Hypertension Editors' Picks: Air Pollution.

Abstract

HomeHypertensionVol. 76, No. 2Hypertension Editors’ Picks Free AccessIn BriefPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessIn BriefPDF/EPUBHypertension Editors’ PicksAir Pollution The Editors The Editors Search for more papers by this author Originally published8 Jul 2020https://doi.org/10.1161/HYPERTENSIONAHA.120.15142Hypertension. 2020;76:e18–e22The following articles are being highlighted as part of Hypertension Editors’ Picks series. According to the report of the Lancet Commission on pollution and health, “Pollution is the largest environmental cause of disease and premature death in the world today. Diseases caused by pollution were responsible for an estimated 9 Mio. premature deaths in 2015 - 16% of all deaths worldwide - three times more deaths than from AIDS, tuberculosis, and malaria combined.” These numbers are further supported by WHO estimations on 12.6 Mio global deaths in 2012 caused by unhealthy environments. These numbers will probably be outcompeted by recent estimations on 9 Mio premature global deaths/y solely caused by air pollution (mainly particulates of diameter ≤2.5 µm [PM2.5]). The GBD Study (Global Burden of Disease) 2015 ranked ambient air pollution fifth as a global risk factor for global mortality closing the gap on traditional cardiovascular risk factors such as diabetes, smoking, and hypertension. The European Union applies an annual mean air quality limit of 25 mg/m3 for PM2.5 since 2015, which is 2.5× higher than the guideline concentration of 10 mg/m3 of the WHO and also higher than the annual mean limit in the United States (12 mg/m3), in Canada (10 mg/m3) and in Australia (8 mg/m3), even if the European Union reaches their exposure reduction targets for 2020 (20 mg/m3). The Hypertension abstracts highlighted here have reported an association of PM1.0 exposure with hypertension in children, of different forms of air pollution with preeclampsia, of acute and chronic high ambient PM2.5 exposure with hypertension in China, of maternal PM2.5 exposure with the blood pressure in their offspring (children aged 3–9 years), and that mitigation measures (eg, decreasing PM2.5) lowered hypertension incidence. We have, therefore, collated for our readers the following articles on air pollution published in our Journal from 2017 to 2020.Effects of Home Particulate Air Filtration on Blood Pressure: A Systematic Review1AbstractAir pollution is a major contributor to cardiovascular morbidity and mortality. Fine particulate matter <2.5 µm in diameter may be a modifiable risk factor for hypertension. The benefits of in-home air filtration on systolic blood pressure (BP) and diastolic BP are unclear. To examine the effects of in-home personal air cleaner use on fine particulate exposure and BP, we queried PubMed, Web of Science, Cochrane Central Register, Inspec, and EBSCO GreenFILE databases for relevant clinical trials. Included studies were limited to nonsmoking participants in smoke-free homes with active or sham filtration on indoor fine particulate concentrations and changes in systolic and diastolic BP. Of 330 articles identified, 10 trials enrolling 604 participants who met inclusion criteria were considered. Over a median 13.5 days, there was a significant reduction of mean systolic BP by ≈4 mm Hg (−3.94 mm Hg [95% CI, −7.00 to −0.89]; P=0.01) but a nonsignificant difference in mean diastolic BP (−0.95 mm Hg [95% CI, −2.81 to 0.91]; P=0.32). Subgroup analyses indicated no heterogeneity of effect by age, level of particulate exposure, or study duration. Given the variation in study design, additional study is warranted to confirm and better quantify the observed benefits in systolic BP found with personal air cleaner use.Wintertime Wood Smoke, Traffic Particle Pollution, and Preeclampsia2AbstractPrevious studies have reported associations between ambient fine particle concentrations and preeclampsia; however, the impact of particulate pollution on early- and late-onset preeclampsia is understudied. Furthermore, few studies have examined the association between source-specific particles, such as markers of traffic pollution or wood combustion on adverse pregnancy outcomes. Electronic medical records and birth certificate data were linked with land-use regression models in Monroe County, New York, for 2009 to 2013 to predict monthly pollutant concentrations for each pregnancy until the date of clinical diagnosis during winter (November–April) for 16 116 births. Up to 30% of ambient wintertime fine particle concentrations in Monroe County, New York, is from wood combustion. Multivariable logistic regression was used to separately estimate the odds of preeclampsia (all, early-, and late-onset) associated with each interquartile range increase in fine particles, traffic pollution, and woodsmoke concentrations during each gestational month, adjusting for maternal characteristics, birth hospital, temperature, and relative humidity. Each 3.64 µg/m3 increase in fine particle concentration was associated with an