Blood Pressure Response to Controlled Diesel Exhaust Exposure in Human Subjects

Cosselman, Kristen; Krishnan, Ramiah; Oron, Assaf P.; Jansen, Karen; Peretz, Alon; Sullivan, Jeffrey; Larson, Timothy V.; Kaufman, Joel D.

doi:10.1161/hypertensionaha.111.186593

Cited by 112 publications

(98 citation statements)

References 21 publications

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“…Assessed as an overall effect, this change in brachial artery caliber is similar to that observed in a previous study by our group (7), which found an average 0.11-mm decrease in BAd 30 minutes after exposure to DE at 200 mg/m 3 . This finding adds to the growing body of literature confirming that acute exposure to traffic-related air pollutants has a consistent and measurable effect on vasocontractility (7,(14)(15)(16)(17)(18) associated with a simultaneous rise in systemic blood pressure (9,19). Interestingly, in this study, we found evidence that both genetic variations and AO supplementation may alter individual susceptibility to the DE exposure.…”

Section: Discussionsupporting

confidence: 75%

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Pretreatment with Antioxidants Augments the Acute Arterial Vasoconstriction Caused by Diesel Exhaust Inhalation

Sack

Jansen

Cosselman

et al. 2016

Am J Respir Crit Care Med

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Rationale: Diesel exhaust inhalation, which is the model trafficrelated air pollutant exposure, is associated with vascular dysfunction.Objectives: To determine whether healthy subjects exposed to diesel exhaust exhibit acute vasoconstriction and whether this effect could be modified by the use of antioxidants or by common variants in the angiotensin II type 1 receptor (AGTR1) and other candidate genes.Methods: In a genotype-stratified, double-blind, four-way crossover study, 21 healthy adult subjects were exposed at rest in a randomized, balanced order to diesel exhaust (200 mg/m 3 particulate matter with an aerodynamic diameter < 2.5 mm [PM 2.5 ]) and filtered air, and to pretreatment with antioxidants (Nacetylcysteine and ascorbate) and placebo. Before and after each exposure, brachial artery diameter (BAd) was assessed using ultrasound. Changes in BAd were compared across pretreatment and exposure sessions. Gene-exposure interactions were evaluated in the AGTR1 A1166C polymorphism, on which recruitment was stratified, and other candidate genes, including TRPV1 and GSTM1. Conclusions: We confirmed that short-term exposure to diesel exhaust in healthy subjects is associated with acute vasoconstriction in a conductance artery and found suggestive evidence of involvement of nociception and renin-angiotensin systems in this effect. Pretreatment with an antioxidant regimen increased vasoconstriction.

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Section: Discussionsupporting

confidence: 75%

“…Some of the results of this study have been previously reported in the form of an abstract (8). Cosselman and colleagues previously published that DE exposure was associated with a rise in systemic blood pressure using data from this experiment combined with two additional studies using our exposure chamber (9).…”

mentioning

confidence: 92%

Pretreatment with Antioxidants Augments the Acute Arterial Vasoconstriction Caused by Diesel Exhaust Inhalation

Sack

Jansen

Cosselman

et al. 2016

Am J Respir Crit Care Med

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“…However, consistent with our findings, several studies measuring the association between exposure to environmental pollutants (other than SHS) and BP have reported increases in the systolic BP, with no similar increase in the diastolic BP. 28,29 In addition, systolic BP has recently been shown to be more important than the diastolic BP in estimating the risk of CVD. 28 This study has numerous strengths.…”

