Several investigators have documented the effect of temperature on mortality, although fewer have studied its impact on morbidity. In addition, little is known about the effectiveness of mitigation strategies such as use of air conditioners (AC). We investigated the association between temperatures and hospital admissions in California from 1999 to 2005. We also determined whether AC ownership and usage, assessed at the zip code level, mitigates this association. Because of the unique spatial pattern of income and climate in the state, confounding of AC effects by other local factors is less likely. We only included individuals who had a temperature monitor within 25 kilometers of their residential zip codes. Using a time-stratified case-crossover approach, we observed a significantly increased risk for hospitalization for multiple diseases including cardiovascular, ischemic heart disease, ischemic stroke, respiratory disease, pneumonia, dehydration, heat stroke, diabetes and acute renal failure with same-day apparent temperature. We also found that ownership and usage of air conditioning significantly reduced the effects of temperature on these health outcomes, after controlling for the potential confounding effects of family income and other socioeconomic factors. Our results demonstrate important effects of temperature on public health and the potential for mitigation. Several investigators have documented the acute effect of temperature on mortality in the U.S. and Europe, and in developing nations(1-3). There are far fewer studies, however, on the effects of temperature on morbidity outcomes, such as hospitalizations (4-6). According to the recent IPCC report (7), temperatures are expected to increase in the future with more frequent and severe heat waves. Therefore, it is important to obtain a better understanding of these heat-associated health risks and susceptible populations for future surveillance and targeted interventions. In addition, relatively little is known about the effectiveness of proposed mitigation strategies, such as cooling shelters, and personal use of air conditioners (AC). Studies on the effects of actual AC use on temperature-related health outcomes, however, are limited, since data are typically available for AC prevalence, rather than AC use, and only for broad geographic regions. Thus, effects of AC may be confounded by other regional characteristics (8) such as demographic and economic factors. As a result, there is need for more localized estimates of the effects of temperature on morbidity and on the effectiveness of AC use in mitigating these effects. For several reasons, California serves as an ideal study area for examining the effects of AC use on temperature-related adverse health. First, it includes a large and diverse population, residing within a wide array of climatic regions. Second, individual-level data at small levels of spatial scale over a majority of the state are available from surveys conducted by the California Public Utilities Commission (9). Finally, income is less likely to confound the estimates of the effects of AC. In general, incomes are higher in the coastal regions, but lower in the inland areas, such as the Central Valley. However, AC use is greater in the Central Valley where the summers are much hotter, and many homes in the coastal areas of California lack AC (9). In this study, we used temperature data during the warm season in California to estimate the impact on several disease-specific categories of hospitalizations. To limit exposure misclassification, we limited our study to buffer areas with individuals living in zip codes within 25 kilometers (km) of a temperature monitor. Next, we quantified the likely reduction in health impacts based on both ownership and use of ACs using individual-level data for each buffer. Finally, we examined the potential confounding effect that local measures of family income may have on our effect estimates.

Background

Exposures to ambient gaseous pollutants have been linked to cardiovascular diseases (CVDs), but the biological mechanisms remain uncertain.

Objectives

This study examined the changes in CVD marker levels resulting from elevated exposure to ambient gaseous pollutants in midlife women.

Methods

Annual repeated measurements of several inflammatory, hemostatic and lipid makers were obtained from 2306 midlife women enrolled in the longitudinal Study of Women's Health Across the Nation (SWAN) between 1999 and 2004. Ambient carbon monoxide (CO), nitrogen dioxide (NO₂), and sulfur dioxide (SO₂) data were assigned to each woman based on proximity of the monitoring station to her residential address. Short- and long-term exposures were calculated, and their associations with markers were examined using linear mixed-effects regression models, adjusted for demographic, health and other factors.

Results

Short-term CO exposure was associated with increased fibrinogen, i.e., every interquartile increase of average prior one-week exposure to CO was associated with 1.3% (95% CI: 0.6%, 2.0%) increase in fibrinogen. Long-term exposures to NO₂ and SO₂ were associated with reduced high-density lipoproteins and apolipoprotein A1, e.g., 4.0% (1.7%, 6.3%) and 4.7% (2.8%, 6.6%) decrease per interquartile increment in prior one-year average NO₂ concentration, respectively. Fine particle (PM_2.5) exposure confounded associations between CO/NO₂ and inflammatory/hemostatic markers, while associations with lipoproteins were generally robust to PM_2.5 adjustment.

