Particulate air pollution and vascular reactivity: the bus stop study

Dales, Robert; Liu, Ling; Szyszkowicz, Mieczysław; Dalipaj, Mary; Willey, Jeff B.; Kulka, Ryan; Ruddy, Terrence D.

doi:10.1007/s00420-007-0199-7

Cited by 71 publications

(44 citation statements)

References 23 publications

(24 reference statements)

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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%

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%

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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“…In healthy adults, very short-term exposure to elevated levels of ambient PM from traffic sources while exercising for 30 minutes near roadways 195 and when resting by bus stops for 2 hours 196 has been related to impaired endothelium-dependent vasodilation. Daily changes in ambient gaseous pollutants (SO 2 and NO x ) in Paris, France, have also been associated with impaired endothelium-dependent vasodilation among nonsmoking men.…”

Section: Vascular Functionmentioning

confidence: 99%

Particulate Matter Air Pollution and Cardiovascular Disease

Brook¹,

Rajagopalan²,

Pope³

et al. 2010

Circulation

5,431

3,225

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Abstract-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 Ͻ2.5 m 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. (Circulation. 2010;121:2331-2378.)

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“…Epidemiological studies demonstrate that present -day levels of PM are capable of elevating arterial blood pressure (BP) within a period of a few days (Linn et al, 1999 ;Brauer et al, 2001 ;Ibald -Mulli et al, 2001, 2004Zanobetti et al, 2004 ;Chuang et al, 2005 ;Santos et al, 2005 ;Harrabi et al, 2006 ;Madsen and Nafstad, 2006 ;Choi et al, 2007 ;Liu et al, 2007 ;McCracken et al, 2007 ;Auchincloss et al, 2008 ;Dvonch et al, 2009 ;Brook et al, 2010 ). Controlled human and animal experiments have corroborated the veracity of this relationship under certain scenarios whereby BP can increase within only hours of exposure (Gong et al, 2003 ;Mills et al, 2005Mills et al, , 2007Mills et al, , 2008Urch et al, 2005 ;Dales et al, 2007 ;Br ä uner et al, 2008 ;Fang et al, 2008 ;Shah et al, 2008 ;Brook et al, 2009 ).…”

Section: Introductionmentioning

confidence: 90%

“…There have been fi ve positive and negative studies each (Table 18.2 ) (Gong et al, 2003 ;Mills et al, 2005Mills et al, , 2007Mills et al, , 2008Urch et al, 2005 ;Dales et al, 2007 ;Br ä uner et al, 2008 ;Fang et al, 2008 ;Shah et al, 2008 ;Brook et al, 2009 ). As with the epidemiology, most of these protocols were not designed with the explicit intent to focus on BP changes as the primary outcome.…”

Section: Controlled Exposure Studiesmentioning

confidence: 99%