Polycyclic aromatic hydrocarbons and childhood asthma

Karimi, Parviz; Peters, Kamau O.; Bidad, Katayoon; Strickland, Paul T.

doi:10.1007/s10654-015-9988-6

Cited by 87 publications

(62 citation statements)

References 139 publications

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“…Exposure to these pollutants has been correlated to various pathological situations, including inflammation, cancer development, cardiovascular and pulmonary diseases 3, 4 . Therefore, PAHs have been classified as priority toxicants by the United States Environmental Protection Agency (US-EPA), the World Health Organization (WHO) and the European Union 5 .…”

Section: Introductionmentioning

confidence: 99%

Benzo(a)pyrene triggers desensitization of β2-adrenergic pathway

Mayati

Podechard

Rineau

et al. 2017

Sci Rep

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Exposure to environmental polycyclic aromatic hydrocarbons (PAHs), such as benzo(a)pyrene (B(a)P), has been linked to several health-threatening risks. PAHs were also shown to hinder adrenergic receptor (ADR) responses. As we previously demonstrated that B(a)P can directly interact with the β2ADR, we investigated here whether B(a)P could decrease β2ADR responsiveness by triggering receptor desensitization phenomena. We firstly showed that exposure to B(a)P reduced β2ADR-mediated epinephrine-induced induction of NR4A gene mRNAs and of intracellular cAMP. Analysis of β2ADR protein expression demonstrated that B(a)P rapidly decreased membrane expression of β2ADR with a subsequent degradation of receptor protein. B(a)P exposure concomitantly rapidly increased the β2ADR mRNA levels. The use of the β-blockers, propranolol and ICI 118.551, demonstrated the involvement of β2ADR itself in this increase. However, sustained exposure to B(a)P induced a diminution of β2ADR mRNA steady-state as a result of the acceleration of its degradation. Together, these results show that, beside the well-known activation of the aryl hydrocarbon receptor, PAH deleterious effects may involve the dysfunction of adrenergic responses through, in part, the desensitization of β2ADR. This may be taken in consideration when β2-agonists/antagonists are administered in patients exposed to important concentrations of PAHs, e.g. in cigarette smokers.

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Section: Introductionmentioning

confidence: 99%

Benzo(a)pyrene triggers desensitization of β2-adrenergic pathway

Mayati

Podechard

Rineau

et al. 2017

Sci Rep

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“…Our analysis identified a significant direct effect of PAHs but not pesticides and PFCs on respiratory tract disease. This was supported by several pieces of evidence, including those suggesting that PAHs are formed mainly by organic fuel combustion and released into the atmosphere (Baek et al, 1991), where they can contribute to risk factors for respiratory cancer and childhood asthma (Bosetti et al, 2007;Karimi et al, 2015;Rota et al, 2014). A meta-analysis study concluded that the relationship between pesticide exposure and respiratory health is controversial (Mamane et al, 2015), and several other studies suggest that occupational exposure to pesticides increases the risks of developing asthma (Fareed et al, 2013;Ye et al, 2013).…”

Section: Discussionmentioning

confidence: 93%

A network biology-based approach to evaluating the effect of environmental contaminants on human interactome and diseases

Iida

Takemoto

2018

Ecotoxicology and Environmental Safety

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Environmental contaminant exposure can pose significant risks to human health. Therefore, evaluating the impact of this exposure is of great importance; however, it is often difficult because both the molecular mechanism of disease and the mode of action of the contaminants are complex. We used network biology techniques to quantitatively assess the impact of environmental contaminants on the human interactome and diseases with a particular focus on seven major contaminant categories: persistent organic pollutants (POPs), dioxins, polycyclic aromatic hydrocarbons (PAHs), pesticides, perfluorochemicals (PFCs), metals, and pharmaceutical and personal care products (PPCPs). We integrated publicly available data on toxicogenomics, the diseasome, protein-protein interactions (PPIs), and gene essentiality and found that a few contaminants were targeted to many genes, and a few genes were targeted by many contaminants. The contaminant targets were hub proteins in the human PPI network, whereas the target proteins in most categories did not contain abundant essential proteins. Generally, contaminant targets and disease-associated proteins were closely associated with the PPI network, and the closeness of the associations depended on the disease type and chemical category. Network biology techniques were used to identify environmental contaminants with broad effects on the human interactome and contaminant-sensitive biomarkers. Moreover, this method enabled us to quantify the relationship between environmental contaminants and human diseases, which was supported by epidemiological and experimental evidence. These methods and findings have facilitated the elucidation of the complex relationship between environmental exposure and adverse health outcomes.

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“…There is reason to believe that traffic pollution could be especially damaging during childhood because burning fossil fuels releases Polycyclic Aromatic Hydrocarbons (PAHs), carbon monoxide, and other toxicants. There are a growing number of epidemiological studies on how PAHs might harm child development, but most of the evidence of the effects of PAHs comes from in-vitro studies of embryonic rodent cells, which have shown that PAHs are potentially mutagenic (Lovasi et al, 2014;Margolis et al, 2016;Perera et al, 2009) or from associational studies that have found increased PAH exposure is associated with increased cases of asthma (Karimi, Peters, Bidad, & Strickland, 2015) and attention deficit hyperactivity disorder and learning disabilities (Abid, Roy, Herbstman, & Ettinger, 2014).…”

Section: Introductionmentioning

confidence: 99%

Does Pollution Drive Achievement? The Effect of Traffic Pollution on Academic Performance

Heissel¹,

Persico²,

Simon³

2019

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Standard-Nutzungsbedingungen:Die Dokumente auf EconStor dürfen zu eigenen wissenschaftlichen Zwecken und zum Privatgebrauch gespeichert und kopiert werden.Sie dürfen die Dokumente nicht für öffentliche oder kommerzielle Zwecke vervielfältigen, öffentlich ausstellen, öffentlich zugänglich machen, vertreiben oder anderweitig nutzen.Sofern die Verfasser die Dokumente unter Open-Content-Lizenzen (insbesondere CC-Lizenzen) zur Verfügung gestellt haben sollten, gelten abweichend von diesen Nutzungsbedingungen die in der dort genannten Lizenz gewährten Nutzungsrechte.We examine the effect of school traffic pollution on student outcomes by leveraging variation in wind patterns for schools the same distance from major highways. We compare within-student achievement for students transitioning between schools near highways, where one school has had greater levels of pollution because it is downwind of a highway.Students who move from an elementary/middle school that feeds into a "downwind" middle/high school in the same zip code experience decreases in test scores, more behavioral incidents, and more absences, relative to when they transition to an upwind school. Even within zip codes, microclimates can contribute to inequality. JEL Classification:Q53, I24, I14

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Polycyclic aromatic hydrocarbons and childhood asthma

Cited by 87 publications

References 139 publications

Benzo(a)pyrene triggers desensitization of β2-adrenergic pathway

Benzo(a)pyrene triggers desensitization of β2-adrenergic pathway

A network biology-based approach to evaluating the effect of environmental contaminants on human interactome and diseases

Does Pollution Drive Achievement? The Effect of Traffic Pollution on Academic Performance

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