extent than temperature and relative humidity. The inclusion of CO in the model did not further improve the prediction of daily mortality. The magnitude of association is small, for instance, a 10% reduction in smoke is estimated to decrease daily mortality by 0.75% (95% confidence interval [CI]: 0.51-0.99). However, it cannot be accounted for by climatic and seasonal effects, so that a causal influence of air pollution on daily mortality seems plausible.
These findings suggest that current air pollution levels in Athens (and many other industrialized cities) may be responsible for substantial numbers of premature deaths, and hence remain an important public health issue.
Data on 1,618 male and 1,669 female adults aged 40-69 yrs, from China in the Beijing Respiratory Health Study, were analysed to investigate the gender differences in effects of smoking on pulmonary function. Smoking was characterized by total smoking-years, smoking status (former, transitional and constant), smoking type (cigarette, cigar and others). The effects of smoking on height-standardized forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) were assessed by multiple regressions adjusting for age, education level, use of an indoor coal stove for heating, passive smoking, occupational dust and gas/fume exposure, and residence. Prediction equations were derived from nonsmoking asymptomatic subjects. As compared to women, men had a much higher smoking prevalence (78 vs 35%) but a lower quitting rate (14 vs 23%). Female lifetime nonsmokers had greater mean percentage predicted lung function values than male lifetime nonsmokers, whilst female cigarette smokers had lower values than their male counterparts. In both sexes, the highest mean percentage predicted lung function values were found in lifetime nonsmokers, whilst the lowest values were found among former smokers, the second lowest among transitional smokers, and constant smokers actually had greater values than both former and transitional smokers. These findings were confirmed by sex-specific regression analyses. A global test on the interactions between smoking and sex was highly significant. This study suggests that adverse smoking effects on pulmonary function were greater in women than in men.(ABSTRACT TRUNCATED AT 250 WORDS)
National vital statistics in the United States present data in terms of race, sex, and age, treated as biological variables. Some races are clearly of more interest than others: data are usually available for whites and blacks, and increasingly for Hispanics, but seldom for Native Americans or Asians and Pacific Islanders. These data indicate that white men and women generally have the best health and that men and women, within each racial/ethnic group, have different patterns of disease. Obviously, the health status of men and women differs for conditions related to reproduction, but it differs for many nonreproductive conditions as well. In national health data, patterns of disease by race and sex are emphasized while social class differences are ignored. This article discusses how race and sex became such all-important, self-evident categories in 19th and 20th century biomedical thought and practice. It examines the consequences of these categories for knowledge about health and for the provision of health care. It then presents alternative approaches to understanding the relationship between race/ethnicity, gender, and health, with reference to the neglected category of social class.
Some individuals, groups, and communities are at special risk from environmental threats. This is especially the case for low income persons, the working class, and people of color whose health may be imperiled by lead in their houses, pollution in their neighborhoods, and hazards in their workplace. Moreover, many of their children face potential health threats in the parks where they play. The environmental justice perspective unmasks the ethical and political questions of "who gets what, why, and in what amounts." An environmental and public health strategy is needed to ensure that all Americans are protected.
Although much of the evidence is anecdotal and circumstantial, there are mounting concerns that environmental health risks are borne disproportionately by members of the population who are poor and nonwhite. We examine the central role of environmental health research in defining the dimensions of the problem, understanding its causes, and identifying solutions. Environmental health sciences, including epidemiology, exposure analysis. pharmacokinetics, toxicology, and surveillance monitoring, must be employed to determine the extent to which society has achieved "equity" and "justice" in safeguarding the health and safety of its citizens. By improving our ability to identify, evaluate, prevent, and/or reduce risks for all members of society, environmental health research can contribute directly to fair and equitable protection for everyone, regardless of age, ethnicity, gender, race, or socioeconomic status.
A study of air pollution and daily hospital admissions for respiratory causes was conducted in Toronto, Ontario. Fine aerosol (da < 2.5 microns) samples were collected daily at a central city site during July and August 1986, 1987, and 1988 and were subsequently extracted and analyzed for daily particulate phase aerosol strong acidity (H+) and sulfates (SO4 =). Daily counts of respiratory admissions to 22 acute care hospitals and daily meteorological and environmental data (e.g. ozone [O3], total suspended particulate matter [TSP], and thoracic particle mass [PM10] were also obtained. Regression analyses indicated that only the O3, H+, and SO4 = associations with respiratory and asthma admissions remained consistently significant after controlling for temperature. Even after excluding days with maximum 1-hr O3 > 120 ppb, O3 was still strongly significant. In the various model specifications considered, the relative particle metric strengths of association with admissions were generally H+ > SO4 = > FP > PM10 > TSP, indicating that particle size and composition are of central importance in defining the adverse human health effects of particulate matter. On average, summertime haze air pollution was associated with 24% of all respiratory admissions (21% with O3, 3% with H+). On peak pollution days, however, aerosol acidity yielded the highest relative risk estimates (e.g., RR = 1.5 at 391 nmole/m3 H+), and summertime haze was associated with roughly half of all respiratory admissions.
