Many epidemiologic studies have evaluated the association between exposure to particulate matter (PM) and elevated blood pressure (BP), a well-established risk factor for cardiovascular disease (CVD) and stroke.1 However, the effects of short-term PM exposure on BP remain inconclusive. Several epidemiologic and controlled human studies have reported higher systolic or diastolic BP with short-term exposure to particulate matter with diameters <10 μm (PM10) and <2.5 μm (PM2.5).2 – 9 Some studies, however, have found small decreases in the systolic and diastolic BP with short-term exposure to either PM10 or PM2.5,10 – 13 whereas others still have found no association.14 – 20 These diverse findings suggest that observed short-term effects of particulate air pollution on the morbidity and mortality of persons with CVD may not be explained by an increase in BP, a hypothesized link between long-term air pollution exposure and progression of CVD.21 In addition, some studies have also reported associations of acute gaseous pollutants with increased BP.3,8,13,15,17
A change in BP is a complicated physiologic response affected by vascular resistance and cardiac output (a product of stroke volume and heart rate). PM may increase the resistance and decrease the compliance of vasculature via plausible biologic mechanisms involving endothelial dysfunction and vasoconstriction.17,19 However, the associations between air pollution and cardiac output or stroke volume have rarely been addressed because of the difficulty of using invasive instruments in human beings to allow for real-time hemodynamic monitoring. The pulse pressure, which is the difference between systolic and diastolic BP, is determined by the ratio of stroke volume to the vascular compliance,22 and is a noninvasive indicator of short-term hemodynamic changes. Pulse pressure was increased by PM exposure in one human study but decreased in an animal study.5,23 We evaluated changes in BP and pulse pressure in nonsmoking adults in response to the short-term exposure to PM and gaseous pollutants in Taiwan.
The study population was selected from a nationwide multiple-disease screening program, the Taiwan Community-based Integrated Screening program. This program was an expansion of the Keelung community-based integrated screening model, and the study design and implementation of this model have been published elsewhere.24 Overall, the attendance rate in this screening program ranged from 55% to 80%. After excluding current smokers and exsmokers, our study population included 9238 subjects >30 years of age who participated in the program in 1 of 6 townships: Renai, Sinjhuang, Nantou, Puli, Jushan, and Renwu. Based on the township type and potential emission sources, these 6 townships were classified into 4 categories for further subgroup analyses: seaport (Renai), urban (Sinjhuang), rural (Nantou, Puli, and Jushan), and industrial (Renwu). The screening periods in the various study areas were as follows: Renai, 1 April to 30 November 2002; Sinjhuang, 1 October to 30 November 2002; Nantou, Puli, and Jushan, 1 June 2003 to 31 August 2005; and Renwu, 1 April to 30 June 2002. This study was approved by the Joint Institutional Review Board of the Public Health College of the National Taiwan University, and all of the participants provided informed consent upon recruitment into the study.
Health Examination and BP Data
The screening program consisted of an interview, a questionnaire, and a physical examination. The questionnaires were in Mandarin, and the subjects were interviewed in person by trained personnel from the Public Health Bureau and local hospitals. Information was collected on personal characteristics, including age, sex, height, weight, body mass index (BMI), education level, alcohol consumption, betel-nut-chewing status, and physician-diagnosed diabetes and hypertension histories. A fasting venous blood sample was collected at physical examination, and analyzed for blood sugar and triglyceride levels. BP measurements were performed by trained medical personnel with electronic sphygmomanometers (Model HEM-770A; Omron Health Care, Kyoto, Japan) according to standard procedures.24 To avoid diurnal variations, BP measurements were performed in the morning (0900 hours to 1200 hours). Following completion of the 30-minute questionnaire, the BP measurement was taken in a seated, upright position. One of 3 cuff sizes (adult standard, large, and thigh-sized) was used depending on the circumference of the subject's right upper arm. To minimize the possible effects of antihypertensive drugs, participants were instructed not to take any medication on the morning of the BP measurement. If systolic and diastolic BP values were greater than 140 and 90 mm Hg, respectively, at the first measurement, the participant was asked to undergo a second measurement with a standard mercury sphygmomanometer after completing other screening steps. We then used the standard mercury sphygmomanometer measurement as the recorded BP value for the participant. The pulse pressure was determined as the difference between systolic and diastolic BP.
