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Particulate matter air pollution and ambient temperature: Opposing effects on blood pressure in high-risk cardiac patients
Abstract
Fine particulate matter air pollution (PM2.5) and extreme temperatures have both been associated with alterations in blood pressure (BP). However, few studies have evaluated their joint haemodynamic actions among individuals at high risk for cardiovascular events.
We assessed the effects of short-term exposures during the prior week to ambient PM2.5 and outdoor temperature levels on resting seated BP among 2078 patients enrolling into a cardiac rehabilitation programme at the University of Michigan (from 2003 to 2011) using multiple linear regression analyses adjusting for age, sex, BMI, ozone and the same-day alternate environmental factor (i.e. PM2.5 or temperature).
Mean PM2.5 and temperature levels were 12.6 ± 8.2 μg/m and 10.3 ± 10.4°C, respectively. Each standard deviation elevation in PM2.5 concentration during lag days 4-6 was associated with significant increases in SBP (2.1-3.5 mmHg) and DBP (1.7-1.8 mmHg). Conversely, higher temperature levels (per 10.4°C) during lag days 4-6 were associated with reductions in both SBP (-3.6 to -2.3 mmHg) and DBP (-2.5 to -1.8 mmHg). There was little evidence for consistent effect modification by other covariates (e.g. demographics, seasons, medication usage).
Short-term exposures to PM2.5, even at low concentrations within current air quality standards, are associated with significant increases in BP. Contrarily, higher ambient temperatures prompt the opposite haemodynamic effect. These findings demonstrate that both ubiquitous environmental exposures have clinically meaningful effects on resting BP among high-risk cardiac patients.
... [2][3][4][5][6] In North America, less than 20% of individuals face levels above AQG compared to more than 99% of those living in East and South Asia. 5 Daily PM 2.5 averages can exceed astounding levels (i.e., 500 µg/m 3 ) in megacities such as Beijing, 2,3,5,6 which are 10-to 50-fold those encountered in urban locations across the United States and Canada. [3][4][5]7,8,9 Due to the enormous population facing extremely poor air quality, the largest public health burden (>50%) due to PM 2.5 disproportionately impacts Asia. 2,3 Nevertheless, recent BACKGROUND Fine particulate matter (PM 2.5 ) air pollution is a leading cause of global cardiovascular mortality. ...
... 1,10 Mounting studies by us and others have provided evidence that a key mechanistic explanation may be PM 2.5 -mediated elevations in arterial blood pressure (BP). 1,8,9,[10][11][12][13] A number of air pollutants are capable of increasing BP over a few hours-to-days of exposure. 8,9,[11][12][13][14][15][16][17][18] Living in a more air polluted environment can even promote the onset of chronic hypertension. ...
... 1,8,9,[10][11][12][13] A number of air pollutants are capable of increasing BP over a few hours-to-days of exposure. 8,9,[11][12][13][14][15][16][17][18] Living in a more air polluted environment can even promote the onset of chronic hypertension. 13,15,17 Several potentially responsible biological pathways have been elucidated including autonomic imbalance favoring sympathetic nervous system activation and vascular dysfunction. ...
Background:
Fine particulate matter (PM2.5) air pollution is a leading cause of global cardiovascular mortality. A key mechanism may be PM2.5-induced blood pressure (BP) elevations. Whether consistent prohypertensive responses persist across the breadth of worldwide pollution concentrations has never been investigated.
Methods:
We evaluated the hemodynamic impact of short-term exposures to ambient PM2.5 in harmonized studies of healthy normotensive adults (4 BP measurements per participant) living in both a highly polluted (Beijing) and clean (Michigan) location.
Results:
Prior 7-day outdoor-ambient and 24-hour personal-level PM2.5 concentration averages were much higher in Beijing (86.7 ± 52.1 and 52.4 ± 79.2 µg/m3) compared to Michigan (9.1 ± 1.8 and 12.2 ± 17.0 µg/m3). In Beijing (n = 73), increased outdoor-ambient exposures (per 10 µg/m3) during the prior 1-7 days were associated with significant elevations in diastolic BP (0.15-0.17 mm Hg). In overweight adults (body mass index ≥25 kg/m2), significant increases in both systolic (0.34-0.44 mm Hg) and diastolic (0.22-0.66 mm Hg) BP levels were observed. Prior 24-hour personal-level exposures also significantly increased BP (0.41/0.61 mm Hg) in overweight participants. Conversely, low PM2.5 concentrations in Michigan (n = 50), on average within Air Quality Guidelines, were not associated with BP elevations.
Conclusions:
Our findings demonstrate that short-term exposures to ambient PM2.5 in a highly polluted environment can promote elevations in BP even among healthy adults. The fact that no adverse hemodynamic responses were observed in a clean location supports the key public health importance of international efforts to improve air quality as part of the global battle against hypertension.
... Additionally, it is possible that the dilatory and BP-lowering effects of other exposures at the fireline counteract the expected BP-raising effect of WFS-associated PM exposure (Cunha et al., 2020;Giorgini et al., 2015;Halliwill, 2001;Halonen et al., 2011;Wu et al., 2015). For example, post-exercise hypotension often occurs after dynamic exercise/training and the magnitude of BP reduction is associated with exercise intensity, exertion duration, and hypertension (Cornelissen and Smart, 2013;Eicher et al., 2010;Gomes Anunciação and Doederlein Polito, 2011;Halliwill, 2001;Rezk et al., 2006). ...
... Moreover, ambient temperature is inversely associated with BP (Giorgini et al., 2015;Halonen et al., 2011;Wu et al., 2015), and exercising in hot environments, such as would be experienced by wildland firefighters at prescribed burns (84.17 ± 6.81 • F in this study, Table 1), can exaggerate the acute hypotensive effect of exercise (Cunha et al., 2020;Halliwill, 2001). In a previous study investigating post-exercise hypotension among 7 men with elevated blood pressure (127.4/83.7 mmHg), SBP measured following two bouts of cycling exercise in hot environment (35 • C) was consistently lower (− 0.3 to − 4.7 mmHg) compared to measurements following the same exercise regime in normal environment (21 • C) across a 21-hr recovery period (Cunha et al., 2020). ...
Wildland firefighters at prescribed burns are exposed to elevated levels of wildland fire smoke (WFS) while performing physically demanding tasks. WFS exposure has been linked to increases in hospital and emergency admissions for cardiovascular disorders in the general population. However, knowledge about the cardiovascular effect of occupational WFS exposure among wildland firefighters is limited. To provide a better understanding of the effect of this exposure scenario on acute hemodynamic responses, resting systolic/diastolic blood pressure (SBP/DBP) and heart rate (HR) of wildland firefighters were measured before (pre-shift), after (post-shift), and the morning (next morning) immediately following prescribed burn shifts (burn days) and regular work shifts (non-burn days). A total of 38 firefighters (34 males and 4 females) participated in this study and resting BP and HR were recorded on 9 burn days and 7 non-burn days. On burn days, HR significantly increased from pre-to post-shift (13.25 bpm, 95% CI: 7.47 to 19.02 bpm) while SBP significantly decreased in the morning following the prescribed burns compared to pre-shift (−6.25 mmHg, 95% CI: −12.30 to −0.20 mmHg). However, this was due to the decrease of SBP in the firefighters who were hypertensive (−8.46 mmHg, 95% CI: −16.08 to −0.84 mmHg). Significant cross-shift reductions (post-shift/next morning vs. pre-shift) were observed in SBP on burn days compared to non-burn days (−7.01 mmHg, 95% CI: −10.94 to −3.09 mmHg and −8.64 mmHg, 95% CI: −13.81 to −3.47 mmHg, respectively). A significant reduction on burn days was also observed from pre-shift to the following morning for HR compared to non-burn days (−7.28 bpm, 95% CI: −13.50 to −1.06 bpm) while HR significantly increased in pre-to post-shift on burn days compared to non-burn days (10.61 bpm, 95% CI: 5.05 to 16.17 bpm). The decreased BP observed in wildland firefighters might be due to a high level of carbon monoxide exposure and exercise-induced hypotension. The increase in HR immediately after prescribed burns might be attributable to WFS exposure and physical exertion in prescribed burn shifts. The results suggest that wildland firefighting exposure might cause a distinct hemodynamic response, including SBP reduction and HR increment, especially for those who have pre-existing hypertension.
... A study on 2078 cardiac rehabilitation patients from Michigan, found a similar inverse association. A reduction in outdoor temperatures by 10.4 o C during the prior 1 to 7 days was associated with a 3.6mm Hg increase in systolic blood pressure [14]. However, some studies have found nocturnal blood pressure to be higher during summer than winter months [12,13,15,16]. ...
... The risk of cardiovascular related mortality increased by around 1% for each 10 mg/m3 ( increase in PM2.5 [36]. A study of 2078 heart disease patients in Michigan, found typical daily variations of ambient PM2.5 within the previous few days to be independently associated with a significant rise in blood pressure [14]. More importantly, average PM2.5 levels were within the day-to-day United States National Ambient Air Quality Standards [36]. ...
Environmental factors are an important cause of poor health globally. Hypertension is known to occur due to complex interactions between adverse lifestyles and environmental factors on a background of polygenic inheritance. Although pharmacological interventions have taken a prominent place, environmental factors and interventions have generally received less consideration. The short-term and long term impact of several environmental factors on blood pressure changes such as cold ambient temperature, exposure to loud noise, air pollution, high altitude, certain organic pollutants, and heavy metals have been recently reported. In this chapter, the current evidence on the effect of such environmental risk factors on blood pressure with its pathophysiological mechanisms and clinical relevance have been described in detail. As some of these effects are clinically relevant, clinicians, patients with hypertension or cardiovascular disease and individuals at high risk for cardiovascular disease would need to be aware of these environmental factors. Furthermore, close attention to monitoring blood pressure during such exposures is necessary and in individuals with hypertension, treatment schedules may need adjustment to ensure more optimal blood pressure control.
... More than a dozen studies have examined the association between ambient temperature and BP (Alpérovitch et al., 2009;Brook et al., 2011b;Giorgini et al., 2015;Halonen et al., 2011;Hampel et al., 2011;Madsen and Nafstad, 2006;Wu et al., 2015;Yang et al., 2015b), most of which observed an inverse relationship although some studies did not find statistically significant associations (Brook et al., 2011b;Saeki et al., 2014). Among the studies with significant inverse association, the magnitude of temperature effects also varied, which may result from differences in study design, measurements of temperature and BP or demographic characteristics. ...
... We included 23 studies (Alpérovitch et al., 2009;Barnett et al., 2007;Brook et al., 2011a;Brook et al., 2011b;Bruce et al., 1991;Chen et al., 2013;Dashti et al., 2016;Giorgini et al., 2015;Halonen et al., 2011;Hampel et al., 2011;Hong et al., 2012;Jansen et al., 2001;Jehn et al., 2002;Kent et al., 2011;Kunutsor and Powles, 2010;Lanzinger et al., 2014b;Madaniyazi et al., 2016;Madsen and Nafstad, 2006;Modesti et al., 2013;Saeki et al., 2014;Woodhouse et al., 1993;Wu et al., 2015;Yang et al., 2015b), among which 14 were used for meta-analysis ( Fig. 1) including six longitudinal studies (Chen et al., 2013;Hong et al., 2012;Lanzinger et al., 2014b;Saeki et al., 2014;Woodhouse et al., 1993;Wu et al., 2015) and eight cross-sectional studies (Barnett et al., 2007;Bruce et al., 1991;Dashti et al., 2016;Jehn et al., 2002;Kent et al., 2011;Kunutsor and Powles, 2010;Madsen and Nafstad, 2006;Yang et al., 2015b) summarized in Table 1. Dashti et al. (2016) reported results from two independent studies: the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study and the Boston Puerto Rican Health Study (BPRHS). ...
Objective:
Although many individual studies have examined the association between temperature and blood pressure (BP), they used different methods and also their results were somewhat inconsistent. The aims of this study are to quantitatively summarize previous studies and to systematically assess the methodological issues to make recommendations for future research.
Methods:
We searched relevant empirical studies published before January 2016 concerning temperature and BP among adults using the MEDLINE, Embase and PubMed databases. Mean changes in systolic (SBP) and diastolic blood pressure (DBP) per 1°C reduction in temperature were pooled using a random-effects meta-analysis.
Results:
Of 23 studies included, 14 were used for meta-analysis. Consistent, statistically significant, inverse associations were observed between ambient temperature (mean, maximum, minimum outdoor temperature and indoor temperature) and BP. An 1°C decrease in mean daily outdoor temperature was associated with an increase in SBP and DBP of 0.26mmHg (95% CI: 0.18-0.33) and 0.13 (95% CI: 0.11-0.16), respectively. The increase was greater in people with conditions related to cardiovascular disease. An 1°C decrease in indoor temperature was associated with 0.38mmHg (0.18-0.58) increase in SBP, while the effects on DBP were not estimated due to limited studies. Among the previous studies on temperature-BP relationship, temperature and BP measurements are not accurate enough and statistical methods need to be improved.
Conclusions:
Lower ambient temperatures seem to increase adults' BP and people with conditions related to cardiovascular disease are more susceptible to drops in temperature. Indoor temperature appeared to have a stronger effect on BP than outdoor temperature. To understand temperature-BP relationship well, a study combining repeated personal temperature exposure and ambulatory BP monitoring, applying improved statistical methods to examine potential non-linear relationship is warranted.
