Daily measures of maximum temperature, particulate matter [less than or equal to] 10 pm in aerodynamic diameter (P[M.sub.10]), and gaseous pollution (ozone; nitrogen dioxide, sulfur dioxide, and carbon monoxide) were collected in Denver, Colorado, in July and August between 1993 and 1997. We then compared these exposures with concurrent data on the number of daily hospital admissions for cardiovascular diseases in men and women > 65 years of age. Generalized linear models, assuming a Poisson error structure for the selected cardiovascular disease hospital admissions, were constructed to evaluate the associations with air pollution and temperature. After adjusting the admission data for yearly trends, day-of-week effects, ambient maximum temperature, and dew point temperature, we studied the associations of the pollutants in single-pollutant models with lag times of 0-4 days. The results suggest that [O.sub.3] is associated with an increase in the risk of hospitalization for acute myocardial infarction, coronary atherosderosis, and pulmonary heart disease. S[O.sub.2] appears to be related to increased hospital stays for cardiac dysthythmias, and CO is significantly associated with congestive heart failure. No association was found between particulate matter or N[O.sub.2] and any of the health outcomes. Males tend to have higher numbers of hospital admissions than do females for all of the selected cardiovascular diseases, except for congestive heart failure. Higher temperatures appear to be an important factor in increasing the frequency of hospitalization for acute myocardial infarction and congestive heart failure, and are associated with a decrease in the frequency of visits for coronary atherosclerosis and pulmonary heart disease. Key words: acute myocardial infarction, air pollution, cardiac dysrhythmias, cardiovascular diseases, CO, congestive heart failure, coronary atherosderosis, generalized estimating equations, N[O.sub.2], [O.sub.3], P[M.sub.10], Poisson regression, pulmonary heart disease, S[O.sub.2], temperature.
There is substantial epidemiologic literature indicating a link between air pollution and cardiovascular morbidity and mortality. This includes not only studies of episodic pollution such as occurred during 1930 in the Meuse Valley (Firket 1931), 1948 in Pennsylvania (Shrenk et al. 1949), and 1952 in London (Ministry of Health 1954) but also of the generally low concentrations found in urban areas. Studies have been carried out in North America (Burnett et al. 1997a, 1997b; Morris et al. 1995; Morris and Naumova 1998; Schwartz 1999; Schwartz and Morris 1995; Zanobetti et al. 2000), in Western Europe (Atkinson et al. 1999; Ballester et al. 2001; Diaz et al. 2001; Hoek et al. 2001; Prescott et al. 1998), in Tokyo, Japan (Piver et al. 1999), and in Hong Kong, China (Wong et al. 1999). Most of these studies showed a predominant effect of particulates and carbon monoxide on cardiovascular admissions (Ballester et al. 2001; Burnett et al. 1997b; Morris et al. 1995; Morris and Naumova 1998; Schwartz 1999; Schwartz and Morris 1995; Wong et al. 1999). However, the Tokyo study (Piver et al. 1999) suggests an independent effect of nitrogen dioxide. Furthermore, the studies in Canada (Burnett et al. 1997a) and Spain (Diaz et al. 2001) demonstrated consistent effects for sulfur dioxide and/or ozone on cardiovascular hospital admissions. Several reports have addressed the issue of weather and mortality; extreme temperatures have been associated with increased daily mortality in numerous regions of the world (Braga et al. 2001; Kunst et al. 1993). Mortality has also been observed to increase during periods of 3 or more days of unusual temperatures during summer or winter, showing that temperature variability is an important determinant of human health effects (Braga et al. 2001, 2002; Saez et al. 1995).
It has been suggested that weather and temperature may modify the effects of air pollution on health both at high temperatures (Katsouyanni et al. 1993) and low temperatures (Morris and Naumova 1998). The Intergovernmental Panel on Climate Change (IPCC; 1996) has projected that atmospheric concentrations of carbon dioxide could double in the next 50-100 years. A doubling of atmospheric concentrations of C[O.sub.2]2 could result in an increase in average global surface air temperatures of 1-3[degrees]C because of the greenhouse effect. In addition, because approximately 65% of atmospheric C[O.sub.2] comes from combustion of fossil fuels, increasing concentrations of C[O.sub.2] could also be accompanied by increasing concentrations of other air pollutants, particularly in large urban areas. An increase in surface air temperatures could accompany a greater frequency and duration of heat waves. According to the IPCC (1996), the frequency of extremely hot days in temperate climates approximately doubles for every 2-3[degrees]C increase in temperature during the average summer. Because heat waves often occur in large metropolitan areas during warm summer months, these large cities could experience an increase in the incidence of heat-related morbidity and mortality (McMichael et al. 1996). To address this specific issue, we focused our research on the months of the year when the frequency of exposure to high daily maximum temperatures ([T.sub.max]) and high air pollutant concentrations would be the greatest. The present study focuses on the months of July and August (1993-1997) in Denver, Colorado.
Studies have documented associations between daily variations in air pollution and cardiovascular deaths and hospital admissions (Dockery et al. 2000). Mechanisms for the effects of air pollution on cardiovascular mortality and morbidity may include changes in blood coagulability (Seaton et al. 1995) and changes in the nervous system control of the heart, possibly leading to arrhythmias (Peters et al. 2000). Mechanisms linking temperature to cardiovascular mortality and morbidity have also been postulated. The blood viscosity and cholesterol levels have been found to increase with high temperatures (Keatinge et al. 1986), whereas blood pressure and fibrinogen levels increase during winter, although outdoor temperature does not seem to determine the seasonal variation in fibrinogen (van der Bom et al. 1997). In many epidemiology studies with respiratory and cardiovascular diseases, regression models include adjustments for seasonal climate variability to isolate the contributions of air pollution on the daily number of deaths or hospital admissions for these diseases. In contrast to using seasonal adjustments for the entire year, we focused on the months of July and August, partially to avoid potential bias in the type of seasonal adjustment to be used and partially to focus on short time-frame changes in temperature.
Materials and Methods
Setting. Denver once was among the most polluted cities in the United States, with a brown cloud as a constant reminder of its air pollution woes. The city regularly exceeded the federal air pollution standards for 200 days/year, every year in the late 1970s. Air pollution in Denver mainly derives from motor vehicle exhaust emissions, with industrial pollution playing a minor role. Denver's air pollution levels are also exacerbated by temperature inversions resulting from Denver's geographic location. During a temperature inversion, a warm, less-dense inversion layer of air overlies colder, denser air, forming a "lid" that traps pollutants below …