Air Pollution and Meteorologic Data
To estimate the exposure of each participant to air pollutants, we used hourly air pollution data on PM10, sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3) obtained from the single general ambient air quality monitoring station in each township. The air quality monitoring stations were built by the Taiwan Environmental Protection Agency (EPA) and located in the downtown school of each study township. Maximum distance from study subjects to the monitoring station was 1.2 km (Renai), 2.5 km (Sinjhuang), 4.8 km (Nantou), 7.2 km (Puli), 8.9 km (Jushan), and 3.4 km (Renwu). The instruments used in these air-quality monitoring stations were a β-gauge analyzer (BAM-1020, MET ONE Inc., Grants Pass, OR) for PM10, an ultraviolet fluorescence analyzer (Ecotech 9850, Blackburn, Victoria, Australia) for SO2, a chemiluminescence analyzer (Ecotech 9841, Blackburn, Victoria, Australia) for NO2, a nondispersed infrared absorption analyzer (APMA-360 CE, Irvine, CA) for CO, and an ultraviolet absorption analyzer (Ecotech 9810B, Blackburn, Victoria, Australia) for O3. All samples were analyzed in the same laboratory, with scheduled quality-control procedures. Meteorologic data, including ambient temperature (Ta) and dew-point temperature (Td), were also obtained by the monitoring stations. Data for a given day were classified as “missing” if more than 20% of the hourly data were invalid. We calculated each subject's exposure to 24-hour average concentrations of PM10, SO2, and NO2, and 1-hour daily maximum concentrations of CO and O3, at 0–23 hours (1-day lag), 24–47 hours (2-day lag), and 48–71 hours (3-day lag) (ie, time preceding the BP measurements). The apparent temperature (AT)—an index of human discomfort—was calculated 1–3 days before the BP measurements by modeling the 24-hour averages of Ta and Td, using the following formula: AT = −2.653 + (0.994 × Ta) + (0.0153 × Td 2).25
We used a generalized additive model to estimate the effects of pollution on systolic and diastolic BP and pulse pressure. This model, with a cutoff level of a 10% change in effect estimates, was applied to selected potential confounding factors,26 including age, sex, BMI, education level, alcohol consumption, betel-nut-chewing status, fasting blood sugar and triglyceride levels, history of physician-diagnosed diabetes and hypertension, and meteorologic conditions (season and the apparent-temperature values 1–3 days before the BP measurements). The lowest Akaike's information criterion (AIC) was then used as the selection criterion to determine goodness of fit. Changes in systolic and diastolic BP and pulse pressure values for 1- to 3-day lags of each of the 5 air pollutants were then estimated using the generalized additive model, adjusting for the selected individual and meteorologic covariates. The smoothing function of the generalized additive model was fit with penalized splines to adjust for nonlinear meteorological covariates.
Because the PM compositions may vary by study site, and may have varying effects on BP,11 subgroup analyses were used to examine whether the associations of PM10 with systolic and diastolic BP and pulse pressure differed among the 6 sites. Possible heterogeneity of effect was also examined by age (60 years vs. <60 years), sex, hypertensive status (yes or no), and season (March–May vs. June–August vs. September–November vs. December–February). Age 60 years is often a cutoff for defining elderly populations, and was close to the median of our study subjects (58 years). All analyses were performed using SAS software (Version 9.1.3; SAS Institute, Cary, NC). The analysis of variance (ANOVA) test was used to compare continuous variables among townships, and the χ2 test was used to test noncontinuous variables. The estimates for effects of air pollutants on BP were expressed as mean and 95% confidence intervals (CIs) for an interquartile range (IQR) increase in each air pollutant at 1- to 3-day lags.
Study Population and Exposure Characteristics
A total of 9238 subjects were recruited for this study, and basic characteristics of the study subjects are shown in Table 1. Characteristics of study subjects varied among the 6 townships, with the exception of diabetes prevalence rate. Systolic BP and pulse pressure were highest in Renai Township, and the lowest in Sinjhuang Township.
eTable 1 (http://links.lww.com/EDE/A546) shows air pollution and meteorologic data for each township. The average concentrations of the 5 air pollutants were all below the accepted National Ambient Air Quality Standards of the Taiwan EPA. The 24-hour average concentration of NO2 and the 1-hour daily maximum concentration of CO were highest in Sinjhuang, the 24-hour average concentration of SO2 was highest in Renwu, and the 24-hour average concentration of PM10, and 1-hour daily maximum concentration of O3 were highest in Jushan. The daily temperature and daily dew point values were typical for this subtropical region.
BP and Pulse Pressure Changes
Using a cutoff level of a 10% change in the effect estimates and the lowest AIC to test the model's goodness of fit, we identified the following covariates as adjustment variables: age, sex, BMI, fasting blood sugar and triglyceride levels, history of physician-diagnosed hypertension, season, and apparent temperature 1–2 days before BP measurements.
