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.
Highlights
Air pollution is among the leading environmental health risk factors, estimated to cause between four and nine million deaths globally [1, 2]
The studies combined support the notion that air-borne polycyclic aromatic hydrocarbons (PAHs) exposure may contribute to development and/or exacerbation of respiratory disease and dysfunction
Human epidemiological studies combined with experimental studies give support to the hypothesis that exposure to air-borne PAHs may contribute to the enhanced risk of non-malignant respiratory diseases associated with air pollution exposure
Summary
Air pollution is among the leading environmental health risk factors, estimated to cause between four and nine million deaths globally [1, 2]. The mechanisms through which PM causes respiratory effects are multifactorial and still discussed [7–9]. It has become increasingly clear that the chemical composition of particles is of importance for many of their biological and toxicological effects [10–13], the precise mechanisms involved may vary with the biological endpoint studied [7, 14]. Incomplete combustion of coal and various organic materials as fossil fuels and cigarette smoking produces a mixture of pollutants including PM. PM typically consists of a carbon core with mixtures of organic chemicals adhered to the surface [15–17]. The specific composition and amount of organic chemicals are highly dependent on fuel burned and combustion technology. The levels of organic chemicals are often found to be in the range 20–30% of total particle mass, but may reach as much as 90% [18, 19]
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