Particle Depletion Does Not Remediate Acute Effects of Traffic-related Air Pollution and Allergen. A Randomized, Double-Blind Crossover Study

Wooding, Denise J.; Ryu, Min Hyung; Hüls, Anke; Lee, Andrew D.; Lin, David; Rider, Christopher F.; Yuen, Alexander K. L.; Carlsten, Chris

doi:10.1164/rccm.201809-1657oc

Cited by 51 publications

(64 citation statements)

References 42 publications

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“…As a final example of minimal coverage of key endpoints, we note that only 2 studies investigated oxidative damage to DNA. There was an absence of attention to the role of co-exposures [41], systemic cellular immune responses (and related genetic predispositions) [42] or anti-microbial defence [43], important within the broader air pollution literature; these gaps should be addressed in future studies.…”

Section: Discussionmentioning

confidence: 99%

Controlled human exposures to wood smoke: a synthesis of the evidence

2020

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Background Exposure to particulate matter (PM) from wood combustion represents a global health risk, encompassing diverse exposure sources; indoor exposures due to cooking in developing countries, ambient PM exposures from residential wood combustion in developed countries, and the predicted increasing number of wildfires due to global warming. Although physicochemical properties of the PM, as well as the exposure levels vary considerably between these sources, controlled human exposure studies may provide valuable insight to the harmful effects of wood smoke (WS) exposures in general. However, no previous review has focused specifically on controlled human exposure studies to WS. Results The 22 publications identified, resulting from 12 controlled human studies, applied a range of combustion conditions, exposure levels and durations, and exercise components in their WS exposure. A range of airway, cardiovascular and systemic endpoints were assessed, including lung function and heart rate measures, inflammation and oxidative stress. However, the possibility for drawing general conclusions was precluded by the large variation in study design, resulting in differences in physicochemical properties of WS, effective dose, as well as included endpoints and time-points for analysis. Overall, there was most consistency in reported effects for airways, while oxidative stress, systemic inflammation and cardiovascular physiology did not show any clear patterns. Conclusion Based on the reviewed controlled human exposure studies, conclusions regarding effects of acute WS exposure on human health are premature. Thus, more carefully conducted human studies are needed. Future studies should pay particular attention to the applied WS exposure, to assure that both exposure levels and PM properties reflect the research question.

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Section: Discussionmentioning

confidence: 99%

Controlled human exposures to wood smoke: a synthesis of the evidence

2020

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“…Of these pollutants, PM has a complex composition that includes metals, elemental carbon and organic carbon (both in hydrocarbons and peptides), sulphates and nitrates, etc. (Ghio et al, 2012;Wooding et al, 2019).…”

Section: Why Did This Coronavirus Spread So Rapidly In Italy?mentioning

confidence: 99%

Factors determining the diffusion of COVID-19 and suggested strategy to prevent future accelerated viral infectivity similar to COVID