Conclusions

Exposures to these gas pollutants at current ambient levels may increase thrombotic potential and disrupt cholesterol metabolism, contributing to greater risk of CVDs in midlife women. Caution should be exercised in evaluating the confounding by PM_2.5 exposure.

Background

Exposure to particulate matter air pollution has been associated with cardiovascular disease (CVD) morbidity and mortality; however, most studies have focused on fine particulate matter (PM_2.5) exposure and CVD. Coarse particulate matter (PM_10-2.5) exposure has not been extensively studied, particularly for long-term exposure, and the biological mechanisms remain uncertain.

Methods

We examined the association between ambient concentrations of PM_10-2.5 and inflammatory and hemostatic makers that have been linked to CVD. Annual questionnaire and clinical data were obtained from 1694 women (≥ 55 years old in 1999) enrolled in the longitudinal Study of Women's Health Across the Nation (SWAN) at six study sites from 1999 to 2004. Residential locations and the USEPA air monitoring network measurements were used to assign exposure to one-year PM_10-2.5, as well as co-pollutants. Linear mixed-effects regression models were used to describe the association between PM_10-2.5 exposure and markers, including demographic, health and other covariates.

Results

Each interquartile (4 μg/m³) increase in one-year PM_10-2.5 exposure was associated with a 5.5% (95% confidence interval [CI]: 1.8, 9.4%) increase in levels of plasminogen activator inhibitor-1 (PAI-1) and 4.1% (95% CI: - 0.1, 8.6%) increase in high-sensitivity C-creative Protein (hs-CRP). Stratified analyses suggested that the association with PAI-1 was particularly strong in some subgroups, including women who were peri-menopausal, were less educated, had a body mass index lower than 25, and reported low alcohol consumption. The association between PM_10-2.5 and PAI-1 remained unchanged with adjustment for PM_2.5, ozone, nitrogen dioxide, and carbon monoxide.

Conclusions

Long-term PM_10-2.5 exposure may be associated with changes in coagulation independently from PM_2.5, and thus, contribute to CVD risk in midlife women.

Fine particles (PM_2.5) are known to increase risks of cardiovascular diseases, but it is unclear how they affect plasma lipid levels. In this study, we examined the associations between PM_2.5 exposure and lipid/lipoprotein levels from 2289 midlife women enrolled in the longitudinal Study of Women's Health Across the Nation. The average exposure to PM_2.5 and gaseous co-pollutants during the prior one year, six months, 30 days, and one day were estimated for each woman based on U.S. Environmental Protection Agency ambient monitoring data. Blood samples were collected annually from 1999 to 2005 and analyzed for lipids/lipoproteins. Mixed-effect models were used to account for repeated measures for each woman, adjusted for demographic, health and behavior covariates. PM_2.5 exposures, especially the long-term exposure, were negatively associated with protective lipoproteins, and positively associated with atherogenic lipoproteins. For example, each 3 μg/m³ increase of one-year PM_2.5 exposure was associated with decreases of -0.7% (-1.4%, -0.1%) in high-density lipoprotein cholesterols and -0.6% (-1.1%, -0.1%) in apolipoprotein A1 (ApoA1), as well as increases of 3.8% (1.0%, 6.6%) in lipoprotein(a) and 1.4% (0.5%, 2.3%) in the ratio of apolipoprotein B (ApoB)/ApoA1. In stratified analysis, increased atherogenic lipoproteins were mainly observed in women without dyslipidemia, and both increased atherogenic lipoproteins and reduced protective lipoproteins were observed among women in perimenopause. In summary, PM_2.5 exposure was associated with adverse lipid level changes, and thus, may increase cardiovascular risks in midlife women.