... The entire analysis is adjusted for the mean temperature on the day of ABPM, due to the known effect of ambient temperature on BP and on the concentration of atmospheric pollutants. 35,36 Focusing on the results for pollutants and BP, it should be noted that, although some recorded values exceeded the values allowed by law (PM 10 annual mean concentrations 40 g/m 3 ; PM 2,5 annual mean 25 g/m 3 ; NO 2 annual limit value 40 g/m 3 ), these are not average values for the whole year but only for those days of the year when ABPM was performed. We would also emphasise that a decreasing progression of pollution has been observed over the years in our register. ...
... 1.4 mmHg elevated SBP and 3.2 mmHg decreased SBP, respectively. Giorgini et al. (Giorgini et al., 2015) examined the effects of short-term exposure to ambient PM 2.5 and temperature on BP of 2078 high-risk cardiac patients, they found that each standard deviation greater PM 2.5 was associated with higher SBP (2.1 to 3.5 mmHg) and higher DBP (1.7 to 1.8 mmHg), and conversely, each 10.4°C greater ambient temperature was associated with decreases in both SBP (−3.6 to −2.3 mmHg) and DBP (−2.5 to −1.8 mmHg). Similar findings were also found in Canada (Goldberg et al., 2015), Germany (Lanzinger et al., 2014), and China (Li et al., 2022). ...
Background:
Little evidence exists regarding the combined effect between ambient temperature and air pollution exposure on maternal blood pressure (BP) and hypertensive disorders of pregnancy (HDP).
Objectives:
To assess effect modification by temperature exposure on the PM1-BP/HDP associations among Chinese pregnant women based on a nationwide study.
Methods:
We conducted a cross-sectional country-based population study in China, enrolling 86,005 participants from November 2017 to December 2021. BP was measured with standardized sphygmomanometers. HDP was defined according to the American College of Obstetricians and Gynecologists' recommendations. Daily temperature data were obtained from the European Centre for Medium-Range Weather Forecasts. PM1 concentrations were evaluated using generalized additive model. Generalized linear mixed models were used to examine the health effects, controlling for multiple covariates. We also performed a series of stratified and sensitivity analyses.
Results:
The pro-hypertensive effect of PM1 was observed in the first trimester. Cold exposure amplifies the first-trimester PM1-BP/HDP associations, with adjusted estimate (aβ) for systolic blood pressure (SBP) of 3.038 (95 % CI: 2.320-3.755), aβ for diastolic blood pressure (DBP) of 2.189 (95 % CI: 1.503-2.875), and aOR for HDP of 1.392 (95 % CI: 1.160-1.670). Pregnant women who were educated longer than 17 years or living in urban areas appeared to be more vulnerable to the modification in the first trimester. These findings remained robust after sensitivity analyses.
Conclusions:
First trimester maybe the critical exposure window for the PM1-BP/HDP associations among Chinese pregnant women. Cold exposure amplifies the associations, and those with higher education level or living in urban areas appeared to be more vulnerable.
... Beyond predictable associations with respiratory disorders [157], air pollution is linked to NCDs including steatohepatitis [158], diabetes [106], neurodegenerative dis-eases [159] and cancers [115,160]. Cardiovascular disorders, such as hypertension [161] and CHD [162,163], are particularly strongly associated with air pollution. Even brief exposure is linked to AMI, stroke, arrhythmias, worsening of heart failure and hypertension [164][165][166][167], while chronic exposure accelerates atherosclerosis, impacts blood pressure control, thrombosis, endothelial function, insulin sensitivity [164,166] and increases the risk of hypertension, Long-term effects of ambient PM2. 5 on hypertension and blood pressure and attributable risk among older Chinese adults [167,168]. ...
Both psychosocial and physical environmental stressors have been linked to chronic mental health and chronic medical conditions. The psycho-immune-neuroendocrine (PINE) network details metabolomic pathways which are responsive to varied stressors and link chronic medical conditions with mental disorders, such as major depressive disorder via a network of pathophysiological pathways. The primary objective of this review is to explore evidence of relationships between airborne particulate matter (PM, as a concrete example of a physical environmental stressor), the PINE network and chronic non-communicable diseases (NCDs), including mental health sequelae, with a view to supporting the assertion that physical environmental stressors (not only psychosocial stressors) disrupt the PINE network, leading to NCDs. Biological links have been established between PM exposure, key sub-networks of the PINE model and mental health sequelae, suggesting that in theory, long-term mental health impacts of PM exposure may exist, driven by the disruption of these biological networks. This disruption could trans-generationally influence health; however, long-term studies and information on chronic outcomes following acute exposure event are still lacking, limiting what is currently known beyond the acute exposure and all-cause mortality. More empirical evidence is needed, especially to link long-term mental health sequelae to PM exposure, arising from PINE pathophysiology. Relationships between physical and psychosocial stressors, and especially the concept of such stressors acting together to impact on PINE network function, leading to linked NCDs, evokes the concept of syndemics, and these are discussed in the context of the PINE network.
... When the system energy reaches the lowest, the current BB-RBM unit fits the data characteristics of the input sample to the greatest possible extent from the perspective of probability. erefore, when the unsupervised training is completed, the output of the BB-RBM unit at this time can be regarded as the high-order feature representation of the input features [12][13][14]. ...
According to the general recognition in the first half of the last century, hypertension was not considered a kind of disease, but was regarded as a compensatory response commonly seen in the elderly, and it would not occur to younger people. Because of this erroneous cognition, many young patients fail to pay attention to their own hypertension, fail to take correct and standardized treatment, and suffer from a series of complications caused by hypertension. This article summarizes the relevant factors that affect the patient’s future blood pressure from three directions: the basic characteristics of adolescent patients, the way they lower blood pressure, and the impact of the external environment. In order to make the model better fit the continuous data in the feature set of adolescents with hypertension, the structure of the internal components of the deep confidence network is optimized. Gaussian noise is introduced into the visible and hidden layers of the internal components of the network so that the stored information of the network changes from discrete to continuous during operation and improves the prediction accuracy of the blood pressure prediction model for adolescents with hypertension.
... mm Hg per each standard deviation towards growth in PM 2.5 concentration. This effect was detected in spite of all research participants constantly being treated with up-todate hypotensive therapy and ambient air quality was quite optimal if taken in remote prospects [38]. R.D. Brook and others assessed impacts exerted by ambient air pollution on blood pressure of 65 people living in Beijing where PM 2.5 concentration varied within 9.0-552 µg/m 3 . ...
Ambient air pollution causes approximately 3.3 million untimely deaths annually (2.1 deaths due to ischemic heart disease and 1.1 million deaths due to stroke). Mortality caused by ambient air pollution is higher than mortality due to such traditional risk factors as smoking, obesity, and elevated dextrose contents in blood. Relative risk of mortality amounts to 1.26 (95 % CI 1.08–1.47) in cities with the highest air pollution against those where air pollution is the lowest. Occupational exposure to various chemical air pollutants can cause more than 1 million untimely deaths all over the world but its contribution to prevalence of cardiovascular diseases has not been determined sufficiently. Aerogenic pollutants are quite variable in their chemical structure and include both particulate matter (PM for short) and gaseous matter. The American Heart Association and the European Society of Cardiology consider PM2.5 to be a risk factor causing cardiovascular diseases. This analytical review presents data on effects produced by aerogenic pollutants on development of cardio-metabolic pathology and population mortality due to vascular and metabolic diseases (arterial hypertension, atherosclerosis and ischemic heart disease, heart rhythm disturbances, and type 2 diabetes mellitus). There are also data on mechanisms of pathogenetic influence exerted by aerogenic pollutants on development of such diseases including generation of anti-inflammatory and oxidative mediators and their release into blood flow; developing imbalance in the autonomic nervous system with prevailing activity of the sympathetic nervous system and disrupted heart rate variability; direct introduction of aerogenic pollutants from the lungs into blood flow with developing direct toxic effects. We have also analyzed literature data on protective effects produced by reduction in ambient air pollution on prevalence of cardiovascular pathology.
... Changes in blood pressure have been related to both small particulate matter air contamination (PM 2.5 ) and high temperatures. Few research, however, have looked at their combined haemodynamic effects in people who are at high risk of cardiovascular events (Giorgini et al. 2015). For a healthier atmosphere and a clean environment, particulate matter (PM) must be eliminated from the air (Yoo et al. 2020). ...
Satellite is used to track air quality around the world in order to provide people with free air quality data. The data are released by global networks. A good example is the CAR-NASRDA network that provides real-time particulate matter data. The data (PM1, PM2.5, PM10, temperature, and humidity) from CAR was used in the study. The data was obtained on NASRDA website, and it covers a period of 5–7 months. The range results are depicted as follows: Lagos - PM1 (15.98-604.09 µg/m3), PM2.5 (23.23-847.75 µg/m3), PM10 (25-753.8 µg/m3), temperature (80-109 oF), and relative humidity (12-77 %); Osun - PM1 (6.53-164.1 µg/m3), PM2.5 (9.1-236.6 µg/m3), PM10 (9.95-260.68 µg/m3), temperature (73.1-108.24 oF), and relative humidity (4.9-72 %); Delta - PM1 (8.23-273 µg/m3), PM2.5 (12.11-487.36 µg/m3), PM10 (12.96-552.51 µg/m3), temperature (74.62-109.59oF), and relative humidity (10.7-60.85 %); Kebbi - PM1 (0-5373.5 µg/m3), PM2.5 (µg/m3), PM10 (µg/m3), temperature (6-125 oF), and relative humidity (0-49 %), and FCT - PM1 (0-847.84 µg/m3), PM2.5 (0-1146.73 µg/m3), PM10 (0-831 µg/m3), temperature (66-115 oF), and humidity (2-90 %). When compared to international benchmarks, the findings are noticeably higher in this case. It has been discovered that PM values, temperature and relative humidity are correlated.
... However, the effect estimate was small (0.22 mmHg per 10 μg/m 3 ), and other parameters from ambulator BP monitors showed no significant relationships. Previous studies have shown conflicting results for short-term relationship between particulate air pollutants and arterial BP [15][16][17][18] . One possible explanation is the lag effect. ...
Air pollution has increasingly been recognized as a major healthcare concern. Air pollution, particularly fine particulate matter (≤ 2.5 μm in aerodynamic diameter [PM2.5]) has demonstrated an increase in adverse cardiovascular events. This study aimed to assess the cardiovascular response to personal exposure to different levels of PM2.5. This prospective cohort study enrolled healthy volunteers aged ≥ 18 years with no cardiovascular disease. Study subjects carried personal exposure monitor of PM2.5, digital thermo-hygrometer for temperature and humidity, 24-h blood pressure monitor, and continuous electrocardiogram monitor. Measurements were repeated twice with an interval of 6-12 months. Statistical models consisted of generalized estimation equations to various repeated measures of each subject. A total of 22 subjects were enrolled in this study between July 2018 and January 2019. Measurement was performed twice in all participants, and a total of 36 data were collected except for insufficient data collection. The mean age of the study population was 41.6 years, and 95% of the subjects were females. No study subjects had hypertension or other cardiovascular diseases. The average systolic blood pressure increased with higher PM2.5 levels with marginal significance (0.22 mmHg [95% confidential intervals - 0.04 to 0.48 mmHg] per 10 μg/m3 of PM2.5). All parameters for heart rate variability significantly decreased with a higher level of PM2.5. In this study, we measured individual personal exposure to PM2.5 by using a portable device. We found that 24-h exposure to high levels of PM2.5 was associated with a significant decrease in heart rate variability, suggesting impaired autonomous nervous function.
... Pathophysiological studies found acute functional consequences of air pollution exposure in both myocardial and pulmonary blood flow regulation, but also in coagulation function, mainly driven by the sharp increase in reactive oxygen species generation, which impairs vasodilatation mediated by nitric oxide and promotes vascular inflammation [50]. Indeed, short-term exposure to PM 2.5 , even at low concentrations within current air quality standards, was associated with significant blood pressure increase in high CV risk patients [51]. Although both the level and duration of exposure are directly associated with increased CV risk, there is no safe threshold below which there is no effect, and concentrations of fine and especially ultrafine particles in ambient air are thought to be strongly underestimated by actual standards and measurements [50]. ...
Tobacco use is one of the major public health concerns and it is the most preventable cause of morbidity and mortality worldwide. Smoking cessation reduces subsequent cardiovascular events and mortality. Smoking is a real chronic disorder characterized by the development of an addiction status mainly due to nicotine. This condition makes the smokers generally unable to quit smoking without help. Different strategies are available to treat smoking dependence that include both non-pharmacological (behavioral counselling) and pharmacological therapies. Currently, it is well accepted that smoking cessation drugs are effective and safe in real-world settings. Nicotine replacement therapy (NRT), varenicline, bupropion and cytisine are the main pharmacological strategies available for smoking cessation. Their efficacy and safety have been proved even in patients with chronic cardiovascular disease. Each of these drugs has peculiar characteristics and the clinician should customize the smoking cessation strategy based on currently available scientific evidence and patient's preference, paying particular attention to those patients having specific cardiovascular and psychiatric comorbidities. The present document aims to summarize the current viable pharmacological strategies for smoking cessation, also discussing the controversial issue regarding the use of alternative tobacco products, in order to provide useful practical indications to all physicians, mainly to those involved in cardiovascular prevention.