To investigate the acute respiratory health effects of ambient air pollution, the number of emergency of urgent daily respiratory admissions to 168 acute care hospitals in Ontario were related to estimates of exposure to ozone and sulfates in the vicinity of each hospital. Ozone levels were obtained from 22 monitoring stations maintained by the Ontario Ministry of the Environment for the period January 1, 1983 to December 31, 1988. Daily levels of sulfates were recorded at nine monitoring stations representing three different networks operated by the Ontario Ministry of the Environment and Environment Canada. Positive and statistically significant associations were found between hospital admissions and both ozone and sulfates recorded on the day of admission and up to 3 days prior to the date of admission. Five percent of daily respiratory admissions in the months of May to August were associated with ozone, with sulfates accounting for an additional 1% of these admissions. Ozone was a stronger predictor of admissions than sulfates. Positive and statistically significant (P < 0.05) associations were observed between the ozone-sulfate pollution mix and admissions for asthma, chronic obstructive pulmonary disease, and infections. Positive associations were also found in all age groups, with the largest impact on infants (15% of admissions associated with the ozone-sulfate pollution mix) and the least effects on the elderly (4%). Temperature had no effect on the air pollution-admission relationship. Ozone (lagged 1 day) and sulfates (lagged 1 day) displayed a positive association with respiratory admissions for 91 and 100% of the 168 acute care hospitals, respectively. Air pollution was not related to a class of nonrespiratory admissions, which served as a negative control, nor was it related to admissions in the winter months of December to March, when ozone and sulfate levels are low and when people spend a considerable amount of time indoors.
The air pollution disasters in London in 1952, the Meuse valley in 1930, and in Donoroa, Pennsylvania, in 1948 made it clear that extremely high levels of particulate-based smog could produce large increases in the daily mortality rate. Recent studies of fluctuations in daily air pollution and daily mortality have reported associations at much lower concentrations in London during the 1960s and in Philadelphia, Steubenville, Santa Clara, St. Louis, Utah valley, Detroit, and eastern Tennessee in the 1970s and 1980s. Whether these associations are causal or not is a matter of considerable public health concern. If the detailed pattern of the deaths at these lower concentrations appeared similar to the pattern in London, this would strengthen the argument for causality. To examine this issue, the death certificates from Philadelphia were examined on the 5% of the days with the highest particulate air pollution and the 5% of the days with the lowest particulate air pollution during the years 1973-1980. There was little difference in weather between the high and low pollution days, but total suspended particulate matter concentrations averaged 141 micrograms/m3 on the high pollution days versus 47 micrograms/m3 on the low pollution days. The relative risk of dying on the high pollution days was 1.08 P < 0.0001. The relative increase was higher for COPD (1.25) and pneumonia (1.13). Deaths were also elevated for heart disease and stroke; however, there was a substantial increase in the reports of respiratory factors as contributing causes for those underlying causes of death. Dead-on-arrival deaths and deaths outside of hospitals and clinics were also disproportionately increased. This paralleled the pattern seen in London in 1952. The age pattern of the relative risk of death was also similar. This adds to the evidence that the association is causal.
An association between sulfur dioxide levels in urban air and the daily number of emergency room admissions for chronic obstructive pulmonary disease was previously reported in Barcelona, Spain, for the period 1985-1986. The present study assesses this association over a longer period of time, 1985-1989. This made it possible to carry out separate analyses for the winter and summer seasons and thus to control more adequately for weather and influenza epidemics. An increase of 25 micrograms/m3 in sulfur dioxide (24-hour average) produced adjusted changes of 6% and 9% in emergency room admissions for chronic obstructive pulmonary disease during winter and summer, respectively. For black smoke, a similar change was found during winter, although the change was smaller in summer. The association of each pollutant with chronic obstructive pulmonary disease admissions remained significant after control for the other pollutant. The present findings support the conclusion that current levels of sulfur dioxide and black smoke may have an effect on the respiratory health of susceptible persons.