Associations between temperature and cardiovascular (CVD) mortality have been reported, but the underlying biological mechanisms remain uncertain. We explored the association between apparent temperature and serum biomarkers for CVD. Using linear mixed effects models, we examined the relationships between residence-proximate apparent temperature (same day and 1, 7, and 30 days prior) and several inflammatory, hemostatic, and lipid biomarkers for midlife women from 1999 through 2004. Our study population consisted of 2,306 women with mean age of 51 years (± 3 years) enrolled in Study of Women's Health Across the Nation (SWAN) in Chicago, Illinois; Detroit, Michigan; Los Angeles and Oakland, California; Newark, New Jersey; and Pittsburgh, Pennsylvania. Mean daily apparent temperature was calculated using temperature and relative humidity data provided by the National Climatic Data Center and the US Environmental Protection Agency, while daily data for fine particles, ozone, carbon monoxide, and nitrogen dioxide from the US Environmental Protection Agency Air Quality Data Mart were considered as confounders. All analyses were stratified by warm and cold seasons. More significant (p < 0.10) negative associations were found during the warm season for various lag times, including hs-CRP, fibrinogen, tissue plasminogen activator antigen (tPA-ag), tissue plasminogen activator antigen (PAI-1), Factor VIIc, high-density lipoprotein (HDL), and total cholesterol. During the cold season, significant negative associations for fibrinogen and HDL, but significant positive associations for tPA-ag, PAI-1, and triglycerides were observed for various lag times. With the exception of ozone, pollutants did not confound these associations. Apparent temperature was associated with several serum biomarkers of CVD risk in midlife women, shedding light on potential mechanisms.

Background

Studies have reported associations between long-term air pollution exposures and cardiovascular mortality. The biological mechanisms connecting them remain uncertain.

Methods

We examined associations of fine particles (PM2.5) and ozone with serum markers of cardiovascular disease risk in a cohort of midlife women. We obtained information from women enrolled at six sites in the multi-ethnic, longitudinal Study of Women's Health Across the Nation, including repeated measurements of high-sensitivity C-reactive protein, fibrinogen, tissue-type plasminogen activator antigen, plasminogen activator inhibitor type 1, and factor VIIc (factor VII coagulant activity). We obtained residence-proximate PM2.5 and ozone monitoring data for a maximum five annual visits, calculating prior year, 6-month, 1-month, and 1-day exposures and their relations to serum markers using longitudinal mixed models.

Results

For the 2,086 women studied from 1999 to 2004, PM2.5 exposures were associated with all blood markers except factor VIIc after adjusting for age, race/ethnicity, education, site, body mass index, smoking, and recent alcohol use. Adjusted associations were strongest for prior year exposures for high-sensitivity C-reactive protein (21% increase per 10 μg/m³ PM2.5, 95% confidence interval [CI]: 6.6, 37), tissue-type plasminogen activator antigen (8.6%, 95% CI: 1.8, 16), and plasminogen activator inhibitor (35%, 95% CI: 19, 53). An association was also observed between year prior ozone exposure and factor VIIc (5.7% increase per 10 ppb ozone, 95% CI: 2.9, 8.5).

Conclusions

Our findings suggest that prior year exposures to PM2.5 and ozone are associated with adverse effects on inflammatory and hemostatic pathways for cardiovascular outcomes in midlife women.

Background

Several cohort studies report associations between chronic exposure to ambient fine particles (PM2.5) and cardiovascular mortality. Uncertainty exists about biological mechanisms responsible for this observation, but systemic inflammation has been postulated. In addition, the subgroups susceptible to inflammation have not been fully elucidated.

Methods

We investigated whether certain subgroups are susceptible to the effects of long-term exposure to PM2.5 on C-reactive protein (CRP), a marker of inflammation directly linked to subsequent cardiovascular disease. We used data from the SWAN cohort of 1923 mid-life women with up to five annual repeated measures of CRP. Linear mixed and GEE models accounting for repeated measurements within an individual were used to estimate the effects of prior-year PM2.5 exposure on CRP. We examined CRP as a continuous and as binary outcome for CRP greater than 3mg/l, a level of clinical significance.

Results

We found strong associations between PM2.5 and CRP among several subgroups. For example a 10 µg/m(3) increase in annual PM2.5 more than doubled the risk of CRP greater than 3mg/l in older diabetics, smokers and the unmarried. Larger effects were also observed among those with low income, high blood pressure, or who were using hormone therapy, with indications of a protective effects for those using statins or consuming moderate amounts of alcohol.

Conclusions

In this study, we observed significant associations between long-term exposure to PM2.5 and CRP in several susceptible subgroups. This suggests a plausible pathway by which exposure to particulate matter may be associated with increased risk of cardiovascular disease.