... For this reason, a greater clinical toxicity of UFP with respect to other particles sizes (PM 2.5 and PM 10 ) has been postulated [25]. It is necessary to take into account the effects of temperature on BP [26] and on the concentration of atmospheric pollutants. For all of this, all the analysis is adjusting for the average environmental temperature of the same day of realization of the ABPM. ...
Introduction:
Air in urban areas is usually contaminated with particle matter. High concentrations lead to a rise in the risk of cardiovascular and respiratory diseases. Some studies have reported that ultrafine particles (UFP) play a greater role in cardiovascular diseases than other particle matter, particularly regarding hypertensive crises and DBP, although in the latter such effects were described concerning clinical blood pressure (BP). In this study, we evaluate the relationship between 24-h ambulatory BP monitoring (ABPM) and atmospheric UFP concentrations in Barcelona.
Methods:
An observational study of individual patients' temporal and geographical characteristics attended in Primary Care Centres and Hypertensive Units during 2009-2014 was performed.
Results:
The participants were 521 hypertensive patients, mean age 56.8 years (SD 14.5), 52.4% were women. Mean BMI was 28.0 kg/m and the most prominent cardiovascular risk factors were diabetes (N = 66, 12.7%) and smoking (N = 79, 15.2%). We describe UFP effects at short-term and up to 1 week (from lag 0 to 7). For every 10 000 particle/cm UFP increase measured at an urban background site, a corresponding statistically significant increase of 2.7 mmHg [95% confidence interval = (0.5-4.8)] in 24-h DBP with ABPM for the following day was observed (lag 1).
Conclusion:
We have observed that a rise in UFP concentrations during the day prior to ABPM is significantly associated with an increase in 24 h and diurnal DBP. It has been increasingly demonstrated that UFP play a key role in cardiovascular risk factors and, as we have demonstrated, in good BP control.
... In addition, opposing actions of warmer outdoor ambient temperatures during the predominately summer months of this study may have countered the effects of TRAP. 42 Nevertheless, we observed that higher exposures to PC and BC were independently associated with the worsening of several aortic hemodynamic parameters. Finally, we observed mixed results regarding the protection afforded by N95 respirators. ...
Background:
The risk for cardiovascular events increases within hours of near-roadway exposures. We aimed to determine the traffic-related air pollutants (TRAP) and biological mechanisms involved and if reducing particulate matter<2.5 µm (PM2.5) inhalation is protective.
Methods:
Fifty healthy-adults underwent multiple 2-hour near-roadway exposures (Tuesdays-Fridays) in Ann Arbor during 2 separate weeks (randomized to wear an N95-respirator during one week). Monday both weeks, participants rested 2-hours in an exam room (once wearing an N95-respirator). Brachial blood pressure, aortic hemodynamics and heart rate variability were repeatedly-measured during exposures. Endothelial function (reactive hyperemia index [RHI]) was measured post-exposures (Thursdays). Black carbon (BC), total particle count (PC), PM2.5, noise and temperature were measured throughout exposures.
Results:
PM2.5 (9.3±7.7 µg/m3), BC (1.3±0.6 µg/m3), PC (8375±4930 particles/cm3) and noise (69.2±4.2 dB) were higher (p-values<0.01) and aortic hemodynamic parameters trended worse while near-roadway (p-values<0.15 versus exam room). Other outcomes were unchanged. Aortic hemodynamics trended towards improvements with N95-respirator usage while near-roadway (p-values<0.15 versus no-use), whereas other outcomes remained unaffected. Higher near-roadway PC and BC exposures were associated with increases in aortic augmentation pressures (p-values<0.05) and trends toward lower RHI (p-values<0.2). N95-respirator usage did not mitigate these adverse responses (non-significant pollutant-respirator interactions). Near-roadway outdoor-temperature and noise were also associated with cardiovascular changes.
Conclusions:
Exposure to real-world combustion-derived particulates in TRAP, even at relatively-low concentrations, acutely worsened aortic hemodynamics. Our mixed findings regarding the health benefits of wearing N95-respirators support that further studies are needed to validate if they adequately-protect against TRAP given their growing worldwide usage.
... 22,23 However, recent studies have found that ambient PM 2.5 can increase SBP and DBP. 24 In this study, DBP was also significantly decreased by LE filtration. These findings suggest that future trials with appropriate power are warranted to determine whether air filtration indeed lowers DBP and not just SBP. ...
Importance
Fine particulate matter (smaller than 2.5 μm) (PM2.5) air pollution is a major global risk factor for cardiovascular (CV) morbidity and mortality. Few studies have tested the benefits of portable air filtration systems in urban settings in the United States.
Objective
To investigate the effectiveness of air filtration at reducing personal exposures to PM2.5 and mitigating related CV health effects among older adults in a typical US urban location.
Design, Setting, and Participants
This randomized, double-blind crossover intervention study was conducted from October 21, 2014, through November 4, 2016, in a low-income senior residential building in Detroit, Michigan. Forty nonsmoking older adults were enrolled, with daily CV health outcome and PM2.5 exposure measurements.
Interventions
Participants were exposed to the following three 3-day scenarios separated by 1-week washout periods: unfiltered air (sham filtration), low-efficiency (LE) high-efficiency particulate arrestance (HEPA)–type filtered air, and high-efficiency (HE) true-HEPA filtered air using filtration systems in their bedroom and living room.
Main Outcomes and Measures
The primary outcome was brachial blood pressure (BP). Secondary outcomes included aortic hemodynamics, pulse-wave velocity, and heart rate variability. Exposures to PM2.5 were measured in the participants’ residences and by personal monitoring.
Results
The 40 participants had a mean (SD) age of 67 (8) years (62% men). Personal PM2.5 exposures were significantly reduced by air filtration from a mean (SD) of 15.5 (10.9) μg/m³ with sham filtration to 10.9 (7.4) μg/m³ with LE fitration and 7.4 (3.3) μg/m³ with HE filtration. Compared with sham filtration, any filtration for 3 days decreased brachial systolic and diastolic BP by 3.2 mm Hg (95% CI, −6.1 to −0.2 mm Hg) and 1.5 mm Hg (95% CI, −3.3 to 0.2 mm Hg), respectively. A continuous decrease occurred in systolic and diastolic BP during the 3-day period of LE filtration, with a mean of 3.4 mm Hg (95% CI, −6.8 to −0.1 mm Hg) and 2.2 mm Hg (95% CI, −4.2 to −0.3 mm Hg), respectively. For HE filtration, systolic and diastolic BP decreased by 2.9 mm Hg (95% CI, −6.2 to 0.5 mm Hg) and 0.8 mm Hg (95% CI, −2.8 to 1.2 mm Hg), respectively. Most secondary outcomes were not significantly improved.
Conclusions and Relevance
Results of this study showed that short-term use of portable air filtration systems reduced personal PM2.5 exposures and systolic BP among older adults living in a typical US urban location. The use of these relatively inexpensive systems is potentially cardioprotective against PM2.5 exposures and warrants further research.
Trial Registration
ClinicalTrials.gov identifier: NCT03334565
... 96038 608 Journal of Environmental Protection sources of air pollution which are responsible for the cardiovascular and other health effects are directly linked with the traffic-related particles [7]. It has been evidenced that the air pollutants PM, which enters the circulatory system easily induces systemic inflammation and hypercoagulability [8] [9], alters cardiac au- tonomic nervous system [10], induces in significant increased blood pressure [11] [12], and promotes cardiovascular diseases through oxidative pathway [13] [14]. Epidemiological studies reported that the air pollution exposure evidenced in the growth of cardiovascular health effects [15] [16] [17]. ...
... Mounting evidence suggests that the long-term PM 2.5 exposure may play a crucial role in the development and progression of atherosclerosis [3][4][5] . Extreme swings in outdoor temperatures are also linked to CV morbidity and mortality [6][7][8] . Epidemiologic studies suggest that PM 2.5 -mediated increases in low-density lipoproteins (LDL) and reductions in high-density lipoproteins (HDL) cause the CV burden 5,[9][10][11][12][13] . ...
Fine particulate matter (PM2.5) air pollution and environmental temperatures influence cardiovascular morbidity and mortality. Recent evidence suggests that several air pollutants can promote dyslipidemia; however, the impact of ambient PM2.5 and temperature on high-density lipoprotein (HDL) function remains unclear. We hypothesized that daily exposures to higher levels of ambient PM2.5 and colder outdoor temperatures would impair HDL functionality. Lipoproteins, serum cholesterol efflux capacity (CEC), and HDL oxidation markers were measured twice in 50 healthy adults (age 32.1 ± 9.6 years) living in southeast Michigan and associated with ambient and personal-level exposures using mixed models. Although previous 7-day mean outdoor temperature (4.4 ± 9.8°C) and PM2.5 levels (9.1 ± 1.8 µg/m³) were low, higher ambient PM2.5 exposures (per 10 µg/m³) were associated with significant increases in the total cholesterol-to-HDL-C ratio (rolling average lag days 1 and 2) as well as reductions in CEC by −1.93% (lag day 5, p = 0.022) and −1.62% (lag day 6, p = 0.032). Colder outdoor temperatures (per 10°C) were also associated with decreases in CEC from −0.62 to −0.63% (rolling average lag days 5 and 7, p = 0.027 and 0.028). Previous 24-hour personal-level PM2.5 and temperature exposures did not impact outcomes, nor were any exposures associated with changes in HDL-oxidation metrics. In conclusion, we provide the first evidence that ambient PM2.5 (even at low levels) and outdoor temperatures may influence serum CEC, a critical antiatherosclerotic HDL function.
... Thus, these findings cannot be extrapolated to older age when other risk factors can affect both parameters. In addition, pollutants can deeply influence BP [32] as well as lung function [33], even in adolescence. The impact of pollution is the focus of separate analyses. ...
... A maximum of one point was given for each item based on the selection and exposure/outcome categories, and a maximum of two points for comparability; thus, each study could achieve a total score ranging from 0 to 9 points, with a higher score indicating higher quality. The results of the scoring Chen et al. 2013Chen et al. 1998Chen et al.-2001Chen et al. 1831 Shanghai China outdoor perspective 0 hypertensive patients gender, age, BMI, urine protein, smoking behavior and drinking behavior 6 Chen et al. 2015Chen et al. 2011Chen et al.-2012 Shanghai China outdoor perspective 0 older hypertensive patients age, sex, education, BMI, antihypertensive use, income 7 Lanzinger et al. 2014Lanzinger et al. 2007Lanzinger et al.-2008 Augsburg Germany outdoor perspective 0 diabetes age, sex, education, BMI, antihypertensive use, smoking behavior, season 6 Modesti et al. 2013Modesti et al. 2005Modesti et al.-2007Modesti et al. 1897 Italy PET perspective 0 hypertensive patients age, sex, BMI, antihypertensive use, HR, humidity, air pressure 7 Woodhouse et al. 1993Woodhouse et al. 1991Woodhouse et al.-1992 Cambridge UK indoor perspective 0 older population sex, BMI, smoking behavior, sport 6 Hampel et al. 2011Hampel et al. 2002Hampel et al.-2006Hampel et al. 1500 France outdoor perspective 0 Pregnant Women age, BMI before pregnancy, gestational age, number of previous pregnancies (none, 1,2), smoking, passive smoking 6 Saeki et al. 2014Saeki et al. 2010Saeki et al.-2013 Japan indoor perspective 0 older population age, sex, BMI, smoking and drinking habits, types of antihypertensive medication, diabetes 7 Kent et al. 2011Kent et al. 2003Kent et al.-2006 USA outdoor cross sectional 0 general population geographic region, population density, individual income, education, race, age, sex, season, BMI, smoking and drinking habits, antihypertensive use 6 Barnetta et al. 2007Barnetta et al. 1979Barnetta et al.-1997 16 countries indoor perspective 0 general population age, sex, BMI 5 Giorgini et al. 2015Giorgini et al. 2003Giorgini et al.-2011Giorgini et al. 2078 USA outdoor perspective 4-6 cardiovascular patients age, sex, BMI, baseline BP level, smoking status, diagnosis of hypertension, O 3 7 Hurk et al. 2015Hurk et al. 2007Hurk et al.-2009 Southeast Netherlands outdoor historical data analysis 0 general population age, BMI, Hb, smoker, antihypertensive use, sport, education, income, other climate parameter 7 Yang et al. 2015Yang et al. 2004Yang et al.-2008 China outdoor perspective 0 general population age, sex, region 6 Madaniyazi et al. 20162006 shan China outdoor cohort 3 general population Relative humidity, age, BMI, seasonal and long-term trends, drinking habit, education level, gender, history of myocardial infarction, hypertension, hypertension history of parent, hyperlipidemia, income, marriage status, physical activities, salt intake, smoking status, work type 8 process are shown in Table 1. ...