increased odds of early-onset preeclampsia during the first (odds ratio, 1.35 [95% CI, 1.08–1.68]), second (odds ratio, 1.51 [95% CI, 1.23–1.86]), and third (odds ratio, 1.25 [95% CI, 1.06–1.46]) gestational months. Increases in traffic pollution and woodsmoke during the first gestational month were also associated with increased odds of early-onset preeclampsia. Increased odds of late-onset preeclampsia were not observed. Our findings suggest that exposure to wintertime particulate pollution may have the greatest effect on maternal cardiovascular health during early pregnancy.Ambient Airborne Particulates of Diameter ≤1 µm, a Leading Contributor to the Association Between Ambient Airborne Particulates of Diameter ≤2.5 µm and Children’s Blood Pressure3AbstractEvidence on the associations between airborne particulates of diameter ≤1 µm (PM1) and airborne particulates of diameter ≤2.5 µm (PM2.5) and childhood blood pressure (BP) is scarce. To help to address this literature gap, we conducted a study to explore the associations in Chinese children. Between 2012 and 2013, we recruited 9354 children, aged 5 to 17 years, from 62 schools in 7 northeastern Chinese cities. We measured their BP with a mercury sphygmomanometer. We used a spatiotemporal model to estimate daily ambient PM1 and PM2.5 exposures, which we assigned to participants’ home addresses. Associations between particulate matter exposure and BP were evaluated with generalized linear mixed regression models. The findings indicated that exposure to each 10 mg/m3 greater PM1 was significantly associated with 2.56 mm Hg (95% CI, 1.47–3.65) higher systolic BP and 61% greater odds for hypertension (odds ratio, 1.61 [95% CI, 1.18–2.18]). PM1 appears to play an important role in associations reported between PM2.5 exposure and BP, and we found that the ambient PM1/PM2.5 ratio (range, 0.80–0.96) was associated with BP and with hypertension. Age and body weight modified associations between air pollutants and BP (P<0.01), with stronger associations among younger (aged ≤11 years) and overweight/obese children. This study provides the first evidence that long-term exposure to PM1 is associated with hypertension in children, and that PM1 might be a leading contributor to the hypertensive effect of PM2.5. Researchers and policymakers should pay closer attention to the potential health impacts of PM1.Acute Effects of High-Level PM2.5 Exposure on Central Blood Pressure4AbstractCentral aortic blood pressure (BP) has been increasingly recognized as having a closer relationship with cardiovascular risks than peripheral BP. However, the effects of particulate matter pollution on central aortic BP have not been clearly demonstrated. In this study, we assessed the association between short-term ambient fine particulate matter (with particulates of diameter ≤2.5 mum; PM2.5) exposure and central aortic BP in a Chinese community-based population. A total of 4715 visits were in our final analysis, including 2151 visits at the baseline and 2564 visits at the follow-up. Central aortic systolic BP (cSBP) was measured noninvasively using the method of radial artery tonometry with Omron HEM-9000AI machine. Data from air pollution monitoring stations were used to estimate daily PM2.5 exposure. Generalized additive mixed models with clinical and meteorologic covariates adjusted were used to examine the association between PM2.5 exposure and cSBP. The relationships between PM2.5 exposure and cSBP were nonlinear, and significant increments of cSBP were observed when the PM2.5 exposure concentration was above 100 µg/cm3. An interquartile range increase (80.25 µg/m3) in daily PM2.5 on the day of cSBP measurement (lag 0 day) was associated with 2.54 mm Hg (95% CI, 0.92–4.16) elevation in cSBP. The associations of PM2.5 with cSBP were not modified by age, sex, body mass index, medications, and comorbid diseases except for cardiovascular disease. Our findings demonstrated that short-term exposure to high concentration of ambient PM2.5 above 100 µg/cm3 was associated with significant increases in central aortic BP in a Chinese community-based population.Dynamic Changes in Long-Term Exposure to Ambient Particulate Matter and Incidence of Hypertension in Adults5AbstractMany countries dedicated in mitigation of air pollution in the past several decades. However, little is known about how air quality improvement affects health. Therefore, we conducted current study to investigate dynamic changes in long-term exposure to ambient particulate matter (particulates of diameter ≤2.5 µm [PM2.5]) and incidence of hypertension in a large longitudinal cohort. We recruited 134 978 adults aged 18 years or above between 2001 and 2014. All the participants received a series of standard medical examinations, including measurements of BP. The PM2.5 concentration was estimated using a satellite-based spatiotemporal model at a high resolution (1×1 km2). The change in long-term exposure to PM2.5 (DeltaPM2.5) was defined as the difference between the values measured during follow-up and during the