Air pollution exposure and self-reported cardiovascular disease

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Abstract

Background

Studies suggest that increases of fine particle concentrations (PM2.5) could be linked with a rise in cardiovascular disease. With approximately 25% of American adults aged 30 and older reporting having either heart disease or hypertension it is possible that exposure to air pollution could have significant public health consequences. This study examined the relationship between PM2.5 and the prevalence of self-reported hypertension and heart disease using data from a large nation-wide survey.

Study design

Adults, 30 years of age or older, who participated in the National Health Interview Survey (NHIS) from 1999 to 2005 were linked to annual PM2.5 data from the US Environmental Protection Agency (N=132,224). Annual air quality estimates were averaged from monitors within 20 miles of the respondent's residential block group. Respondents who reported being told they had hypertension by a health professional on two or more separate occasions were defined as hypertensive. Heart disease was defined as answering, “yes” to one or more of three NHIS questions on heart disease.

Results

A 10 μg/m3 increase in PM2.5 exposure was associated with a small elevated risk of hypertension (adjusted odds ratio (OR) 1.05, 95% confidence interval (CI) 1.00–1.10) risk of heart disease (1.08 95% CI 1.00–1.16). The association between PM2.5 and hypertension was found in non-Hispanic white adults (OR 1.10 95% CI 1.04–1.17) but not in non-Hispanic black or Hispanic adults.

Conclusions

Findings from this study complement those from other studies and indicate that PM2.5 adversely affects cardiovascular health. Our results are consistent with other studies in showing a small association between exposure to PM2.5 and cardiovascular outcomes.

Introduction

The health effects of air pollution exposure are of interest to policy makers and scientists. In an effort to monitor air quality, the US Environmental Protection Agency (EPA) currently measures six criteria pollutants (nitrogen dioxide, sulfur dioxide, carbon monoxide, lead, ozone, and particulate matter—PM) for regulatory purposes (US Environmental Protection Agency, 2007a, US Environmental Protection Agency, 2007b). Much of the recent interest in air pollution has centered on particulate matter, which is a composite of other types of pollution ranging from solid to liquid particles emitted from various sources. This study focuses on the effects of PM with an aerodynamic diameter of less than or equal to 2.5 μm (PM2.5), which is sometimes referred to as “fine particles” (US Environmental Protection Agency, 2007a, US Environmental Protection Agency, 2007b). Fine PM remains suspended in the air longer and has been shown to have different associations with health than larger PM (Le Tertre et al., 2002; Samet et al., 2000; Schulz et al., 2005).

Associations between short-term exposure to PM2.5 and acute mortality (Le Tertre et al., 2002; Goldberg et al., 2003; Pope et al., 2006; Toren et al., 2007), hospital admissions for cardiac morbidity (Dominici et al., 2006; Tonne et al., 2007), and other cardiovascular markers, such as blood pressure (Urch et al., 2005), arrhythmia (Rich et al., 2005), and heart rate variability (Adar et al., 2007; Park et al., 2005) have been documented in several studies. Other studies have examined these outcomes as being associated with other specific air pollutants or traffic exposure (Gehring et al., 2006; Hoek et al., 2002).

Fewer studies have explored the health effects of long-term exposure to PM2.5 or other air pollutants. Some of these long-term exposure studies attempt to assess the temporal variability in pollution exposure through “natural experiments” such as the 13-month closure of a Utah Valley steel mill that was associated with a reduction in hospitalizations for cardiovascular events (Pope, 1996). A ban on sulfur-containing fuels was associated with a reduction in cardiovascular health problems in Hong Kong (Hedley et al., 2002). In the Southwestern United States, an 8-month strike at a copper smelter was associated with a large drop in sulfate PM and a slight reduction in hospitalizations (Pope et al., 2007).

In the United States, the Harvard Six Cities study, a long-term cohort study, showed that cardiovascular mortality due to an increase in pollution exposure remained after controlling for smoking and other individual factors (Dockery et al., 1993). The American Cancer Society (ACS) prospective cohort study on pollution exposure and mortality from 1982 to 1998 found that increases in PM2.5 were associated with cardiopulmonary mortality and lung cancer mortality (Pope III et al., 1995, Pope et al., 2002). A later analysis of women using data from the Women's Health Initiative (WHI; Miller et al., 2007) found similar results for mortality as well as increased non-fatal cardiac events. Cohort studies from Europe have also documented increased cardiovascular mortality with increased exposure to ambient air pollution (Nafstad et al., 2004) and increased exposure to traffic-related air pollution (Gehring et al., 2006; Rosenlund et al., 2008). For example, Hoek et al. (2002) found that cardiopulmonary mortality was associated with the distance a resident lived from a major road.

Other studies have examined the association between long-term exposure to air pollution and cardiovascular morbidities (Balluz et al., 2007; Rosenlund et al., 2008). Residential traffic studies have shown increases in acute myocardial infarction (Tonne et al., 2007) and clinical coronary heart disease (Hoffmann et al., 2006) among adults living close to major roadways. The increased long-term and short-term mortality associated with exposure to air pollution could be due to the exacerbation of underlying morbidities (Brook, 2005). With approximately 29% of American adults aged 18 years or older being hypertensive and 12% of adults reporting heart disease (NCHS, 2007), increasing our understanding of the possible effects of exposure to air pollution on cardiovascular morbidities could have implications for many people.

The aim of this study is to examine the associations between exposure to PM2.5 and two self-reported cardiovascular outcomes, hypertension, and heart disease, using a large nation-wide survey. Specifically, the objectives are to: (1) determine if there are relationships between PM2.5 exposure and self-reported rates of hypertension and heart disease, (2) determine whether there are factors that affect the associations between PM2.5 exposure and cardiovascular outcomes, and (3) determine if associations differ among subgroups defined by demographic or health-related factors.

Section snippets

National Health Interview Survey

This analysis is based on 1999–2005 data collected from the National Center for Health Statistics (NCHS) National Health Interview Survey (NHIS) and the EPA Air Quality System (AQS) database. The NHIS is a nationally representative health survey of the United States’ non-institutionalized civilian population (NCHS, NHIS, 2007). Data for the NHIS are collected from approximately 35,000 households annually, comprising nearly 100,000 people. One adult is randomly selected from each family to

Study subjects

Among sample adults that matched our study criteria, 25% (weighted percent) reported being told they had hypertension and 11.9% (weighted percent) reported heart disease (Table 1). The majority of the respondents were non-Hispanic white and between the ages of 30 and 49. High pollution levels were distributed evenly across most variables with a few exceptions. For example, more non-Hispanic black and Hispanic adults lived in areas with higher exposure values than non-Hispanic white adults (P

Discussion

We found that a 10 μg/m3 increase of PM2.5 was associated with a slight increase in self-reported adverse cardiovascular outcomes. After adjusting for the potentially confounding effects of smoking and health insurance, PM2.5 continued to be significantly associated with adverse cardiovascular outcomes. Associations were similar after adjustment for BMI and diabetes. Sensitivity analysis using different monitor radii to calculate pollution exposure led to results similar to those of our main

Conclusion

Studies of the relationship between diseases and long-term exposure to air pollution in the United States have been relatively few. Better exposure measures are being developed for local areas describing the pollution exposure levels within urban areas that may reduce exposure misclassification (Finkelstein et al., 2005). Developing nation-wide exposure measures to complement the large ongoing national surveys will help us understand associations and monitor trends. The findings from this

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