Recent epidemiologic studies suggest increased mortality among the elderly in association with particulate air pollution. We investigated the variability in fractional deposition (DF) of inhaled particles (2 microns mass median aerodynamic diameter [MMAD]) in 62 subjects with normal lung function, aged 18 to 80 yr. Each subject inhaled 2-microns monodisperse carnauba wax particles while following a breathing pattern previously determined by respiratory inductance plethysmography in that subject (i.e., particles inhaled) was determined by laser aerosol photometry and pneumotachometry at the mouth. DF (mean DF = 0.29 +/- 0.06 (ages 18 to 40 yr), 0.29 +/- 0.07 (ages 41 to 60 yr), and 0.26 +/- 0.06 (age over 60 yr) was independent of age. There was a tendency toward greater DF in female than in male subjects; DF = 0.30 +/- 0.07 (females) and 0.27 +/- 0.06 (males) (p = 0.06); however, because the males had 45% higher minute ventilations than the females, the deposition rate (Drate), or particles depositing per unit of time, was 30% greater in males than in females (p = 0.004). Multiple regression analysis showed that among all subjects, the variability in DF was best predicted by variability in the breathing period (T) associated with the pattern used to breathe the particles, and by the subject's specific airway resistance (sRAW). These results may prove useful in determining age- and gender-relative risks that may be associated with the inhalation of pollutant particles in ambient air.
Several recent studies have reported associations between short-term changes in air pollution and respiratory hospital admissions. Most of those studies analyzed locations where there was a high correlation between airborne particles and sulfur dioxide (SO2), and between all air pollutants and temperature. Here, I seek to replicate the previous findings in a location where SO2 concentrations were trivial, and the correlation between both airborne particles and ozone with temperature was considerably lower than in previous studies. I constructed daily counts of admissions to all hospitals in Spokane, WA, for respiratory disease (International Classification of Diseases, 9th revision, codes 460-519) for persons age 65 years and older. I computed average daily concentrations of airborne particles whose diameter is 10 microns or less (PM10) and ozone (O3) from all monitors in each city, and I obtained daily average temperature and humidity from the U.S. weather service. SO2 concentrations in Spokane were so low that monitoring was discontinued. I regressed daily respiratory admission counts on temperature, humidity, day of the week indicators, and air pollution. I used a Poisson regression analysis and removed long wavelength patterns using a nonparametric smooth function of day of study. I dealt with a possible U-shaped dependence of admissions on temperature and/or humidity by using nonparametric smooth functions of weather variables as well. I then examined sensitivity analyses to control for weather. Both PM10 and ozone were associated with increased risk of respiratory hospital admissions [relative risk (RR) = 1.085; 95% confidence interval (CI) = 1.036-1.136 for a 50-microgram per m3 increase in PM10, and RR = 1.244; 95% CI = 1.002-1.544 for a 50-microgram per m3 increase in peak-hour ozone]. The PM10 association was insensitive to alternative methods of control for weather, including exclusion of extreme temperature days and control for temperature on multiple days. The ozone results were more sensitive to the approach for weather control. The magnitude of the PM10 effect in this location, where SO2 was essentially not present, and where the correlation between PM10 and temperature was close to zero, was similar to that reported in other locations in the eastern United States and Europe, where confounding by weather and SO2 is a more substantial concern.
Few data are available on the association between the present low levels of air pollution in Western Europe and mortality. Daily mortality counts and the concentrations of black smoke, inhalable particles (PM10), sulfur dioxide (SO2), carbon monoxide (CO), and ozone (O3) were available for Amsterdam from 1986 to 1992. We used Poisson regression analysis to control for seasonal and other long-term temporal patterns. Black smoke and PM10 were positively associated with increased risk of mortality. The relative risk for a 100-micrograms per m3 increase in black smoke on the same day was 1.19 [95% confidence interval (CI) = 1.02-1.38], and that for a 100-micrograms per m3 increase in PM10 was 1.06 (95% CI = 0.99-1.14). The relative risk for individuals over 64 years of age was higher. We found no consistent association between the levels of SO2 or CO and daily mortality, but ozone lagged 2 days was positively associated with daily mortality. The effect of particulates on acute mortality was independent of these pollutants. The results of the present study are consistent with the relation reported between particulate air pollution and daily mortality in other communities in Europe and the United States.