Background: Hypertension is a major worldwide public health problem. Previous studies have indicated that ambient temperature is associated with blood pressure, but the nature of this association remains unclear. Objective: The objective of this meta-analysis was to investigate the relationship between ambient temperature and blood pressure. Methods: We performed a systematic search of the literature indexed in PubMed, Web of Science, and Science Direct between 1980 and 2016. The pooled effect sizes for exposure to low/moderate temperatures, as well as high temperature exposure, were calculated using a random effects model. Results: Fifteen studies were included in this meta-analysis. Twelve of these reported the effects of low/ moderate temperature exposure, two reported the effects of high temperature exposure, and one reported the effects of both low/moderate and high temperature exposure. For low/moderate temperature exposure, a 1°C decrease in temperature was associated with a 0.40 mmHg (95% CI: 0.34-0.46) increase in systolic blood pressure and a 0.13 mmHg (95% CI: 0.08-0.18) increase in diastolic blood pressure. For high temperature exposure, the relationship between BP and temperature was not statistically significant. Conclusion: For low/moderate temperature exposure, a decrease in temperature was associated with an increase in blood pressure. In contrast, the relationship between high temperature exposure and blood pressure was not statistically significant.
... Thus, these findings cannot be extrapolated to older age when other risk factors can affect both parameters. In addition, pollutants can deeply influence BP [32] as well as lung function [33], even in adolescence. The impact of pollution is the focus of separate analyses. ...
Background:
Vascular and lung function develop and decline over the life course; both predict cardiovascular events and mortality but little is known of how they develop over time. We analysed their relationship in a multiethnic cohort study to test whether lung function from early adolescence to young adulthood affected vascular indices.
Methods:
'DASH' (http://dash.sphsu.mrc.ac.uk) included 6643 children aged 11-13 years in 2003; a representative 10% sample (n = 665) participated in a pilot follow-up in 2013. Psychosocial, anthropometric, blood pressure (BP), and lung function measures were collected in both surveys; aortic pulse wave velocity (PWV) and augmentation index (AIx) were measured at aged 21-23 years. Relationships between forced expiratory volume Z-scores in 1 s (zFEV1), after global initiative-ethnic adjustments and BP, PWV, and AIx were tested in linear regression and general estimating statistical models.
Results:
In total, 488 people with complete data were included. At 11-13 years, SBP was positively associated with zFEV1 (coefficient = 1.90, 95% confidence interval 1.11-2.68, P < 0.001); but not at 21-23 years. The 10-year increase in zFEV1 was associated with rise in SBP (1.38, 0.25-1.51, P < 0.05) in mixed effect models adjusted for age, sex, ethnicity, waist to height ratio, employment, reported racism, smoking, and alcohol use but DBP change was unrelated. In fully adjusted models, neither PWV nor central AIx were associated with zFEV1 at 11-13 years or 21-23 years (P > 0.05).
Conclusion:
Forced expiratory volume change is positively and independently associated with SBP change from adolescence to young adulthood, suggesting earlier lung function plays important roles in SBP development. Vascular indices were unrelated to lung function or its change.
... 1. Increased surface blood circulation and sweating, followed by dehydration and salt depletion leading to (a) Increased cardiac work load as a compensational reaction of the circulation to maintain the heart minute volume [20,33] and falling blood pressure. For example, higher temperature levels (per 10.4°C) were associated with reductions in both systolic and diastolic blood pressure in a panel of cardiac rehabilitation patients [34]. ...
Purpose of the review:
The purpose of this review is to highlight the latest developments in the field of weather and health with a focus on the elderly. The current state of knowledge is summarized and open questions and emerging fields of research are discussed.
Recent findings:
It is expected that climate change will lead to higher global average surface temperatures and more extreme climatic conditions. Previous studies have shown that non-optimal temperatures are associated with increased morbidity and mortality, specifically in elderly people. Future research fields comprise e.g., synergistic effects between meteorological variables and air pollution; long-term impacts of temperature changes; novel unraveling the underlying pathways using blood biomarkers; the association between temperature and mental health; and urban planning and adaptation processes. Understanding the health impacts associated with changes in thermal conditions requires multidisciplinary approaches. Adaptation processes, as well as improvements in urban planning and warning systems, can help reduce the predicted burden of climate change, especially in the elderly.
Aims:
To examine the associations between environmental determinants of health and blood pressure and whether age, sex, or race moderated the associations among 18,754 adolescents and adults from the type 1 diabetes (T1D) Exchange Clinic Registry.
Methods:
We used multivariable linear regression. Environmental determinants included exposure to ambient fine particulate matter (PM2.5, obtained from an integrated model), nitrogen dioxide (NO2), noise and light pollution, and the normalized difference vegetation index (NDVI, a marker of green space) at the ZIP code level of residence.
Results:
Higher exposure to PM2.5 and NO2, and lower NDVI, was associated with higher systolic and diastolic blood pressure, and higher light pollution exposure were similarly associated with higher diastolic blood pressure. These associations between environmental exposures and blood pressure remained significant after accounting for other covariates (age, sex, race/ethnicity, BMI, and T1D duration). With aging, the negative association between NDVI and blood pressure weakened.
Conclusions:
These findings emphasize the significance of minimizing exposure to environmental pollutants, including PM2.5 and NO2, as well as ensuring access to areas with higher NDVI, to promote cardiovascular health in individuals with T1D.
This study quantified the effect of cold or heat exposure of ambient temperature on the alteration of well-known cardiac markers. A meta-analysis was performed using the PRISMA guidelines. Peer-reviewed studies on ambient temperature and cardiac biomarkers were retrieved from MEDLINE, ScienceDirect and Google Scholar from January 2000 to February 2022. The pooled effect sizes of ambient temperature on cardiac biomarkers c-reactive protein, soluble-cell adhesion-molecule-1, soluble-intercellular-adhesion-molecule-1, total cholesterol, low-densitylipoprotein, interleukin-6, B-type-Natriuretic-Peptide; systolic/diastolic blood pressure were quantified using a random-effects meta-analysis. A total of 26 articles were included in the metaanalysis after screening the titles, abstracts and full texts. The pooled results for a 1°C decrease of ambient temperature showed an increase of 0.31% (95% CI= 0.26 to 0.38) in cardiac biomarkers (p=0.00; I-squared=99.2%; Cochran’s Q=5636.8). In contrast, the pooled results for a 1°C increase in ambient temperature showed an increase of 2.03% (95% CI= 1.08 to 3.82) in cardiac biomarkers (p=0.00; I-squared=95.7%; Cochran’s Q=235.2). In the cardiovascular (CV) population, the percent increase in cardiac biomarkers levels due to a decrease/increase in ambient temperature was greater. This study showed the decrease/increase in ambient temperature has a direct correlation with the alterations in cardiac biomarkers. These findings are useful for managing temperatureassociated cardiovascular mortality.
Registration
This meta-analysis is registered on the National Institute for Health and Care Research (NIHCR) for the PROSPERO with registration ID CRD42022320505.
Growing literatures have explored the cardiorespiratory health effects of the daily temperature, but such effects of temperature variability remain unclear. We investigated the acute associations of personal levels of temperature variability with cardiorespiratory biomarkers. This is a panel study with four repeated measurements among forty eligible college students in Hefei, Anhui Province, China. We collected personal-level temperature data using temperature/humidity data loggers. Temperature variability parameters included diurnal temperature range (DTR), the standard-deviation of temperature (SDT) and temperature variability (TV). Cardiorespiratory health indicators included three BP parameters [systolic BP (SBP), diastolic BP (DBP) and mean article pressure (MAP)], fractional exhaled nitric oxide (FeNO), and four saliva biomarkers [C-reactive protein (CRP), cortisol, alpha-amylase and lysozyme]. Linear mixed-effect models were then used to assess the associations of temperature variability with these cardiorespiratory biomarkers. We found that short-term exposure to the three temperature variability parameters was associated with these cardiorespiratory biomarkers. The magnitude, direction and significance of these associations varied by temperature variability parameters, by biomarkers and by lags of exposure. Specifically, temperature variability parameters were inversely associated with BP and saliva lysozyme; positively associated with airway inflammation biomarkers (FeNO and saliva CRP) and stress response biomarkers (saliva cortisol and alpha-amylase). The results were robust to further control for air pollutants, and these associations were more prominent in females and in subjects with abnormal body mass index. Our findings suggested that acute exposure to temperature variability could significantly alter cardiorespiratory biomarker profiles among healthy young adults in China.
The utilization of artificial intelligence (AI) has become a valuable part of medical research. Diabetes is one of the top maladies on the planet, and it is a long-term disease that happens if the body cannot utilize glucose appropriately. This paper indicates the demand for the right procedures, advancement, and usage of successful well-being observing strategies ought to be selected to battle against diabetes. So early discovery and treatment with the utilization of different procedures must be preferred. Our model consists of four machine learning algorithms which are K-Nearest Neighbor, Random Forest, Decision Tree, and Logistic Regression. These algorithms are used on a dataset of 15,000 diabetes mellitus patients along with nine features, where the results are compared to show which algorithm gives the best accuracy, including statistical analysis to get a more perfect result of our model. Among all four algorithms, the random forest gives the best accuracy of around 92%, where the rest of the algorithms give between 78 and 90%. Hopefully, this study could be very helpful in medical science to predict the risk score of diabetes mellitus (DM) early and to classify them.
Der aktuelle Versorgungs-Report geht der Frage nach, welche Auswirkungen der Klimawandel auf unsere Gesundheit hat und welche Konsequenzen sich daraus für die medizinische Versorgung in Deutschland ergeben. Dabei bringt er die unterschiedlichen Perspektiven von Umweltepidemiologie, Medizin und Gesundheitspolitik zusammen. Expertinnen und Experten analysieren in insgesamt 16 Fachbeiträgen den Einfluss des Klimawandels auf Erkrankungshäufigkeiten, gefährdete Bevölkerungsgruppen und Infrastrukturen der Gesundheitsversorgung. Der Report verfolgt das Ziel, aktuelle wissenschaftliche Erkenntnisse für die Versorgungspraxis aufzubereiten und so zu einer stärkeren Sensibilisierung für die gesundheitlichen Folgen des Klimawandels in der Gesellschaft beizutragen. Dargelegt werden: - klimawissenschaftliche Grundlagen und Gesundheitsfolgen der Klimaveränderungen - versorgungsbezogene Analysen zu bedeutsamen Gesundheitsrisiken und Präventionsempfehlungen - Verhalten der Bevölkerung auf Basis einer aktuellen deutschlandweiten Befragung - Anpassungsbedarf auf infrastrukturell-organisatorischer Ebene Der Teil „Daten und Analysen“ informiert umfassend über die Häufigkeit von Erkrankungen und Behandlungen in Deutschland.
Objectives:
To explore whether lower outdoor temperature increases cardio-cerebrovascular disease risk through regulating blood pressure and whether indoor heating in winter is beneficial to prevent cardio-cerebrovascular disease in cold areas.
Methods:
We analyzed the data of 38 589 participants in Harbin from the China Kadoorie Biobank (CKB) during 2004-2008, with an average of 7.14-year follow-up. Linear regression analysis was performed to estimate the relationship between outdoor temperature and blood pressure. Cox regression analysis and logistic regression analysis were used to analyze the association of blood pressure with cardio-cerebrovascular event risk. Mediation analysis was performed to explore the role of blood pressure in the association between outdoor temperature and cardio-cerebrovascular events risk.
Results:
There was an increase of 6.7 mmHg in SBP and 2.1 mmHg in DBP for each 10 °C decrease in outdoor temperature when outdoor temperature was higher than 5 °C. There was an inverse association between outdoor temperature and cardio-cerebrovascular event morbidity. The increases in blood pressure and cardio-cerebrovascular event morbidity were attenuated in months when central heating was fully provided. Participants with hypertension have higher risks of cardio-cerebrovascular disease (hazard ratio 1.347; 95% CI 1.281--1.415), CVD (hazard ratio 1.347; 95% CI 1.282--1.416), MACE (hazard ratio 1.670; 95% CI 1.560--1.788) and stroke (hazard ratio 1.683; 95% CI 1.571--1.803). Mediation analysis demonstrated that the association between outdoor temperature and cardio-cerebrovascular events risk was potentially mediated by blood pressure.
Conclusion:
Temperature-driven blood pressure potentially mediates the association between outdoor temperature and cardio-cerebrovascular events risk. Indoor heating in winter is probably beneficial to cardio-cerebrovascular disease prevention by inhibition of blood pressure increase.
: Blood pressure (BP) exhibits seasonal variation with lower levels at higher environmental temperatures and higher at lower temperatures. This is a global phenomenon affecting both sexes, all age groups, normotensive individuals, and hypertensive patients. In treated hypertensive patients it may result in excessive BP decline in summer, or rise in winter, possibly deserving treatment modification. This Consensus Statement by the European Society of Hypertension Working Group on BP Monitoring and Cardiovascular Variability provides a review of the evidence on the seasonal BP variation regarding its epidemiology, pathophysiology, relevance, magnitude, and the findings using different measurement methods. Consensus recommendations are provided for health professionals on how to evaluate the seasonal BP changes in treated hypertensive patients and when treatment modification might be justified. (i) In treated hypertensive patients symptoms appearing with temperature rise and suggesting overtreatment must be investigated for possible excessive BP drop due to seasonal variation. On the other hand, a BP rise during cold weather, might be due to seasonal variation. (ii) The seasonal BP changes should be confirmed by repeated office measurements; preferably with home or ambulatory BP monitoring. Other reasons for BP change must be excluded. (iii) Similar issues might appear in people traveling from cold to hot places, or the reverse. (iv) BP levels below the recommended treatment goal should be considered for possible down-titration, particularly if there are symptoms suggesting overtreatment. SBP less than 110 mmHg requires consideration for treatment down-titration, even in asymptomatic patients. Further research is needed on the optimal management of the seasonal BP changes.
