Nasal challenge with diesel exhaust particles can induce sensitization to a neoallergen in the human mucosa☆☆☆★

Díaz-Sánchez, David; Garcia, Marisol Penichet; Wang, Margaret; Jyrala, Minna; Saxon, Andrew

doi:10.1016/s0091-6749(99)70011-4

Cited by 300 publications

(191 citation statements)

References 24 publications

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“…These acute exacerbations are characterized by increased symptom score as well as the requirement for more frequent medication and hospitalization [39,40]. In addition to these acute effects, which are likely caused by an exacerbation of already existing airway inflammation and airway hyperreactivity, there is increasing evidence that particulate pollutants act as an adjuvant for allergic sensitization to common environmental allergens [25,[42][43][44][45][46]. This raises the possibility that long-term PM exposures may lead to increased prevalence of asthma and allergic diseases.…”

Section: The Impact Of Particulate Pollutants On Asthmamentioning

confidence: 99%

“…The adjuvant effects of ambient PM and DEP have been demonstrated in a number of human and animal studies [42][43][44][45][46]. Combined DEP and ragweed nasal challenge significantly enhances ragweed-specific IgE and IL-4 production in humans [44].…”

Section: The Impact Of Particulate Pollutants On Asthmamentioning

confidence: 99%

“…Combined DEP and ragweed nasal challenge significantly enhances ragweed-specific IgE and IL-4 production in humans [44]. In addition, intranasal instillation of DEP also increased the expression of several CC chemokines including RANTES, MIP-1α, and MCP-1 in the human nose [43]. Gilliland et al reported that individuals with GST M1 null genotype exhibit increased nasal allergic and allergen-specific IgE response to nasal DEP challenge, thereby demonstrating the possible linkage of these responses to an oxidative stress mechanism [73].…”

Section: The Impact Of Particulate Pollutants On Asthmamentioning

confidence: 99%

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The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Xia

Nel

2008

Free Radical Biology and Medicine

821

529

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Ambient particulate matter (PM) is an environmental factor that has been associated with increased respiratory morbidity and mortality. The major effect of ambient PM on the pulmonary system is the exacerbation of inflammation, especially in susceptible people. One of the mechanisms by which ambient PM exerts its proinflammatory effects is the generation of oxidative stress by its chemical compounds and metals. Cellular responses to PM-induced oxidative stress include activation of antioxidant defense, inflammation, and toxicity. The pro-inflammatory effect of PM in the lung is characterized by increased cytokine/chemokine production and adhesion molecule expression. Moreover, there is evidence that ambient PM can act as an adjuvant for allergic sensitization, which raises the possibility that long-term PM exposure may lead to increased prevalence of asthma. In addition to ambient PM, rapid expansion of nanotechnology has introduced the potential that engineered NP may also become airborne and may contribute to pulmonary diseases by novel mechanisms that could include oxidant injury. Currently, little is known about the potential adverse health effect of these particles. In this communication, the mechanisms by which particulate pollutants, including ambient PM and engineered NP, exert their adverse effects through the generation of oxidative stress and the impacts of oxidant injury in the respiratory tract will be reviewed. The importance of cellular antioxidant and detoxification pathways in protecting against particle-induced lung damage will also be discussed.

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Section: The Impact Of Particulate Pollutants On Asthmamentioning

confidence: 99%

Section: The Impact Of Particulate Pollutants On Asthmamentioning

confidence: 99%

Section: The Impact Of Particulate Pollutants On Asthmamentioning

confidence: 99%

See 1 more Smart Citation

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Xia

Nel

2008

Free Radical Biology and Medicine

821

529

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“…In previous work from the CCCEH, pregnant Dominican and AfricanAmerican women, aged [18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35] (2,15). A PAH mixture that reproduced the PAH exposure of the CCCEH participants (Table 1) was produced for our cellular experiments.…”

Section: Pah Mixturementioning

confidence: 99%

“…In one, air pollutants such as diesel, particulate matter, and metals, known triggers of asthma, may induce oxidative stress pathways, causing the formation of excessive reactive oxygen species in the airways and tissue inflammation (3,4,(26)(27)(28)(29). In a second pathway, exposure to diesel may provide a strong adjuvant for allergic sensitization, and such exposure was shown to up-regulate allergic immune mechanisms in the airways (4,(30)(31)(32)(33). PAHs, which are components of exhaust from the incomplete combustion of diesel fuel, were linked directly with the development of respiratory disease by our group (2,7).…”

Section: Treatment With Pahs Reduces the Function Of B 2 Ar (Procatermentioning

confidence: 99%

Polycyclic Aromatic Hydrocarbons Impair Function of β₂-Adrenergic Receptors in Airway Epithelial and Smooth Muscle Cells