Recent time-series epidemiological studies have reported significant associations between daily air pollution and mortality. These studies typically report a short-term excess increase in deaths as the fractional increase of total (nonaccidental) deaths per unit of air pollutant. The relative risk (RR) calculated for the total population in these studies, however, may underestimate the risk for the most sensitive subpopulation(s) at risk. In this study, race, gender, and cause-specific counts of daily mortality in Cook County, Illinois (which encompasses the city of Chicago) during 1985-1990 were analyzed to determine if there was any heterogeneity in air pollution/weather/mortality associations across these various population subcategories. Seasonal cross-correlations between mortality and environmental variables first were examined to identify appropriate lag structures. Of the pollution variables considered-particulate matter less than 10 microns (PM10), ozone, carbon monoxide, sulfur dioxide, and visual range-derived extinction coefficient-both PM10 and ozone showed significant associations with same-day and next-day mortality. The Poisson regression models employed included seasonal cycles (sine/cosine series), square and linear terms of lagged temperature, trend line, day-of-week dummy variables, and the average of the same day's and previous day's PM10 or ozone. The RR for total nonaccidental mortality per 100 micrograms/m3 increase in PM10 was 1.05 (95% CI: 1.03-1.08). The respiratory (RR = 1.14; 95% CI: 1.04-1.25) and cancer (RR = 1.12; 95% CI: 1.06-1.18) categories showed higher estimates than the circulatory category (RR = 1.03; 95% CI: 0.98-1.07), while the residual of the total from these three categories showed no association with PM10 (RR = 1.01; 95% CI: 0.95-1.08). Among the race- and gender-specific categories, black (African-American) females showed the higher RRs for the total (RR = 1.11; 95% CI: 1.03-1.21), respiratory (RR = 1.31; 95% CI: 0.98-1.75), and cancer (RR = 1.25; 95% CI: 1.07-1.46) mortality categories. Neither ozone nor hot temperature showed such cause-specificity in mortality associations. Cold temperature lagged by two days was a significant predictor of circulatory and respiratory mortality. This study suggests the importance of race- and gender-specific analysis. The greater mortality risk to Chicago's black women from exposure to urban air pollution indicated by this finding should be tested in other metropolitan areas.
Female sex-steroid hormones may play an important influence in asthma. The aim of this study was to compare airway reactivity to adenosine monophosphate (AMP) in female asthmatics with natural menstrual cycles and those taking the oral combined contraceptive pill (OCP). Eighteen asthmatic subjects were evaluated. Nine subjects, mean (SEM) age, 24 (6) years, FEV1 93% (10) predicted, with natural cycles (group 1) were compared with nine subjects, age 24 (6) years, FEV1 93% (9) predicted taking the OCP (group 2). Group 1 subjects were evaluated at the follicular (visit 1) and luteal (visit 2) phases; group 2 subjects were evaluated during the week off OCP (visit 1) and at the end of the OCP cycle (visit 2). At each visit, serum progesterone and estradiol were measured. Airway reactivity to AMP was evaluated and expressed as PC20 (FEV1; mg/ml). Morning and evening peak expiratory flow rates (PEFR) were monitored throughout the study. In group 1, there was a significant increase in serum progesterone (nmol/l) and estradiol (pmol/l). (Visit 1 vs. 2): 2.5 vs. 13.5 (95% CI 2.1 to 19.9; p = 0.02) and 152.3 vs. 358.1 (95% CI 113.0 to 298.5; p < 0.001), respectively. In group 2, however, there was no increase between visit 1 vs. 2 in hormones: 0.9 vs. 1.0 and 75.7 vs. 21.8 for progesterone and estradiol, respectively. There was a significant increase in airway reactivity in group 1 during the luteal phase. Geometric mean PC20 (mg/ml) was 18.8 and 4.7 at visit 1 and 2, respectively: a 4.0-fold difference (95% CI 1.25 to 13.03; p = 0.03) amounting to two doubling doses. In contrast, there was no change in PC20 in group 2. Geometric mean PC20 was 23.5 and 21.4: a 1.06-fold difference (95% CI 0.41 to 2.78; p = 0.83). In group 1, morning and evening PEFR (l/min) were significantly different at both visits: at visit 1 (A.M. PEFR vs. P.M. PEFR) 403 vs. 430 (95% CI 5 to 50; p < 0.001) and visit 2, 415 vs. 439 (95% CI 1 to 46; p < 0.001). In group 2, there was no significant difference in diurnal PEFR variability at both visits; 411 vs. 417 at visit 1 and 413 vs. 427 at visit 2. In conclusion, asthmatic patients receiving the OCP had attenuated cyclical change in airway reactivity as well as reduced diurnal PEFR variability, which was associated with suppression of the normal luteal phase rise in sex-hormones.
Increasing social inequalities in health in the United States and elsewhere, coupled with growing inequalities in income and wealth, have refocused attention on social class as a key determinant of population health. Routine analysis using conceptually coherent and consistent measures of socioeconomic position in US public health research and surveillance, however, remains rare. This review discusses concepts and methodologies concerning, and guidelines for measuring, social class and other aspects of socioeconomic position (e.g. income, poverty, deprivation, wealth, education). These data should be collected at the individual, household, and neighborhood level, to characterize both childhood and adult socioeconomic position; fluctuations in economic resources during these time periods also merit consideration. Guidelines for linking census-based socioeconomic measures and health data are presented, as are recommendations for analyses involving social class, race/ethnicity, and gender. Suggestions for research on socioeconomic measures are provided, to aid monitoring steps toward social equity in health.