immediately preceding visit, and a negative value indicated an improvement in PM2.5 air quality. Time-varying Cox model was used to examine the associations between DeltaPM2.5 and the development of hypertension. The results show that PM2.5 concentrations increased in 2002, 2003, and 2004 but began to decrease in 2005. Every 5 µg/m3 change in exposure to PM2.5 (ie, a DeltaPM2.5 of 5 µg/m3) was associated with a 16% change in the incidence of hypertension (hazard ratio, 0.84 [95% CI, 0.82–0.86]). Both stratified and sensitivity analyses generally yielded similar results. We found that an improvement in PM2.5 exposure is associated with a decreased incidence of hypertension. Our findings demonstrate that air pollution mitigation is an effective strategy to reduce the risk of cardiovascular disease.Differential Effect of Ambient Air Pollution Exposure on Risk of Gestational Hypertension and Preeclampsia6AbstractAlthough ambient air pollution may increase hypertension risk through endothelial damage and oxidative stress, evidence is inconsistent regarding its effect on hypertension in pregnancy. Prior research has evaluated a limited scope of pollution species and often not differentiated preeclampsia, which may have a placental origin, from gestational hypertension. Among 49 607 women with at least 2 singleton deliveries in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Consecutive Pregnancies Study (2002–2010), we estimated criteria pollutant and volatile organic compound levels during pregnancy using Community Multiscale Air Quality models and abstracted gestational hypertension and preeclampsia diagnoses from medical records. Generalized estimating equations accounted for repeat pregnancies and adjusted for ambient temperature and maternal age, race/ethnicity, body mass index, smoking, alcohol, parity, insurance, marital status, and asthma. Air pollution levels were low to moderate (eg, median 41.6 ppb [interquartile range, 38.9–43.7 ppb] for ozone and 35.1 ppb [28.9–40.3 ppb] for nitrogen oxides). Higher levels of most criteria pollutants during preconception and the first trimester were associated with lower preeclampsia risk, whereas higher second-trimester levels were associated with greater gestational hypertension risk. For example, an interquartile increase in first-trimester carbon monoxide was associated with a relative risk of 0.88 (95% CI, 0.81–0.95) for preeclampsia and second-trimester carbon monoxide a relative risk of 1.14 (95% CI, 1.07–1.22) for gestational hypertension. Volatile organic compounds, conversely, were not associated with gestational hypertension but consistently associated with higher preeclampsia risk. These findings further suggest air pollution may affect the development of hypertension in pregnancy, although differing causes of preeclampsia and gestational hypertension may alter these relationships.Long-Term Exposure to Fine Particulate Matter and Hypertension Incidence in China7AbstractThe risk of incident hypertension associated with long-term exposure to fine particulate matter (particulates of diameter ≤2.5 µm [PM2.5]) was still unclear by studies conducted in North America and Europe, and this relationship has rarely been quantified at higher ambient concentrations typically found in developing countries. We aimed to investigate the association between PM2.5 and incident hypertension using the large-scale prospective cohorts in China. We included 59 456 participants without hypertension aged ≥18 years from the China-PAR (Prediction for Atherosclerotic Cardiovascular Disease Risk in China) project. Data on ambient PM2.5 at participants’ residential address were obtained from 2004 to 2015 using a satellite-based spatial-temporal model. Hazard ratios and 95% CIs were calculated for incident hypertension using stratified Cox proportional hazards models with adjustment of potential confounders. The findings indicated that average PM2.5 concentration from 2004 to 2015 at study participants’ address was 77.7 µg/m3. During the follow-up of 364 947 person-years, we identified 13 981 incident hypertension cases. Compared with the lowest quartile exposure of PM2.5, participants in the highest quartile had an increased risk of incident hypertension with a hazard ratio (95% CI) of 1.77 (1.56–2.00). Each 10 µg/m3 increment of PM2.5 concentration could increase 11% risk of hypertension (hazard ratio, 1.11 [95% CI, 1.05–1.17]). This cohort study provided the first evidence from China that long-term exposure to PM2.5 was independently associated with incident hypertension at relatively high ambient concentrations. Stringent strategies on PM2.5 pollution control are warranted to improve the air quality and contribute to the reduction of disease burden of hypertension in China.Maternal Exposure to Ambient Particulate Matter ≤2.5 µm During Pregnancy and the Risk for High Blood Pressure in Childhood8AbstractExposure to ambient air pollution has been associated with greater risk of elevated blood pressure (BP) in adults and children. Recent evidence suggests that air pollution