Nonparametric regression has received considerable attention in biomedical research because it allows for data-driven dependence of the response variable on covariates. In the presence of missing data, doubly robust estimators have been proposed for nonparametric regression, which allow one model for the missingness mechanism and one model for the outcome regression. We propose multiply robust kernel estimating equations (MRKEEs) for nonparametric regression that can accommodate multiple working models for either the missingness mechanism or the outcome regression, or both. The resulting estimator is consistent if any one of those models is correctly specified. When including correctly specified models for both the missingness mechanism and the outcome regression, the proposed estimator achieves the optimal efficiency within the class of augmented inverse propensity weighted (AIPW) kernel estimators. We conduct simulation studies to evaluate the finite sample performance of the proposed method and further demonstrate it through a real-data example.
Hypertension is currently one of the most common chronic diseases with high global prevalence associated with a huge social and economic burden. In recent years, air pollution has become a focus of research, especially the effects of PM2.5 on hypertension. However, few studies have considered the spatial properties of the sample; thus, the results might be unreliable. Based on the China Health and Retirement Longitudinal Study (CHARLS) and the Environmental Status Bulletin for each province in China, we used the extended shared component model (SCM) to fit the spatial variation of hypertension risk and to reveal the impact of PM2.5 on hypertension in males and females. Our results revealed that the crude prevalence of hypertension for the whole population in China was 32.74% in 2015, with the prevalence in men experiencing slightly higher than that in women (32.92% vs. 32.58%). We found that the distribution of hypertension prevalence exhibited obvious spatial aggregation for the whole population in China (Moran’s I = 0.39, P = 0.001), with similar results in both men (Moran’s I = 0.18, P = 0.027) and women (Moran’s I = 0.52, P = 0.001). Furthermore, the smoothed results obtained using the SCM indicated that some eastern and central provinces had relatively higher hypertension risk, while the risk in southeastern provinces was much lower. The risk was also relatively lower in most western provinces, except for some northwestern regions. Notably, our results showed that PM2.5 was a risk factor for hypertension, and the impact of PM2.5 on women was slightly greater than that on men, with odds ratios (OR) of 1.063 (1.041, 1.086) and 1.048 (1.025, 1.071), respectively. Our findings suggest the existence of distinct spatial differences in the prevalence of hypertension and small sex-related differences in the risk of hypertension in China.
Although several studies have demonstrated a short-term association between outdoor temperature and blood pressure (BP) among various adult groups, evidence among children and adolescents is lacking. One hundred ninety-four thousand one hundred four participants from 2016 Health Promotion Program for Children and Adolescents (HPPCA) were analyzed through generalized linear mixed-effects models to estimate the short-term effects of two outdoor temperature variables (average and minimum temperature) on participants’ BP. Decreasing outdoor temperature was associated with significant increases in systolic BP (SBP), diastolic BP (DBP), and prevalence of hypertension during lag 0 through lag 6. Additionally, daily minimum temperature showed a more apparent association with participants’ BP. The estimated increases (95% confidence interval) in SBP and DBP at lag 0 were 0.82 (0.72, 0.92) mmHg and 2.28 (2.20, 2.35) mmHg for a 1 °C decrease in daily minimum temperature, while those values were 0.11 (0.10, 0.12) mmHg and 0.25 (0.24, 0.26) mmHg for a 1 °C decrease in daily average temperature, respectively. The effects of temperature on BP were stronger among female, as well as those with young age and low body mass index. It demonstrated that short-term decreases in outdoor temperature were significantly associated with rises in BP among children and adolescents. This founding has some implications for clinical management and research of BP. Meanwhile, public health intervention should be designed to reduce the exposure to cold temperature for protecting children and adolescents’ BP.
High blood pressure (BP) affects over one billion people and is the leading risk factor for global mortality. While many lifestyle and genetic risk factors are well-accepted to increase BP, the role of the external environment is typically overlooked. Mounting evidence now supports that numerous environmental factors can promote an elevation in BP. Broadly speaking these include aspects of the natural environment (e.g., cold temperatures, higher altitude, and winter season), natural disasters (e.g., earthquakes, volcanic eruptions), and man-made exposures (e.g., noise, air pollutants, and toxins/chemicals). This is important for health care providers to recognize as one (or several) of these environmental factors could be playing a clinically meaningful role in elevating BP or disrupting hypertension control among their patients. At the population level, certain environmental exposures may even be contributing to the growing pandemic of hypertension. Here we provide an updated review of the literature linking environment exposures with high BP and outline practical recommendations for clinicians.
Environmental temperatures influence cardiovascular physiology. However, the majority of time is spent indoors, making outdoor-ambient temperatures inaccurate estimates of true exposures encountered by most individuals. We evaluated in 50 healthy adults the associations between previous 7-day outdoor-ambient (four occasions) and prior 24-hour personal-level (two occasions) environmental temperature exposures with blood pressure, heart rate variability, sleep parameters, and endothelial-dependent vasodilatation (brachial flow-mediated dilatation [FMD]) using generalized estimating equations. Participants (34 females; age, 32.1 ± 9.6 years) had normal blood pressures (107.8 ± 13.3/70.2 ± 9.4 mm Hg), FMD (7.4 ± 2.8%), as well as sleep and heart rate variability parameters. Mean 7-day outdoor-ambient (4.6 ± 9.7°C) differed from personal-level temperature exposures (22.0 ± 3.0°C). Colder outdoor-ambient temperatures (per -10°C) over the previous 1-6 days (rolling averages) were associated with decreases in FMD: -0.57% (95% confidence interval [CI]: -1.14% to 0.01%, P = .055) to -0.62% (95% CI: -1.07% to -0.18%, P = .006). However, a 10°C decrease in personal-level temperature during the prior 24 hours was associated with a greater decrement in FMD: -2.44% (95% CI: -4.74% to -0.13%, P = .038). Both were also linearly related to FMD during all seasons and without a threshold temperature. Other end points were not significantly related to either temperature level in this study. Short-term exposures to colder environmental temperatures reduced endothelial-dependent vasodilatation, supporting the epidemiologic associations with heightened cardiovascular risk. We show here for the first time that temperature exposures characterized at the personal level may be more robust predictors of endothelial function than outdoor-ambient levels.
An elevated systolic but not diastolic blood pressure level represents a common finding in elderly patients and is associated with an increased risk for developing coronary artery disease, cerebrovascular disease, peripheral artery disease, progressive cognitive decline and renal failure. Although less frequently, elderly patients manifest not only with systolic but also diastolic hypertension. Also in this case, the elderly patient will present an increased risk for developing hypertension-related abnormalities. Based on several trials conducted in patients ≥65 years and one single trial in patients ≥80 years the most recent European guidelines recommend antihypertensive treatment in elderly hypertensive patients with a systolic blood pressure ≥60 mmHg, with a systolic target between 140 and 150 mmHg. In fit elderly patients <80 years treatment may be considered at a systolic level ≥140 mmHg with a target SBP <140 mmHg if treatment is well tolerated. Despite of the above, at least three issues related to antihypertensive drug treatment in aged individuals are still debated, particularly after the publication of a recent large scale clinical trial that included also 2.636 patients ≥75 years and a study in nursing home residents ≥80 years, i.e. the frailest oldest patients: (1) the blood pressure threshold at which antihypertensive drug should be initiated, (2) the blood pressure targets of the therapeutic intervention, and (3) the approach to frail elderly hypertensive patients. This review will critically review the evidence available so far on these important issues as well as the position of current guidelines and consensus statements.
A host of environmental factors can significantly increase arterial blood pressure (BP) including cold temperature, high altitude, loud noises, and ambient air pollutants. Although brief exposures acutely elevate BP, over the long term, chronic exposures may be capable of promoting the development of sustained hypertension. Given their omnipresent nature, environmental factors may play a role in worsening BP control and heightening overall cardiovascular risk at the global public health level.
Background:
Long-term exposure to air pollution has been hypothesized to elevate arterial blood pressure (BP). The existing evidence is scarce and country specific.
Objectives:
We investigated the cross-sectional association of long-term traffic-related air pollution with BP and prevalent hypertension in European populations.
Methods:
We analyzed 15 population-based cohorts, participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE). We modeled residential exposure to particulate matter and nitrogen oxides with land use regression using a uniform protocol. We assessed traffic exposure with traffic indicator variables. We analyzed systolic and diastolic BP in participants medicated and nonmedicated with BP-lowering medication (BPLM) separately, adjusting for personal and area-level risk factors and environmental noise. Prevalent hypertension was defined as ≥ 140 mmHg systolic BP, or ≥ 90 mmHg diastolic BP, or intake of BPLM. We combined cohort-specific results using random-effects meta-analysis.
Results:
In the main meta-analysis of 113,926 participants, traffic load on major roads within 100 m of the residence was associated with increased systolic and diastolic BP in nonmedicated participants [0.35 mmHg (95% CI: 0.02, 0.68) and 0.22 mmHg (95% CI: 0.04, 0.40) per 4,000,000 vehicles × m/day, respectively]. The estimated odds ratio (OR) for prevalent hypertension was 1.05 (95% CI: 0.99, 1.11) per 4,000,000 vehicles × m/day. Modeled air pollutants and BP were not clearly associated.
Conclusions:
In this first comprehensive meta-analysis of European population-based cohorts, we observed a weak positive association of high residential traffic exposure with BP in nonmedicated participants, and an elevated OR for prevalent hypertension. The relationship of modeled air pollutants with BP was inconsistent.
Particulate matter less than 2.5μm in diameter (PM2.5) exposure increases blood pressure (BP) in humans and animal models. Abnormal sympathetic nervous system (SNS) activation has been implicated in the acute BP response to PM2.5 exposure. The mechanisms responsible for SNS activation and its role in chronic sustenance of hypertension (HTN) in response to PM2.5 exposure are currently unknown.
We postulated that central nervous system (CNS) inflammation may be implicated in chronic PM2.5 exposure-induced increases in BP and SNS activation.
C57Bl/6j mice were exposed to concentrated ambient PM2.5 (CAPs) for 6 months, and BP was analyzed by radioactive telemetric transmitters. Sympathetic tone was assessed by measurements of low frequency blood pressure variability (LF-BPV) and urinary norepinephrine (NE) excretion. Additionally the effects of acute pharmacologic inhibitors of the SNS and parasympathetic nervous system were tested.
Our results show that long term CAPs exposure significantly increased basal blood pressure, paralleled by increases in LF-BPV and urinary NE excretion. The increased basal blood pressure was attenuated by the centrally acting α2A agonist guanfacine, suggesting a role of increased sympathetic tone in CAPs exposure-induced hypertension. The increase in sympathetic tone was accompanied by an inflammatory response in the arcuate nucleus of the hypothalamus, evidenced by increased expression of pro-inflammatory genes and inhibitor kappaB kinase (IKK)/nuclear factor-kappaB (NF-kB) pathway activation.
Long-term CAPs exposure increases BP through activation of SNS, which may involve hypothalamic inflammation.
Laboratory studies suggest that exposure to fine particulate matter (2.5μm in diameter or less; PM2.5) can trigger a combination of pathophysiological responses that may induce the development of hypertension. However, epidemiological evidence relating PM2.5 and hypertension is sparse. We thus conducted a population-based cohort study to determine whether exposure to ambient PM2.5 is associated with incident hypertension.
We assembled a cohort of 35,303 non-hypertensive adults from Ontario, Canada who responded to one of four population-based health surveys between 1996 and 2005 and were followed-up until December 31, 2010. Incident diagnoses of hypertension were ascertained from the Ontario Hypertension Database, a validated registry of persons diagnosed with hypertension in Ontario (sensitivity=72%, specificity=95%). Estimates of long-term exposure to PM2.5 at participants' postal-code residences were derived from satellite observations. We used Cox proportional hazards models, adjusting for various individual and contextual risk factors including body mass index, smoking, physical activity, and neighbourhood-level unemployment rates. We conducted various sensitivity analyses to assess the robustness of the effect estimate, such as investigating several time windows of exposure and controlling for potential changes in the risk of hypertension over time. Between 1996 and 2010, we identified 8,649 incident cases of hypertension and 2,296 deaths. For every 10µg/m(3) increase of PPM2.5, the adjusted hazard ratio (HR10) of incident hypertension was 1.13 (95% confidence interval (CI): 1.05-1.22). Estimated associations were comparable among all sensitivity analyses.
This study supports an association between PM2.5 and incident hypertension.
Seasonal blood pressure (BP) changes have been found to be related to either outdoor or indoor temperature. No information regarding the independent effects of temperature measured proximally to the patient, the personal-level environmental temperature (PET), is available. Inclusion of daylight hours in multivariate analysis might allow exploring the independent interaction of BP with seasonality. To investigate whether ambulatory BP monitoring is affected by PET or by seasonality, 1897 patients referred to our hypertension units underwent ambulatory BP monitoring with a battery-powered temperature data logger fitted to the carrying pouch of the monitor. Predictors of 24-hour daytime and nighttime BP and of morning BP surge were investigated with a multivariate stepwise regression model, including age, sex, body mass index, antihypertensive treatment, office BP, ambulatory heart rate, PET, relative humidity, atmospheric pressure, and daylight hours as independent variables. At adjusted regression analysis, daytime systolic BP was negatively related to PET (-0.14; 95% confidence interval, -0.25 to -0.02); nighttime BP was positively related to daylight hours (0.63; 0.37-0.90); and morning BP surge was negatively related to daylight hours (-0.54; -0.87 to -0.21). These results provide new evidence that PET and seasonality (daylight hours) are 2 independent predictors of ambulatory BP monitoring.