Factor

Akhmedov

McDonald

et al. 2011

Am J Respir Cell Mol Biol

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Incomplete combustion produces a pollutant mixture that includes polycyclic aromatic hydrocarbons (PAHs). Previous work by the Columbia Center for Children's Environmental Health (CCCEH) and others linked exposure to PAH with symptoms of asthma and other adverse health effects in young children. Inhaled b 2 -adrenergic agonists are mainstays in the treatment of reactive airway diseases. These exogenous catecholamines engage membrane-bound b 2 -adrenergic receptors (b 2 AR) on airway epithelial and smooth muscle cells to cause airway dilation. We hypothesized that exposure to PAH might similarly interfere with the function of b 2 AR in airway epithelial or smooth muscle cells, reducing the efficacy of a medication important for the treatment of asthma symptoms. A PAH mixture was devised, based on ambient levels measured prenatally among a cohort of pregnant women participating at the CCCEH. Primary airway epithelial and smooth muscle cells were exposed to varying concentrations of the PAH mixture, and expression, function, and signaling of b 2 AR were assessed. Murine tracheal epithelial cells and human airway smooth muscle cells, after exposure to a PAH mixture, exhibited reduced expression and function of b 2 AR. These findings support our hypothesis that environmentally relevant PAHs can impede b 2 AR-mediated airway relaxation, and suggest a new paradigm where air pollutants not only contribute to the pathogenesis of childhood asthma, but also diminish responsiveness to standard therapy.

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Early-Life Exposure to Air Pollution and Childhood Asthma Cumulative Incidence in the ECHO CREW Consortium

Zanobetti,

Ryan,

Coull

et al. 2024

JAMA Netw Open

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ImportanceExposure to outdoor air pollution contributes to childhood asthma development, but many studies lack the geographic, racial and ethnic, and socioeconomic diversity to evaluate susceptibility by individual-level and community-level contextual factors.ObjectiveTo examine early life exposure to fine particulate matter (PM2.5) and nitrogen oxide (NO2) air pollution and asthma risk by early and middle childhood, and whether individual and community-level characteristics modify associations between air pollution exposure and asthma.Design, Setting, and ParticipantsThis cohort study included children enrolled in cohorts participating in the Children’s Respiratory and Environmental Workgroup consortium. The birth cohorts were located throughout the US, recruited between 1987 and 2007, and followed up through age 11 years. The survival analysis was adjusted for mother’s education, parental asthma, smoking during pregnancy, child’s race and ethnicity, sex, neighborhood characteristics, and cohort. Statistical analysis was performed from February 2022 to December 2023.ExposureEarly-life exposures to PM2.5 and NO2 according to participants’ birth address.Main Outcomes and MeasuresCaregiver report of physician-diagnosed asthma through early (age 4 years) and middle (age 11 years) childhood.ResultsAmong 5279 children included, 1659 (31.4%) were Black, 835 (15.8%) were Hispanic, 2555 (48.4%) where White, and 229 (4.3%) were other race or ethnicity; 2721 (51.5%) were male and 2596 (49.2%) were female; 1305 children (24.7%) had asthma by 11 years of age and 954 (18.1%) had asthma by 4 years of age. Mean values of pollutants over the first 3 years of life were associated with asthma incidence. A 1 IQR increase in NO2 (6.1 μg/m3) was associated with increased asthma incidence among children younger than 5 years (HR, 1.25 [95% CI, 1.03-1.52]) and children younger than 11 years (HR, 1.22 [95% CI, 1.04-1.44]). A 1 IQR increase in PM2.5 (3.4 μg/m3) was associated with increased asthma incidence among children younger than 5 years (HR, 1.31 [95% CI, 1.04-1.66]) and children younger than 11 years (OR, 1.23 [95% CI, 1.01-1.50]). Associations of PM2.5 or NO2 with asthma were increased when mothers had less than a high school diploma, among Black children, in communities with fewer child opportunities, and in census tracts with higher percentage Black population and population density; for example, there was a significantly higher association between PM2.5 and asthma incidence by younger than 5 years of age in Black children (HR, 1.60 [95% CI, 1.15-2.22]) compared with White children (HR, 1.17 [95% CI, 0.90-1.52]).Conclusions and RelevanceIn this cohort study, early life air pollution was associated with increased asthma incidence by early and middle childhood, with higher risk among minoritized families living in urban communities characterized by fewer opportunities and resources and multiple environmental coexposures. Reducing asthma risk in the US requires air pollution regulation and reduction combined with greater environmental, educational, and health equity at the community level.

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Nasal challenge with diesel exhaust particles can induce sensitization to a neoallergen in the human mucosa☆☆☆★

Cited by 300 publications

References 24 publications

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Polycyclic Aromatic Hydrocarbons Impair Function of β₂-Adrenergic Receptors in Airway Epithelial and Smooth Muscle Cells

Early-Life Exposure to Air Pollution and Childhood Asthma Cumulative Incidence in the ECHO CREW Consortium

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Nasal challenge with diesel exhaust particles can induce sensitization to a neoallergen in the human mucosa☆☆☆★

Cited by 300 publications

References 24 publications

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Polycyclic Aromatic Hydrocarbons Impair Function of β2-Adrenergic Receptors in Airway Epithelial and Smooth Muscle Cells

Early-Life Exposure to Air Pollution and Childhood Asthma Cumulative Incidence in the ECHO CREW Consortium

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Product

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About

Polycyclic Aromatic Hydrocarbons Impair Function of β₂-Adrenergic Receptors in Airway Epithelial and Smooth Muscle Cells