exposure in pregnancy may also portend increased risk for the next generation; however, few studies have examined this relationship. We conducted a prospective study of 1293 mothers in the Boston Birth Cohort (enrolled 1998–2012) and their children who had follow-up visits between 3 and 9 years of age and complete exposure and outcome data. Our primary exposure, ambient particulates of diameter ≤2.5 mum (PM2.5) concentration during pregnancy, was estimated by matching mother’s residential address to the US Environmental Protection Agency’s air quality monitors. We defined our primary outcome child systolic BP (SBP) percentile according to US reference (Fourth Report) and classified elevated BP as SBP ≥90th percentile. Our multivariable-adjusted cubic spline showed a sharp increase in offspring SBP percentile and risk for elevated BP when third-trimester PM2.5 concentration was ≥13 µg/m3. The highest versus lowest tertile of third-trimester PM2.5 exposure was associated with a 4.85 (95% CI, 1.38–8.37) percentile increase in child SBP or a 1.61 (95% CI: 1.13–2.30) times higher risk of child elevated BP. A 5-µg/m3 increment in PM2.5 during the third trimester was associated with a 3.49 (95% CI, 0.71–6.26) percentile increase in child SBP or a 1.47 (95% CI, 1.17–1.85) times higher risk of elevated BP. Our findings suggest that exposure to ambient PM2.5 during the third trimester of pregnancy is associated with elevated BP in children, ages 3 to 9 years.Association Between Hypertensive Disorders in Pregnancy and Particulate Matter in the Contiguous United States, 1999–20049AbstractHypertensive disorders in pregnancy harm both maternal and infant health and have been linked to ambient particulate matter. However, existing studies are restricted to a local scale and remain inconsistent. A large-scale study is required to enrich the epidemiological evidence and explore the potential sources of the inconsistency. Making use of US birth certificates (1999–2004), and monitoring data from the environmental protection agency air quality networks, we associated hypertensive disorders in pregnancy with maternal exposure to fine particles or coarse particles using logistic regression analysis after adjusting for many covariates among >5 million subjects in the contiguous United States. Additional analyses were conducted to examine variations in the associations according to (1) census divisions; (2) individual-level factors; (3) a socioeconomic indicator, county-level poverty; and (4) the concentration of ambient particles. The results indicated that hypertensive disorders in pregnancy were robustly linked to maternal exposure to fine particles with an adjusted odds ratio of 1.10 (95% CIs, 1.08–1.12) per 5 µg/m3 increment in terms of the entire pregnancy mean. Stronger associations were found among white mothers. There were also considerable variations in the association by census division or poverty level among counties. Nonlinear analysis indicated a sublinear dose-response function with a threshold concentration of 9 µg/m3. Based on the national study, we calculated the population attributable fractions and found that 8.1% (6.8%–9.4%) of hypertensive disorder cases were attributable to an entire pregnancy exposure of fine particles. These findings can help policymakers to plan related interventions.Long-Term Effects of Ambient PM2.5 on Hypertension and Blood Pressure and Attributable Risk Among Older Chinese Adults10AbstractLong-term exposure to ambient fine particulate pollution (particulates of diameter ≤2.5 µm [PM2.5]) has been associated with cardiovascular diseases. Hypertension, a major risk factor for cardiovascular diseases, has also been hypothesized to be linked to PM2.5 However, epidemiological evidence has been mixed. We examined long-term association between ambient PM2.5 and hypertension and blood pressure. We interviewed 12 665 participants aged 50 years and older and measured their blood pressures. Annual average PM2.5 concentrations were estimated for each community using satellite data. We applied 2-level logistic regression models to examine the associations and estimated hypertension burden attributable to ambient PM2.5 For each 10 µg/m3 increase in ambient PM2.5, the adjusted odds ratio of hypertension was 1.14 (95% CI, 1.07–1.22). Stratified analyses found that overweight and obesity could enhance the association, and consumption of fruit was associated with lower risk. We further estimated that 11.75% (95% CI, 5.82%–18.53%) of the hypertension cases (corresponding to 914, 95% CI, 453–1442 cases) could be attributable to ambient PM2.5 in the study population. Findings suggest that long-term exposure to ambient PM2.5 might be an important risk factor of hypertension and is responsible for significant hypertension burden in adults in China. A higher consumption of fruit may mitigate, whereas overweight and obesity could enhance this effect.AcknowledgmentsWe thank Thomas Münzel and Andreas Daiber for contributing the introduction to this article.Sources of FundingNone.DisclosuresNone.