Quantification of the disease burden caused by different risks informs prevention by providing an account of health loss different to that provided by a disease-by-disease analysis. No complete revision of global disease burden caused by risk factors has been done since a comparative risk assessment in 2000, and no previous analysis has assessed changes in burden attributable to risk factors over time.
METHODS We estimated deaths and disability-adjusted life years (DALYs; sum of years lived with disability [YLD] and years of life lost [YLL]) attributable to the independent effects of 67 risk factors and clusters of risk factors for 21 regions in 1990 and 2010. We estimated exposure distributions for each year, region, sex, and age group, and relative risks per unit of exposure by systematically reviewing and synthesising published and unpublished data. We used these estimates, together with estimates of cause-specific deaths and DALYs from the Global Burden of Disease Study 2010, to calculate the burden attributable to each risk factor exposure compared with the theoretical-minimum-risk exposure. We incorporated uncertainty in disease burden, relative risks, and exposures into our estimates of attributable burden.
FINDINGS In 2010, the three leading risk factors for global disease burden were high blood pressure (7·0% [95% uncertainty interval 6·2-7·7] of global DALYs), tobacco smoking including second-hand smoke (6·3% [5·5-7·0]), and alcohol use (5·5% [5·0-5·9]). In 1990, the leading risks were childhood underweight (7·9% [6·8-9·4]), household air pollution from solid fuels (HAP; 7·0% [5·6-8·3]), and tobacco smoking including second-hand smoke (6·1% [5·4-6·8]). Dietary risk factors and physical inactivity collectively accounted for 10·0% (95% UI 9·2-10·8) of global DALYs in 2010, with the most prominent dietary risks being diets low in fruits and those high in sodium. Several risks that primarily affect childhood communicable diseases, including unimproved water and sanitation and childhood micronutrient deficiencies, fell in rank between 1990 and 2010, with unimproved water and sanitation accounting for 0·9% (0·4-1·6) of global DALYs in 2010. However, in most of sub-Saharan Africa childhood underweight, HAP, and non-exclusive and discontinued breastfeeding were the leading risks in 2010, while HAP was the leading risk in south Asia. The leading risk factor in Eastern Europe, most of Latin America, and southern sub-Saharan Africa in 2010 was alcohol use; in most of Asia, North Africa and Middle East, and central Europe it was high blood pressure. Despite declines, tobacco smoking including second-hand smoke remained the leading risk in high-income north America and western Europe. High body-mass index has increased globally and it is the leading risk in Australasia and southern Latin America, and also ranks high in other high-income regions, North Africa and Middle East, and Oceania.
INTERPRETATION Worldwide, the contribution of different risk factors to disease burden has changed substantially, with a shift away from risks for communicable diseases in children towards those for non-communicable diseases in adults. These changes are related to the ageing population, decreased mortality among children younger than 5 years, changes in cause-of-death composition, and changes in risk factor exposures. New evidence has led to changes in the magnitude of key risks including unimproved water and sanitation, vitamin A and zinc deficiencies, and ambient particulate matter pollution. The extent to which the epidemiological shift has occurred and what the leading risks currently are varies greatly across regions. In much of sub-Saharan Africa, the leading risks are still those associated with poverty and those that affect children.
FUNDING Bill & Melinda Gates Foundation.
Short-term exposure to high levels of air pollution may trigger myocardial infarction (MI), but this association remains unclear.
To assess and quantify the association between short-term exposure to major air pollutants (ozone, carbon monoxide, nitrogen dioxide, sulfur dioxide, and particulate matter ≤10 μm [PM(10)] and ≤2.5 μm [PM(2.5)] in diameter) on MI risk.
EMBASE, Ovid MEDLINE in-process and other nonindexed citations, and Ovid MEDLINE (between 1948 and November 28, 2011), and EBM Reviews-Cochrane Central Register of Controlled Trials and EBM Reviews-Cochrane Database of Systematic Reviews (between 2005 and November 28, 2011) were searched for a combination of keywords related to the type of exposure (air pollution, ozone, carbon monoxide, nitrogen dioxide, sulfur dioxide, PM(10), and PM(2.5)) and to the type of outcome (MI, heart attack, acute coronary syndrome).
Two independent reviewers selected studies of any study design and in any language, using original data and investigating the association between short-term exposure (for up to 7 days) to 1 or more air pollutants and subsequent MI risk. Selection was performed from abstracts and titles and pursued by reviewing the full text of potentially eligible studies.
Descriptive and quantitative information was extracted from each selected study. Using a random effects model, relative risks (RRs) and 95% CIs were calculated for each increment of 10 μg/m(3) in pollutant concentration, with the exception of carbon monoxide, for which an increase of 1 mg/m(3) was considered.
After a detailed screening of 117 studies, 34 studies were identified. All the main air pollutants, with the exception of ozone, were significantly associated with an increase in MI risk (carbon monoxide: 1.048; 95% CI, 1.026-1.070; nitrogen dioxide: 1.011; 95% CI, 1.006-1.016; sulfur dioxide: 1.010; 95% CI, 1.003-1.017; PM(10): 1.006; 95% CI, 1.002-1.009; and PM(2.5): 1.025; 95% CI, 1.015-1.036). For ozone, the RR was 1.003 (95% CI, 0.997-1.010; P = .36). Subgroup analyses provided results comparable with those of the overall analyses. Population attributable fractions ranged between 0.6% and 4.5%, depending on the air pollutant.
All the main air pollutants, with the exception of ozone, were significantly associated with a near-term increase in MI risk.
Diabetes increases the risk of hypertension and orthostatic hypotension and raises the risk of cardiovascular death during heat waves and high pollution episodes.
We examined whether short-term exposures to air pollution (fine particles, ozone) and heat resulted in perturbation of arterial blood pressure (BP) in persons with type 2 diabetes mellitus (T2DM).
We conducted a panel study in 70 subjects with T2DM, measuring BP by automated oscillometric sphygmomanometer and pulse wave analysis every 2 weeks on up to five occasions (355 repeated measures). Hourly central site measurements of fine particles, ozone, and meteorology were conducted. We applied linear mixed models with random participant intercepts to investigate the association of fine particles, ozone, and ambient temperature with systolic, diastolic, and mean arterial BP in a multipollutant model, controlling for season, meteorological variables, and subject characteristics.
An interquartile increase in ambient fine particle mass [particulate matter (PM) with an aerodynamic diameter of ≤ 2.5 μm (PM2.5)] and in the traffic component black carbon in the previous 5 days (3.54 and 0.25 μg/m3, respectively) predicted increases of 1.4 mmHg [95% confidence interval (CI): 0.0, 2.9 mmHg] and 2.2 mmHg (95% CI: 0.4, 4.0 mmHg) in systolic BP (SBP) at the population geometric mean, respectively. In contrast, an interquartile increase in the 5-day mean of ozone (13.3 ppb) was associated with a 5.2 mmHg (95% CI: -8.6, -1.8 mmHg) decrease in SBP. Higher temperatures were associated with a marginal decrease in BP.
In subjects with T2DM, PM was associated with increased BP, and ozone was associated with decreased BP. These effects may be clinically important in patients with already compromised autoregulatory function.
In this paper, we review the epidemiological evidence on the relationship between ambient temperature and morbidity. We assessed the methodological issues in previous studies and proposed future research directions. DATA SOURCES AND DATA EXTRACTION: We searched the PubMed database for epidemiological studies on ambient temperature and morbidity of noncommunicable diseases published in refereed English journals before 30 June 2010. Forty relevant studies were identified. Of these, 24 examined the relationship between ambient temperature and morbidity, 15 investigated the short-term effects of heat wave on morbidity, and 1 assessed both temperature and heat wave effects.
Descriptive and time-series studies were the two main research designs used to investigate the temperature-morbidity relationship. Measurements of temperature exposure and health outcomes used in these studies differed widely. The majority of studies reported a significant relationship between ambient temperature and total or cause-specific morbidities. However, there were some inconsistencies in the direction and magnitude of nonlinear lag effects. The lag effect of hot temperature on morbidity was shorter (several days) compared with that of cold temperature (up to a few weeks). The temperature-morbidity relationship may be confounded or modified by sociodemographic factors and air pollution.
There is a significant short-term effect of ambient temperature on total and cause-specific morbidities. However, further research is needed to determine an appropriate temperature measure, consider a diverse range of morbidities, and to use consistent methodology to make different studies more comparable.
While the effects of weather and, in particular, ambient temperature on overall mortality are well documented, the strength of the evidence base for the effects on acute myocardial infarction (MI) are less clear.
To systematically review studies specifically focusing on the effects of temperature on MI.
Medline, Embase, and GeoBase publication databases, as well as reference lists, and the websites of a number of relevant public organisations.
Studies of original data in which ambient temperature was an exposure of interest and MI a specific outcome were selected.
The reported effects of ambient temperature on the risk of MI, including effect sizes and confidence intervals, where possible, were recorded. Methodological details were also extracted, including study population, location and setting, ascertainment of MI events, adjustment for potential confounders and consideration of lagged effects.
19 studies were identified, of which 14 considered the short-term effects of temperature on a daily timescale, the remainder looking at longer-term effects. Overall, 8 of the 12 studies which included relevant data from the winter season reported a statistically significant short-term increased risk of MI at lower temperatures, while increases in risk at higher temperatures were reported in 7 of the 13 studies with relevant data. A number of differences were identified between studies in the population included demographics, location, local climate, study design and statistical methodology.
A number of studies, including some that were large and relatively well controlled, suggested that both hot and cold weather had detrimental effects on the short-term risk of MI. However, further research with consistent methodology is needed to clarify the magnitude of these effects and to show which populations and individuals are vulnerable.
Seasonal variations of blood pressure-related diseases have been described in several populations. However, few studies have examined the seasonal variations of blood pressure in the elderly, a segment of the population particularly exposed to vascular diseases. The association of blood pressure with season and outdoor temperature was examined in 8801 subjects 65 years or older from the Three-City study, a population-based longitudinal study.
Blood pressure was measured at baseline and 2-year follow-up examinations. Daily outdoor temperature measured at 11 am was provided by the local meteorological offices.
Both systolic and diastolic blood pressure values differed significantly across the 4 seasons and across the quintiles of the distribution of outdoor temperature. Systolic blood pressure decreased with increasing temperature, with an 8.0-mm Hg decrease between the lowest (< 7.9 degrees C) and the highest (> or = 21.2 degrees C) temperature quintile. Intraindividual differences in blood pressure between follow-up and baseline examinations were strongly correlated with differences in outdoor temperature. The higher the temperature at follow-up compared with baseline, the greater the decrease in blood pressure. Longitudinal changes in blood pressure according to difference in outdoor temperature were larger in subjects 80 years or older than in younger participants.
Outdoor temperature and blood pressure are strongly correlated in the elderly, especially in those 80 years or older. During periods of extreme temperatures, a careful monitoring of blood pressure and antihypertensive treatment could contribute to reducing the consequences of blood pressure variations in the elderly.
"The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure" provides a new guideline for hypertension prevention and management. The following are the key messages(1) In persons older than 50 years, systolic blood pressure (BP) of more than 140 mm Hg is a much more important cardiovascular disease (CVD) risk factor than diastolic BP; (2) The risk of CVD, beginning at 115/75 mm Hg, doubles with each increment of 20/10 mm Hg; individuals who are normotensive at 55 years of age have a 90% lifetime risk for developing hypertension; (3) Individuals with a systolic BP of 120 to 139 mm Hg or a diastolic BP of 80 to 89 mm Hg should be considered as prehypertensive and require health-promoting lifestyle modifications to prevent CVD; (4) Thiazide-type diuretics should be used in drug treatment for most patients with uncomplicated hypertension, either alone or combined with drugs from other classes. Certain high-risk conditions are compelling indications for the initial use of other antihypertensive drug classes (angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, beta-blockers, calcium channel blockers); (5) Most patients with hypertension will require 2 or more antihypertensive medications to achieve goal BP (<140/90 mm Hg, or <130/80 mm Hg for patients with diabetes or chronic kidney disease); (6) If BP is more than 20/10 mm Hg above goal BP, consideration should be given to initiating therapy with 2 agents, 1 of which usually should be a thiazide-type diuretic; and (7) The most effective therapy prescribed by the most careful clinician will control hypertension only if patients are motivated. Motivation improves when patients have positive experiences with and trust in the clinician. Empathy builds trust and is a potent motivator. Finally, in presenting these guidelines, the committee recognizes that the responsible physician's judgment remains paramount.
Major changes in the health profile of many developing countries are taking place. Life expectancy in these countries is increasing, and people are more exposed to diseases of old age like hypertension and cardiovascular diseases. Scientific research in the developing world -including this area - is lagging behind. However, high-quality research can still be carried out in spite of the limited resources. This paper identifies the different material and psychological barriers to scientific research. Epidemiological and clinical research represent high priorities in hypertension research in developing countries, and international cooperation is essential to improve the understanding of hypertension.
Background:
Comprehensive studies have confirmed that particulate matter air pollution could trigger myocardial infarction, heart failure and reduce heart rate variability; however, its effect on blood pressure (BP) remains controversial. Therefore, we did a systematic review and meta-analysis to investigate the association and its magnitude between exposure to PM2.5 and BP.