Table 2 shows the changes in BP with an exposure to the 5 air pollutants. Systolic BP decreased with exposure to each of the 5 air pollutants. Diastolic BP increased with exposure to SO2, NO2, and O3 at various lag times, but not with exposure to PM10 or CO. Pulse pressure was consistently reduced with exposure to the air pollutants at 1- to 3-day lags.
eTable 2 (http://links.lww.com/EDE/A546) summarizes previous studies on BP changes in response to short-term exposure to PM. PM levels in Taiwanese studies were higher than those in other countries.
Susceptibility to PM10 Effect
Figure 1 illustrates the township-specific estimates of the effect of PM10 on BP with various lag times. Systolic BP was decreased at several sites and lags times, whereas diastolic BP was both higher and lower. Diastolic BP increased at the urban and industrial sites, but decreased at the seaport and rural sites. Pulse pressure was reduced at the industrial and rural sites, with the strongest reduction at the industrial site (−15 mm Hg for an IQR increase in PM10 at 1-day lag (95% CI = −18 to −12)). PM10 was not associated with pulse pressure at the seaport and urban sites.
Figure 2 illustrates the effects of PM10 stratified by age, sex, and hypertensive status. The associations of PM10 with systolic BP and pulse pressure were strongest in the older subjects after a 1-day lag (−2 mm Hg of systolic BP [95% CI = −3 to −1] and −3 mm Hg of pulse pressure [95% CI = −4 to −2]). Men appeared generally more vulnerable than women, and those with hypertension were more vulnerable than those without. There was a tendency toward stronger reductions in pulse pressure with exposure to PM10 in March–May compared with June–August (eFigure 1, http://links.lww.com/EDE/A546).
These data from Taiwan suggest that short-term air pollution exposure reduces pulse pressure. Associations appeared stronger among men, persons >60 years of age, those with hypertension, and those living in an industrial township.
BP is determined by peripheral resistance and the elastic properties of arterial walls. Peripheral resistance increases and elasticity decreases with the progression of CVD,1 and these changes may also be accelerated by air pollution exposure.21 However, previous studies, including observational and controlled human studies, have not provided convincing evidence of an association between short-term air pollution exposure and an increase in BP (eTable 2, http://links.lww.com/EDE/A546). Epidemiologic studies have reported inconsistent results for the short-term effects of PM on the BP, with most controlled human studies demonstrating minimal changes in BP with short-term PM exposure.14 – 16,18 – 20 The diverse BP response patterns in other observational studies may be due to different PM concentrations and differing study populations.
Smoking may also contribute to the inconsistent associations of air pollution with BP. Cigarette smoking causes hypertension, endothelial dysfunction, and impaired cardiac remodeling.27 Because most studies investigating BP changes with air pollution exposure have not excluded smokers, the small effects of air pollution on BP could be masked or attenuated by smoking. Brook et al9 found that PM mixed with secondhand smoke was associated with an increase in BP, but such associations were not observed in subjects exposed only to ambient PM. We excluded smokers and exsmokers as study subjects to minimize the confounding effects of smoking on BP. Our results may therefore better reflect the changes in BP in response to air pollution.
BP is a complicated physiologic state, regulated by vascular homeostatic mechanisms including the autonomic system, heart rate, cardiac contractility, and arterial tone to maintain a steady flow of blood and oxygen to vital organs and peripheral tissues. There is strong evidence that short-term air pollution exposure can lead to endothelial dysfunction and vasoconstriction and can, consequently, cause an increase in BP.4,9,28 Even so, studies have found inconsistent BP changes with short-term air pollution exposure. This may be because cardiac output (the other important determinant of BP) plays a role in counterbalancing the changes in BP after short-term air pollution exposure.
We observed opposing changes with short-term air pollution exposure, with a decrease in the systolic BP and an increase in the diastolic BP. These findings may hint at the delicate physiologic balance of hemodynamic systems involved in BP regulation in response to short-term exposures. A decrease in systolic BP may reflect a decrease in cardiac contractility. Prior studies on heart rate variability have demonstrated a slight increase in high-frequency power, a parameter influenced mainly by vagal tone.7,29,30 A shift of sympathovagal balance to increased vagal tone may reduce cardiac contractility or heart rate. Animal studies have also demonstrated major reductions in cardiac fractional shortening in rats with particle exposure that supported lowered myocardial contractility.31,32
The observed increase in diastolic BP with short-term exposure to air pollution is consistent with a recent study in which PM increased diastolic BP with air pollution inhalation, through acute autonomic imbalance.7 Other potential biologic mechanisms include acute systemic inflammation and oxidative stress, which may be responsible for triggering endothelial and vasomotor dysfunction.4,9
In this study, the reductions in pulse pressure by PM10, SO2, NO2, CO, and O3 over various lag periods were consistent even after adjustment for individual and meteorologic factors. A study in dogs also found that exposure to PM2.5 for 5 hours resulted in increased systolic and diastolic BP but a lower pulse pressure.23 The independent decrease in systolic BP or increase in diastolic BP after acute diesel exhaust or ambient particles exposure in controlled or observational human studies also indirectly supports our findings.3,4,7,13 Pulse pressure is associated with cardiovascular morbidity and mortality, and is a common surrogate measure for arterial stiffness.33 Elevated pulse pressure is strongly associated with endothelial dysfunction, a major factor in the development of atherosclerosis.34 However, in addition to vascular compliance, the pulse pressure is also closely correlated with left-ventricle stroke volume.22 Because several studies have demonstrated a decrease in vascular compliance following air pollution exposure,20,28 the observed pulse pressure reductions with air pollution exposure in our study may indicate that stroke volume decreased in response to short-term exposure to both particulate and gaseous pollutants. The decrease in stroke volume may further indicate an inappropriate cardiac contractility and impaired vasodilation of resistance vessels after short-term air pollutant exposure.