Section: Discussionmentioning

confidence: 99%

Association of Serum Cotinine Levels and Hypertension in Never Smokers

2013

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Seated systolic and diastolic BPs were measured using a mercury sphygmomanometer according to the American Heart Association and the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7). 13,14 Up to 3 measurements were averaged for systolic and diastolic pressures. Patients were considered hypertensive if they reported physician diagnosis of hypertension, current BP-reducing medication use, or had systolic BP ≥140 mm Hg and diastolic BP ≥90 mm Hg based on JNC 7 criteria. 13Abstract-Hypertension is a major public health problem. Identifying novel risk factors for hypertension, including widely prevalent environmental exposures, is therefore important. Active smoking is a well-known risk factor for hypertension and cardiovascular diseases. However, there are no studies investigating the relationship between secondhand smoke exposure, measured objectively by serum cotinine, and high blood pressure among never smokers. We examined 2889 never smokers from the National Health and Nutrition Examination Survey 2005-2008. Our exposure of interest was secondhand smoke exposure among never smokers, estimated by serum cotinine level, and our main outcome was hypertension (n=1004). We found that in never smokers, higher serum cotinine levels were positively associated with hypertension. In comparison with those with serum cotinine levels ≤0.025 ng/mL, the multivariable odds ratio (95% confidence interval) of hypertension among those with serum cotinine levels ≥0.218 ng/mL was 1.44 (1.01-2.04). In addition, higher serum cotinine was positively associated with mean change in systolic blood pressure (odds ratio [95% confidence interval], 3.24 [0.86-5.63]; P=0.0061). However, no association was present with diastolic blood pressure. In conclusion, in never smokers, higher secondhand smoke exposure measured objectively by serum cotinine levels was found to be associated with systolic blood pressure and hypertension independent of age, sex, ethnicity, education, alcohol drinking, body mass index, glycohemoglobin, total cholesterol, and other confounders. Briefly, the serum sample was spiked with methyl-D3 cotinine as an internal standard, and after an equilibration period, the sample was applied to a basified solid-phase extraction column. Cotinine was extracted off the column with methylene chloride, the organic extract was concentrated, and the residue was injected onto a short, C18 high-performance liquid chromatography column. The eluant from these injections was monitored by atmospheric pressure chemical ionization-tandem mass spectrometry, and the m/z 80 daughter ion from the m/z 177 quasimolecular ion was quantitated, along with additional ions for the internal standard, external standard, and for confirmation. Cotinine concentrations were derived from the ratio of native/labeled cotinine in the sample, by comparisons to a standard curve. Detailed description of serum cotinine measurement in NHANES is available online.12 Serum total cholesterol was...

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“…Another recent controlled human inhalation study reported that exposure to diesel exhaust was associated with a rapid and measureable increase in SBP but not DBP. 15 Furthermore, some authors even reported that there was a small significant decrease in DBP and SBP and hypertension in association with particulate air pollution. 16 The reasons for inconsistent effects of ambient air…”

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confidence: 99%

Association Between Long-Term Air Pollution and Increased Blood Pressure and Hypertension in China

Qian²,

et al. 2013

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http://hyper.ahajournals.org/ Downloaded from Dong et al Effects of Air Pollution on Blood Pressure 579pollution on BP in different parts of the world are unclear but may result from spatial and temporal variability in pollution sources and composition. 17,18 Compared with short-term effects of air pollution, there is little information on the relation between chronic exposure to air pollution and prevalent hypertension. Inconsistent results have also been reported on the association between incident hypertension and air pollution. For instance, Coogan et al 19 showed in a 10-year follow-up for incident hypertension and diabetes mellitus of black women from Los Angeles that NO X (but less PM 2.5 ) borderline increased the risk of becoming hypertensive. However, Sørensen et al 20 reported that longterm exposure (1 and 5 years) to NO X was not associated with incident self-reported hypertension in a Danish cohort. We hypothesized that at the population level, long-term exposure to ambient air pollution is associated with higher BP and higher prevalence of hypertension among humans. In this study, we tested this hypothesis in the 11 Districts Chinese Study, a cross-sectional study of air pollution and adult health in a large, well-characterized population-based sample, residing in northeast China, where there are wide differences in inter-and intracity gradients and ambient pollutant levels, offering a valuable opportunity to assess the associations between exposure and response. Methods Study Cities Selection and Subject RecruitmentMore than 20 million people reside in 14 cities in Liaoning province in northeast China. To maximize the inter-and intracity gradients of the pollutants of interest and minimize the correlation between district-specific ambient pollutants, in April 2009, we selected 3 cities (Shenyang, Anshan, and Jinzhou) based on the results of air pollution measurements between 2006 and 2008. There are 5, well-identified geographic districts in Shenyang, and 3 districts in Anshan and Jinzhou, respectively. Three communities within 1 km of air-monitoring sites were randomly chosen from these districts resulting in 33 locales, and from each of these, 700 to 1000 households were randomly identified. One participant, aged 18 to 74 years, was selected from each household without replacement. Our entry criterion was that the subject should have lived at that place for at least 5 years. The design and conduct of this investigation was reviewed and approved by Human Studies Committee of China Medical University. Before data collection, a written informed consent form was obtained from each participant. Ambient Air PollutionIn each of the selected study districts, there was only 1 municipal air pollution monitoring station, which was located 1 mile from the participants' homes. Measurements of PM 10 , SO 2 , NO 2 , and O 3 concentrations from 2006 to 2008 were obtained at the stations. The measurements were subject to uniform criteria for monitoring, siting, instrumentation, and quality assurance. Thes...

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Blood Pressure Response to Controlled Diesel Exhaust Exposure in Human Subjects

Cited by 112 publications

References 21 publications

Pretreatment with Antioxidants Augments the Acute Arterial Vasoconstriction Caused by Diesel Exhaust Inhalation

Pretreatment with Antioxidants Augments the Acute Arterial Vasoconstriction Caused by Diesel Exhaust Inhalation

Association of Serum Cotinine Levels and Hypertension in Never Smokers

Association Between Long-Term Air Pollution and Increased Blood Pressure and Hypertension in China

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