Methods:
The databases of PubMed, Ovid Medline and Embase between 1948 and 15 November 2013 were searched to identify the studies exploring the association between particulate matters (diameter <2.5 μm) (PM2.5) and BP. Selection was performed by screening abstracts and titles and then reviewing the full text of potentially eligible studies. We extracted descriptive and quantitative information from each study and used a random-effects model to calculate BP change and 95% confidence interval (95% CI) for each increment of 10 μg/m in PM2.5. Meta-regression and subgroup analyses were conducted to explore the source of heterogeneity and the impact of possible confounding factors.
Results:
Of 1028 identified articles, after screening and reviewing in detail, 22 studies were included in our meta-analysis. The overall analysis suggested that BP was positively related to PM2.5 exposure with an elevation of 1.393 mmHg, 95% CI (0.874-1.912) and 0.895 mmHg, 95% CI (0.49-1.299) per 10 μg/m increase for SBP and DBP, respectively. Long-term exposure showed the strongest associations with BP. And for short-term effect, the largest magnitude was seen at the lag of the previous 5 days average prior to BP measurement. Subgroup analyses yielded consistent results with the overall analyses. Meta-regression of SBP did not identify any significant potential causes of heterogeneity. For DBP, study design, the method of BP monitoring, publication year, study design, study period and sample size were significant modifiers of the relationship between DBP and PM2.5.
Conclusion:
Exposure to PM2.5 had a statistically significant impact on BP and the magnitude of this effect may have substantially clinical implication.
Few prospective studies have assessed the blood pressure effect of extremely high air pollution encountered in Asia's megacities. The objective of this study was to evaluate the association between combustion-related air pollution with ambulatory blood pressure and autonomic function. During February to July 2012, personal black carbon was determined for 5 consecutive days using microaethalometers in patients with metabolic syndrome in Beijing, China. Simultaneous ambient fine particulate matter concentration was obtained from the Beijing Municipal Environmental Monitoring Center and the US Embassy. Twenty-four-hour ambulatory blood pressure and heart rate variability were measured from day 4. Arterial stiffness and endothelial function were obtained at the end of day 5. For statistical analysis, we used generalized additive mixed models for repeated outcomes and generalized linear models for single/summary outcomes. Mean (SD) of personal black carbon and fine particulate matter during 24 hours was 4.66 (2.89) and 64.2 (36.9) μg/m(3). Exposure to high levels of black carbon in the preceding hours was associated significantly with adverse cardiovascular responses. A unit increase in personal black carbon during the previous 10 hours was associated with an increase in systolic blood pressure of 0.53 mm Hg and diastolic blood pressure of 0.37 mm Hg (95% confidence interval, 0.17-0.89 and 0.10-0.65 mm Hg, respectively), a percentage change in low frequency to high frequency ratio of 5.11 and mean interbeat interval of -0.06 (95% confidence interval, 0.62-9.60 and -0.11 to -0.01, respectively). These findings highlight the public health effect of air pollution and the importance of reducing air pollution.
Acute exposure to air pollution has been linked to myocardial infarction, but its effect on heart failure is uncertain. We did a systematic review and meta-analysis to assess the association between air pollution and acute decompensated heart failure including hospitalisation and heart failure mortality.
Five databases were searched for studies investigating the association between daily increases in gaseous (carbon monoxide, sulphur dioxide, nitrogen dioxide, ozone) and particulate (diameter <2·5 μm [PM2·5] or <10 μm [PM10]) air pollutants, and heart failure hospitalisations or heart failure mortality. We used a random-effects model to derive overall risk estimates per pollutant.
Of 1146 identified articles, 195 were reviewed in-depth with 35 satisfying inclusion criteria. Heart failure hospitalisation or death was associated with increases in carbon monoxide (3·52% per 1 part per million; 95% CI 2·52-4·54), sulphur dioxide (2·36% per 10 parts per billion; 1·35-3·38), and nitrogen dioxide (1·70% per 10 parts per billion; 1·25-2·16), but not ozone (0·46% per 10 parts per billion; -0·10 to 1·02) concentrations. Increases in particulate matter concentration were associated with heart failure hospitalisation or death (PM2·5 2·12% per 10 μg/m(3), 95% CI 1·42-2·82; PM10 1·63% per 10 μg/m(3), 95% CI 1·20-2·07). Strongest associations were seen on the day of exposure, with more persistent effects for PM2·5. In the USA, we estimate that a mean reduction in PM2·5 of 3·9 μg/m(3) would prevent 7978 heart failure hospitalisations and save a third of a billion US dollars a year.
Air pollution has a close temporal association with heart failure hospitalisation and heart failure mortality. Although more studies from developing nations are required, air pollution is a pervasive public health issue with major cardiovascular and health economic consequences, and it should remain a key target for global health policy.
British Heart Foundation.
To determine the effects of longer term modest salt reduction on blood pressure, hormones, and lipids.
Systematic review and meta-analysis.
Medline, Embase, Cochrane Hypertension Group Specialised Register, Cochrane Central Register of Controlled Trials, and reference list of relevant articles.
Randomised trials with a modest reduction in salt intake and duration of at least four weeks.
Data were extracted independently by two reviewers. Random effects meta-analyses, subgroup analyses, and meta-regression were performed.
Thirty four trials (3230 participants) were included. Meta-analysis showed that the mean change in urinary sodium (reduced salt v usual salt) was -75 mmol/24 h (equivalent to a reduction of 4.4 g/day salt), and with this reduction in salt intake, the mean change in blood pressure was -4.18 mm Hg (95% confidence interval -5.18 to -3.18, I(2)=75%) for systolic blood pressure and -2.06 mm Hg (-2.67 to -1.45, I(2)=68%) for diastolic blood pressure. Meta-regression showed that age, ethnic group, blood pressure status (hypertensive or normotensive), and the change in 24 hour urinary sodium were all significantly associated with the fall in systolic blood pressure, explaining 68% of the variance between studies. A 100 mmol reduction in 24 hour urinary sodium (6 g/day salt) was associated with a fall in systolic blood pressure of 5.8 mm Hg (2.5 to 9.2, P=0.001) after adjustment for age, ethnic group, and blood pressure status. For diastolic blood pressure, age, ethnic group, blood pressure status, and the change in 24 hour urinary sodium explained 41% of the variance between studies. Meta-analysis by subgroup showed that in people with hypertension the mean effect was -5.39 mm Hg (-6.62 to -4.15, I(2)=61%) for systolic blood pressure and -2.82 mm Hg (-3.54 to -2.11, I(2)=52%) for diastolic blood pressure. In normotensive people, the figures were -2.42 mm Hg (-3.56 to -1.29, I(2)=66%) and -1.00 mm Hg (-1.85 to -0.15, I(2)=66%), respectively. Further subgroup analysis showed that the decrease in systolic blood pressure was significant in both white and black people and in men and women. Meta-analysis of data on hormones and lipids showed that the mean change was 0.26 ng/mL/h (0.17 to 0.36, I(2)=70%) for plasma renin activity, 73.20 pmol/L (44.92 to 101.48, I(2)=62%) for aldosterone, 187 pmol/L (39 to 336, I(2)=5%) for noradrenaline (norepinephrine), 37 pmol/L (-1 to 74, I(2)=12%) for adrenaline (epinephrine), 0.05 mmol/L (-0.02 to 0.11, I(2)=0%) for total cholesterol, 0.05 mmol/L (-0.01 to 0.12, I(2)=0%) for low density lipoprotein cholesterol, -0.02 mmol/L (-0.06 to 0.01, I(2)=16%) for high density lipoprotein cholesterol, and 0.04 mmol/L (-0.02 to 0.09, I(2)=0%) for triglycerides.
A modest reduction in salt intake for four or more weeks causes significant and, from a population viewpoint, important falls in blood pressure in both hypertensive and normotensive individuals, irrespective of sex and ethnic group. Salt reduction is associated with a small physiological increase in plasma renin activity, aldosterone, and noradrenaline and no significant change in lipid concentrations. These results support a reduction in population salt intake, which will lower population blood pressure and thereby reduce cardiovascular disease. The observed significant association between the reduction in 24 hour urinary sodium and the fall in systolic blood pressure, indicates that larger reductions in salt intake will lead to larger falls in systolic blood pressure. The current recommendations to reduce salt intake from 9-12 to 5-6 g/day will have a major effect on blood pressure, but a further reduction to 3 g/day will have a greater effect and should become the long term target for population salt intake.
Several studies have investigated the short-term effects of ambient air pollutants in the development of high blood pressure and hypertension. However, little information exists regarding the health effects of long-term exposure. To investigate the association between residential long-term exposure to air pollution and blood pressure and hypertension, we studied 24 845 Chinese adults in 11 districts of 3 northeastern cities from 2009 to 2010. Three-year average concentration of particles with an aerodynamic diameter ≤10 µm (PM(10)), sulfur dioxide (SO(2)), nitrogen dioxides (NO(2)), and ozone (O(3)) were calculated from monitoring stations in the 11 districts. We used generalized additive models and 2-level logistic regressions models to examine the health effects. The results showed that the odds ratio for hypertension increased by 1.12 (95% confidence interval [CI], 1.08-1.16) per 19 μg/m(3) increase in PM(10), 1.11 (95% CI, 1.04-1.18) per 20 μg/m(3) increase in SO(2), and 1.13 (95% CI, 1.06-1.20) per 22 μg/m(3) increase in O(3). The estimated increases in mean systolic and diastolic blood pressure were 0.87 mm Hg (95% CI, 0.48-1.27) and 0.32 mm Hg (95% CI, 0.08-0.56) per 19 μg/m(3) interquartile increase in PM(10), 0.80 mm Hg (95% CI, 0.46-1.14) and 0.31 mm Hg (95% CI, 0.10-0.51) per 20 μg/m(3) interquartile increase in SO(2), and 0.73 mm Hg (95% CI, 0.35-1.11) and 0.37 mm Hg (95% CI, 0.14-0.61) per 22 μg/m(3) interquartile increase in O(3). These associations were only statistically significant in men. In conclusion, long-term exposure to PM(10), SO(2), and O(3) was associated with increased arterial blood pressure and hypertension in the study population.
J Clin Hypertens (Greenwich). 2011;13:836–842. ©2011 Wiley Periodicals, Inc.
Blood pressure (BP) is affected by many environmental factors including ambient temperature, altitude, latitude, noise, and air pollutants. Given their pervasiveness, it is plausible that such factors may also have an impact on hypertension prevalence and control rates. Health care providers should be aware that the environment can play a significant role in altering BP. Although not among the established modifiable risk factors (eg, obesity) for hypertension, reducing exposures when pertinent should be considered to prevent or control hypertension. The authors provide a concise review of the evidence linking diverse environmental factors with BP and suggest an approach for incorporating this knowledge into clinical practice. The authors propose using the term environmental hypertensionology to refer to the study of the effects of environmental factors on BP in clinical and research settings.
Higher ambient fine particulate matter (PM₂.₅) levels can be associated with increased blood pressure and vascular dysfunction.
To determine the differential effects on blood pressure and vascular function of daily changes in community ambient- versus personal-level PM₂.₅ measurements.
Cardiovascular outcomes included vascular tone and function and blood pressure measured in 65 non-smoking subjects. PM₂.₅ exposure metrics included 24 h integrated personal- (by vest monitors) and community-based ambient levels measured for up to 5 consecutive days (357 observations). Associations between community- and personal-level PM₂.₅ exposures with alterations in cardiovascular outcomes were assessed by linear mixed models.
Mean daily personal and community measures of PM₂.₅ were 21.9±24.8 and 15.4±7.5 μg/m³, respectively. Community PM₂.₅ levels were not associated with cardiovascular outcomes. However, a 10 μg/m³ increase in total personal-level PM₂.₅ exposure (TPE) was associated with systolic blood pressure elevation (+1.41 mm Hg; lag day 1, p<0.001) and trends towards vasoconstriction in subsets of individuals (0.08 mm; lag day 2 among subjects with low secondhand smoke exposure, p=0.07). TPE and secondhand smoke were associated with elevated systolic blood pressure on lag day 1. Flow-mediated dilatation was not associated with any exposure.
Exposure to higher personal-level PM₂.₅ during routine daily activity measured with low-bias and minimally-confounded personal monitors was associated with modest increases in systolic blood pressure and trends towards arterial vasoconstriction. Comparable elevations in community PM₂.₅ levels were not related to these outcomes, suggesting that specific components within personal and background ambient PM₂.₅ may elicit differing cardiovascular responses.
In 2004, the first American Heart Association scientific statement on "Air Pollution and Cardiovascular Disease" concluded that exposure to particulate matter (PM) air pollution contributes to cardiovascular morbidity and mortality. In the interim, numerous studies have expanded our understanding of this association and further elucidated the physiological and molecular mechanisms involved. The main objective of this updated American Heart Association scientific statement is to provide a comprehensive review of the new evidence linking PM exposure with cardiovascular disease, with a specific focus on highlighting the clinical implications for researchers and healthcare providers. The writing group also sought to provide expert consensus opinions on many aspects of the current state of science and updated suggestions for areas of future research. On the basis of the findings of this review, several new conclusions were reached, including the following: Exposure to PM <2.5 microm in diameter (PM(2.5)) over a few hours to weeks can trigger cardiovascular disease-related mortality and nonfatal events; longer-term exposure (eg, a few years) increases the risk for cardiovascular mortality to an even greater extent than exposures over a few days and reduces life expectancy within more highly exposed segments of the population by several months to a few years; reductions in PM levels are associated with decreases in cardiovascular mortality within a time frame as short as a few years; and many credible pathological mechanisms have been elucidated that lend biological plausibility to these findings. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM(2.5) exposure and cardiovascular morbidity and mortality. This body of evidence has grown and been strengthened substantially since the first American Heart Association scientific statement was published. Finally, PM(2.5) exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality.