The township-specific effect of PM10 on pulse pressure also suggests that chemical compositions of aerosols may play a role. It is likely that the chemical composition of PM10 differed among these 4 sites, and may have accounted for differences in response patterns (Fig. 1). The industrial site, Renwu Township, is the center of Taiwan's petrochemical industry and is exposed to volatile organic compounds (VOCs), nitrogen oxides (NOx), and PM10 emissions. The rural sites, especially Jushan Township, have higher concentrations of PM10 and O3, and the transport of VOCs, O3 precursors, and NOx from upwind industry or vehicle emissions can contribute to high air pollution levels in these downwind rural sites.35 PM comprises a chemically heterogeneous mixture of solid and liquid particles, and may cause a variety of health effects. VOCs, including propane, isobutane, and benzene, were found to have same-day effects on cardiovascular mortality in central Taiwan.36 Further studies are needed to evaluate the toxicity of particles from different sources and to explore possible differences in their effects on hemodynamic response.
We found that subjects who were older, male, or hypertensive exhibited greater reductions in their pulse pressures. Potential interactions among individual characteristics, air pollution, and pulse pressure have rarely been addressed. A decrease in systolic BP after short-term PM10 exposure was more pronounced in subjects with a history of myocardial infarction, probably because of medication intake and disease status.11 However, Dvonch et al6 found that young age and not taking BP medications could be predictors of increased BP and pulse pressure with PM2.5 exposure. In contrast, a population-based study found that the increases in both systolic BP and pulse pressure were stronger in subjects taking BP medications and those who were hypertensive.5 More studies are warranted to explore these inconsistent findings and to determine how potential modifiers affect hemodynamic changes caused by air pollution.
Several limitations of our study should be noted. First, personal air pollutant exposures were not measured directly but rather were estimated using fixed-site ambient monitoring data. The use of fixed-site pollution measurements to assess personal air pollution exposure can lead to measurement error, and may underestimate the effects of pollution.9 Second, the potential effect of antihypertensive drugs was not considered because of the lack of relevant information. However, participants were instructed not to take any medication on the morning before BP measurement to minimize possible antihypertensive drug effects. Third, the reproducibility of the blood pressure measurements with the electronic instrument was not tested for bias. The manufacturer stated that all instruments had satisfied the validation standards of international organizations such as the Association for the Advancement of Medical Instruments. To minimize possible measurement error, quality control procedures were arranged for all electronic sphygmomanometers twice per year.
We found reductions in pulse pressure after short-term air pollution exposure that resulted from both decreases in systolic BP and increases in diastolic BP. This suggests that short-term air pollution may decrease stroke volume by decreasing cardiac contractility or increasing vascular resistance. Age, sex, and hypertensive status may modify the effects of PM10 on pulse pressure. Short-term air pollution-mediated hemodynamic changes may be particularly important for vulnerable subjects, especially those with pre-existing cardiovascular disease. Furthermore, particles from industrial emissions may contribute to the magnitude of pulse pressure changes. Although the observed hemodynamic changes after short-term air pollution exposure were small, the subsequent reduced cardiac flow, autonomic system dysregulation, and vasomotor dysfunction may be considerable. Studies are needed to clarify the possible mechanisms and causal relationship between the air pollutants and the regulation of pulse pressure.
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We thank Tony Hsiu-Hsi Chen for organizing the Taiwan Community-based Integrated Screening (TCIS) program and controlling the data quality. We also thank Ming-Neng Shiu, head of the Public Health Bureau of Taipei County, Taiwan, Bo-En Wang, head of the Public Health Bureau of Keelung City, Taiwan, and Long-Ren Liao, head of Public Health Bureau of Nantou County, Taiwan for helping with the implementation of the TCIS program.