Potential role of polycyclic aromatic hydrocarbons in air pollution-induced non-malignant respiratory diseases

Abstract

Epidemiological studies have found strong associations between air pollution and respiratory effects including development and/or exacerbation of asthma and chronic obstructive pulmonary disease (COPD) as well as increased occurrence of respiratory infections and lung cancer. It has become increasingly clear that also polycyclic aromatic hydrocarbons (PAHs) may affect processes linked to non-malignant diseases in the airways. The aim of the present paper was to review epidemiological studies on associations between gas phase and particle-bound PAHs in ambient air and non-malignant respiratory diseases or closely related physiological processes, to assess whether PAH-exposure may explain some of the effects associated with air pollution. Based on experimental in vivo and in vitro studies, we also explore possible mechanisms for how different PAHs may contribute to such events. Epidemiological studies show strongest evidence for an association between PAHs and asthma development and respiratory function in children. This is supported by studies on prenatal and postnatal exposure. Exposure to PAHs in adults seems to be linked to respiratory functions, exacerbation of asthma and increased morbidity/mortality of obstructive lung diseases. However, available studies are few and weak. Notably, the PAHs measured in plasma/urine also represent other exposure routes than inhalation. Furthermore, the role of PAHs measured in air is difficult to disentangle from that of other air pollution components originating from combustion processes. Experimental studies show that PAHs may trigger various processes linked to non-malignant respiratory diseases. Physiological- and pathological responses include redox imbalance, oxidative stress, inflammation both from the innate and adaptive immune systems, smooth muscle constriction, epithelial- and endothelial dysfunction and dysregulated lung development. Such biological responses may at the molecular level be initiated by PAH-binding to the aryl hydrocarbon receptor (AhR), but possibly also through interactions with beta-adrenergic receptors. In addition, reactive PAH metabolites or reactive oxygen species (ROS) may interfere directly with ion transporters and enzymes involved in signal transduction. Overall, the reviewed literature shows that respiratory effects of PAH-exposure in ambient air may extend beyond lung cancer. The relative importance of the specific PAHs ability to induce disease may differ between the biological endpoint in question.

Scoping Review—The Association between Asthma and Environmental Chemicals

“…Humans are exposed directly to PAHs and PAH derivatives or through bioaccumulation in the food chain [7,18,27]. PAHs are known or suspected to be mutagenic, carcinogenic and teratogenic, yet, toxicity between PAHs and their derivatives varies and depends on concentration, time and route of the exposure [7,25,30]. There are legislation and regulations for PAHs in the EU and separate countries [7,25].…”

“…According to epidemiological studies, there is an association between exposure to PAHs, concentrations of air pollutants and the development of allergic and non-allergic asthma, increased symptoms of asthma, risk of asthma exacerbations and lung function decrease, yet according to current data there is a low level of evidence. The strongest evidence is shown for the association between development of asthma and lung function in children [18,27,30,31]. Various mechanisms are likely to play a role in these pathophysiological processes including inflammation, immunoglobulin E (IgE), mast cells' and eosinophils' mediated reactions, oxidative stress, and epithelial and endothelial dysfunction [18,27,32,33].…”

“…The risk of asthma is associated with the duration and dose of exposure to PAHs. However, normally, PAHs are one of many air pollutants, and therefore it is difficult to study the effects of each single chemical (mixed exposure) [27,30,31].…”

“…However, there is no proven causal association between occupational exposure to PAHs and asthma. As an exception, occupational external tobacco smoke might be associated with onset of adult asthma [7,18,27,30].…”

The effects of traffic-related air pollutants on chronic obstructive pulmonary disease in the community-based general population

“…We did not collect chemical composition data of PM 2.5 such as polycyclic aromatic hydrocarbons or heavy metals in this study. However, it is suggested that PAHs or heavy metals in PM 2.5 may have a positive association with development of COPD [ 42 , 43 ]. We recommended that follow-up studies could further analyze the impact of PM 2.5 components on COPD to understand the mechanisms of PM 2.5 on COPD.…”