A short-term increase in fine particulate matter air pollution (PM(2.5)) concentration increases the risk for myocardial infarctions, strokes, and heart failure exacerbations. An important mechanism likely contributing to these associations is an elevation in arterial blood pressure (BP). Exposure to ambient PM(2.5) even at present-day concentrations can increase BP within a period of a few days while long-term exposure might also promote the development of chronic hypertension. Controlled human and animal experiments have corroborated the veracity of these findings and elucidated plausible biological mechanisms. PM(2.5) deposition within the pulmonary tree is capable of rapidly triggering autonomic nervous system imbalance, thereby increasing BP within minutes of inhalation. In addition, fine particles can instigate a systemic pro-inflammatory response over a more prolonged period of exposure. Higher circulating levels of activated immune cells and inflammatory cytokines could consequently cause vascular endothelial dysfunction leading to an imbalance in vascular homeostatic responses. Indeed, chronic PM(2.5) exposure augments pro-vasoconstrictive pathways while blunting vasodilator capacity. Finally, certain particle constituents (e.g., metals, organic compounds, and ultra-fine particles) might also be capable of reaching the systemic circulation upon inhalation and thereafter directly impair vascular function. At the molecular level, the generation of oxidative stress with the consequent up-regulation of redox sensitive pathways appears to be a common and fundamental mechanism involved in the instigation of these pro-hypertensive responses. Due to the ubiquitous, continuous and often involuntary nature of exposure, PM(2.5) may be an important and under-appreciated worldwide environmental risk factor for increased arterial BP.
Associations between blood pressure (BP) and ambient air pollution have been inconsistent. No studies have used ambulatory BP monitoring and outdoor home air-pollutant measurements with time-activity-location data. We address these gaps in a study of 64 elderly subjects with coronary artery disease, living in retirement communities in the Los Angeles basin.
Subjects were followed up for 10 days with hourly waking ambulatory BP monitoring (n = 6539 total measurements), hourly electronic diaries for perceived exertion and location, and real-time activity monitors (actigraphs). We measured hourly outdoor home pollutant gases, particle number, PM2.5, organic carbon, and black carbon. Data were analyzed with mixed models controlling for temperature, posture, actigraph activity, hour, community, and season.
We found positive associations of systolic and diastolic BP with air pollutants. The strongest associations were with organic carbon (especially its estimated fossil-fuel- combustion fraction), multiday average exposures, and time periods when subjects were at home. An interquartile increase in 5-day average organic carbon (5.2 microg/m) was associated with 8.2 mm Hg higher mean systolic BP (95% confidence interval = 3.0-13.4) and 5.8 mm Hg higher mean diastolic BP (3.0-8.6). Associations of BP with 1-8 hour average air pollution were stronger with reports of moderate to strenuous physical exertion but not with higher actigraph motion. Associations were also stronger among 12 obese subjects.
Exposure to primary organic components of fossil fuel combustion near the home were strongly associated with increased ambulatory BP in a population at potential risk of heart attack. Low fitness or obesity may increase the effects of pollutants.
Fine particulate matter air pollution plus ozone impairs vascular function and raises diastolic blood pressure. We aimed to determine the mechanism and air pollutant responsible. The effects of pollution on heart rate variability, blood pressure, biomarkers, and brachial flow-mediated dilatation were determined in 2 randomized, double-blind, crossover studies. In Ann Arbor, 50 subjects were exposed to fine particles (150 microg/m(3)) plus ozone (120 parts per billion) for 2 hours on 3 occasions with pretreatments of an endothelin antagonist (Bosentan, 250 mg), antioxidant (Vitamin C, 2 g), or placebo. In Toronto, 31 subjects were exposed to 4 different conditions (particles plus ozone, particles, ozone, and filtered air). In Toronto, diastolic blood pressure significantly increased (2.9 and 3.6 mm Hg) only during particle-containing exposures in association with particulate matter concentration and reductions in heart rate variability. Flow-mediated dilatation significantly decreased (2.0% and 2.9%) only 24 hours after particle-containing exposures in association with particulate matter concentration and increases in blood tumor necrosis factor alpha. In Ann Arbor, diastolic blood pressure significantly similarly increased during all of the exposures (2.5 to 4.0 mm Hg), a response not mitigated by pretreatments. Flow-mediated dilatation remained unaltered. Particulate matter, not ozone, was responsible for increasing diastolic blood pressure during air pollution inhalation, most plausibly by instigating acute autonomic imbalance. Only particles from urban Toronto additionally impaired endothelial function, likely via slower proinflammatory pathways. Our findings demonstrate credible mechanisms whereby fine particulate matter could trigger acute cardiovascular events and that aspects of exposure location may be an important determinant of the health consequences.
Exposure to ambient air pollution has been associated with increases in blood pressure. We have previously demonstrated activation of the Rho/Rho kinase pathway in experimental hypertension in rats. In this investigation, we evaluated the effects of particulate matter of < 2.5 microm (PM(2.5)) exposure on cardiovascular responses and remodeling and tested the effect of Rho kinase inhibition on these effects. C57BL/6 mice were exposed to concentrated ambient PM(2.5) or filtered air for 12 wk followed by a 14-day ANG II infusion in conjunction with fasudil, a Rho kinase antagonist, or placebo treatment. Blood pressure was monitored, followed by analysis of vascular function and ventricular remodeling indexes. PM(2.5) exposure potentiated ANG II-induced hypertension, and this effect was abolished by fasudil treatment. Cardiac and vascular RhoA activation was enhanced by PM(2.5) exposure along with increased expression of the guanine exchange factors (GEFs) PDZ-RhoGEF and p115 RhoGEF in PM(2.5)-exposed mice. Parallel with increased RhoA activation, PM(2.5) exposure increased ANG II-induced cardiac hypertrophy and collagen deposition, with these increases being normalized by fasudil treatment. In conclusion, PM(2.5) potentiates cardiac remodeling in response to ANG II through RhoA/Rho kinase-dependent mechanisms. These findings have implications for the chronic cardiovascular health effects of air pollution.
Recent studies have suggested a link between exposure to ambient particulate matter <2.5 microm in diameter (PM(2.5)) and adverse cardiovascular outcomes. The objective of this study was to examine the effects of differing community-level exposure to PM(2.5) on daily measures of blood pressure (BP) among an adult population. During the period May 2002 through April 2003, BP was examined at 2 time points for 347 adults residing in 3 distinct communities of Detroit, Michigan. Exposure to PM(2.5) was assessed in each community during this period, along with multivariate associations between PM(2.5) and BP. In models combining all 3 of the communities, PM(2.5) was significantly associated with systolic blood pressure; a 10-microg/m(3) increase in daily PM(2.5) was associated with a 3.2-mm Hg increase in systolic blood pressure (P=0.05). However, in models that added a location interaction, larger effects were observed for systolic blood pressure within the community with highest PM(2.5) levels; a 10-microg/m(3) increase in daily PM(2.5) was associated with a 8.6-mm Hg increase in systolic blood pressure (P=0.01). We also found young age (<55 years) and not taking BP medications to be significant predictors of increased BP effects. Among those taking BP medications, the PM(2.5) effect on BP appeared to be mitigated, partially explaining the age effect, because those participants <55 years of age were less likely to take BP medications. Short-term increases in exposure to ambient PM(2.5) are associated with acute increases in BP in adults, especially within communities with elevated levels of exposure.
The effects of climate and altitude on casual blood pressure are examined from the perspectives of initial exposure, acclimatization, long-term residence, and birthplace. Hot arid and hot humid climates seem to have little effect on blood pressure, although a slight reduction may be found in some naturally acclimatized groups. Exposure of the total body to mild cold likewise has little apparent effect. Local exposure of the extremities to severe cold occasions significant increases in blood pressure during exposure but not at other times. Acclimatization reduces but does not eliminate that response. The effects of altitude on blood pressure are variable. There is initial hypertension, followed by gradual normalization. After years of residence at high altitude blood pressure may actually be lower than that observed among residents at sea level.
The age-specific relevance of blood pressure to cause-specific mortality is best assessed by collaborative meta-analysis of individual participant data from the separate prospective studies.
Information was obtained on each of one million adults with no previous vascular disease recorded at baseline in 61 prospective observational studies of blood pressure and mortality. During 12.7 million person-years at risk, there were about 56000 vascular deaths (12000 stroke, 34000 ischaemic heart disease [IHD], 10000 other vascular) and 66000 other deaths at ages 40-89 years. Meta-analyses, involving "time-dependent" correction for regression dilution, related mortality during each decade of age at death to the estimated usual blood pressure at the start of that decade.
Within each decade of age at death, the proportional difference in the risk of vascular death associated with a given absolute difference in usual blood pressure is about the same down to at least 115 mm Hg usual systolic blood pressure (SBP) and 75 mm Hg usual diastolic blood pressure (DBP), below which there is little evidence. At ages 40-69 years, each difference of 20 mm Hg usual SBP (or, approximately equivalently, 10 mm Hg usual DBP) is associated with more than a twofold difference in the stroke death rate, and with twofold differences in the death rates from IHD and from other vascular causes. All of these proportional differences in vascular mortality are about half as extreme at ages 80-89 years as at ages 40-49 years, but the annual absolute differences in risk are greater in old age. The age-specific associations are similar for men and women, and for cerebral haemorrhage and cerebral ischaemia. For predicting vascular mortality from a single blood pressure measurement, the average of SBP and DBP is slightly more informative than either alone, and pulse pressure is much less informative.
Throughout middle and old age, usual blood pressure is strongly and directly related to vascular (and overall) mortality, without any evidence of a threshold down to at least 115/75 mm Hg.
Multiple studies have demonstrated a consistent association between ambient particulate air pollution and increased risk of hospital admissions and deaths for cardiovascular causes. We investigated the associations between fine particulate pollution (PM2.5) and blood pressure during 631 repeated visits for cardiac rehabilitation in 62 Boston residents with cardiovascular disease.
Blood pressure, cardiac risk factor, and exercise data were abstracted from records of rehabilitation visits between 1999 and 2001. We applied mixed-effect models, controlling for body mass index, age, gender, number of visits, hour of day, and weather variables. For an increase from the 10th to the 90th percentile in mean PM2.5 level during the 5 days before the visit (10.5 microg/m3), there was a 2.8-mm Hg (95% CI, 0.1 to 5.5) increase in resting systolic, a 2.7-mm Hg (95% CI, 1.2 to 4.3) increase in resting diastolic, and a 2.7-mm Hg (95% CI, 1.0 to 4.5) increase in resting mean arterial blood pressure. The mean PM2.5 level during the 2 preceding days (13.9 microg/m3) was associated with a 7.0-mm Hg (95% CI, 2.3 to 12.1) increase in diastolic and a 4.7-mm Hg (95% CI, 0.5 to 9.1) increase in mean arterial blood pressure during exercise in persons with resting heart rate > or =70 bpm, but it was not associated with an increase in blood pressure during exercise in persons with heart rate <70 bpm.
In patients with preexisting cardiac disease, particle pollution may contribute to increased risk of cardiac morbidity and mortality through short-term increases in systemic arterial vascular narrowing, as manifested by increased peripheral blood pressure.
Multiple studies have documented an increased incidence of cardiovascular events in the winter, but the pathophysiologic mechanisms remain incompletely understood. It was hypothesized that brachial flow and flow-mediated dilation (FMD) would vary by season and temperature. Season and temperature were related to ultrasonic brachial artery endothelium-dependent FMD% (n = 2,587), baseline flow velocity, and maximal reactive hyperemia (n = 1,973) in the Framingham Offspring Cohort (mean age 61 +/- 10 years, 53% women). Outdoor temperatures were obtained from National Climate Data Center records for Bedford, Massachusetts (about 14 miles from the testing site), and the examination room temperature was measured. In multivariate models, FMD% was highest in summer and lowest in winter (3.01 +/- 0.09% vs 2.56 +/- 0.10%, respectively, p = 0.02 for differences across all 4 seasons). FMD% was highest in the warmest and lowest in the coldest outdoor-temperature quartiles. In stepwise models adjusting for risk factors and selecting among season, outdoor temperature, and room temperature, FMD% was associated with season (p = 0.02); temperature did not enter the model. In contrast, hyperemic flow velocity was significantly lower for cooler and higher for warmer room temperatures (p = 0.02 overall); season did not enter the model. Season and outdoor and room temperature were each retained in a stepwise model of baseline flow velocity (p <0.0001, p = 0.02, and p <0.0001, respectively). In conclusion, a significant association was observed between season and FMD%. Microvascular vasodilator function, as reflected by hyperemic flow velocity, was more strongly related to temperature than season. Endothelial dysfunction may be 1 of the mechanisms influencing seasonal variation in cardiovascular events.