Coccia

2020

Science of The Total Environment

564

568

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This study has two goals. The first is to explain the geo-environmental determinants of the accelerated diffusion of COVID-19 in Italy that is generating a high level of deaths. The second is to suggest a strategy to cope with future epidemic threats having accelerated viral infectivity in society. Using data on N=55 Italian province capitals, and data of infected individuals at as of April 7 th , 2020, results reveal that the accelerate and vast diffusion of COVID-19 in North Italy has a high association with air pollution of cities measured with days exceeding the limits set for PM10 (particulate matter 10 micrometers or less in diameter) or ozone in previous years. In particular, hinterland cities with average higher number of days exceeding the limits set for PM10 (and a low intensity of wind speed) have a very high number of infected people on 7 th April, 2020 (arithmetic mean about 2,200 infected, with average polluted days greater than 80), than coastal cities also having days of exceeding the limits set for PM10 or ozone but with high intensity of wind speed (arithmetic mean about 944.70 infected individuals, with about 60 average polluted days); moreover, cities having more than 100 days of air pollution (exceeding the limits set for PM10), they have a very high average number of infected people (about 3,350 infected individuals, 7 th April 2020), whereas cities having less than 100 days of air pollution, they have a lower average number of infected individuals (about 1014). The findings here also suggest that to minimize the impact of future epidemics similar to COVID-19, the max number of days per year in which Italian provincial capitals can exceed the limits set for PM10 or for ozone, considering their meteorological conditions, is about 48 days. Moreover, results here reveal that the explanatory variable of air pollution in cities under study seems to be a more important predictor in the initial phase of diffusion (on 17 th March 2020, b1 = 1.27, p<0.001) than interpersonal contacts (b2 = 0.31, p<0.05). In the second phase of maturity of the transmission dynamics of COVID-19, air pollution reduces intensity (on 7 th April, 2020 with b'1 = .81, p<0.001) also because of indirect effect of lockdown, whereas coefficient of transmission by interpersonal contacts has stability (b'2 = 0.31, p<0.01). This result reveals that accelerated transmissions dynamics of COVID-19 is due to mainly to the mechanism of "air pollution-to-human transmission" rather than "human-to-human transmission". Overall, then, transmission dynamics of viral infectivity, such as COVID-19, is due to systemic causes: general factors that are the same for all regions (e.g., biological characteristics of virus, incubation period, etc.) and specific factors which are different for each region (e.g., complex interaction between air pollution, meteorological conditions and biological characteristics of viral infectivity) and health level of individuals (habits, immune system, age, sex, etc.). Lessons learned for COVID-19 in the case study o...

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“…39 DE and allergen coexposure negatively impacts lung function, increases CD4, IL-4, CD138, and nasal elastase in the respiratory submucosa of AR subjects; increases in blood neutrophils (24 hours) and eosinophils (24 and 48 hours) postexposure were also found. 39,40 Additionally, co-exposure to allergen and DE alters the expression of allergen-induced secreted proteins linked to the protein phosphatase 2A pathway and the MAPK1-ERK1/3 axis, which regulates the response to oxidative stress and inflammation, respectively. 41 Other forms of air pollutant exposure include oil fly ash, a particulate produced from coal combustion.…”

Section: Recent Studies and Current Treatmentsmentioning

confidence: 99%

“…(Continued) studies demonstrating that NO 2 can enhance airway response to an allergen, but a definite cause is unclear. 40,49…”

Section: Recent Studies and Current Treatmentsmentioning

confidence: 99%

<p>Air Pollution and Allergic Rhinitis: Role in Symptom Exacerbation and Strategies for Management</p>

Li¹,

Sayeau²,

Ellis³

2020

JAA

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This article reviews the current understanding of the role of air pollution in both the symptom exacerbation and rising prevalence of allergic rhinitis (AR) for the development of future AR therapeutics and management strategies. We discuss the epidemiological evidence for this relationship through birth cohort studies, the economic impact of AR, and the influence of air pollution through the lens of the exposome framework of allergic disease development. This is followed by a discussion on the influence of diesel exhaust and diesel exhaust particles (DEP) from motor vehicle emissions and their implication in the rising prevalence of allergic disease and allergic sensitization through triggering inflammatory signalling pathways that exacerbate AR symptoms. Finally, a summary is provided of clinical trials assessing the influence of air pollution on AR with a depiction of currently available therapies and management strategies. Future directions in the development of AR modalities given the air pollution-mediated symptom exacerbation are challenged with unfolding the complex gene-environment interaction product of heterogenous AR presentation.

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Particle Depletion Does Not Remediate Acute Effects of Traffic-related Air Pollution and Allergen. A Randomized, Double-Blind Crossover Study

Cited by 51 publications

References 42 publications

Controlled human exposures to wood smoke: a synthesis of the evidence

Controlled human exposures to wood smoke: a synthesis of the evidence

Factors determining the diffusion of COVID-19 and suggested strategy to prevent future accelerated viral infectivity similar to COVID

<p>Air Pollution and Allergic Rhinitis: Role in Symptom Exacerbation and Strategies for Management</p>

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