Perspective: Ambient Air Pollution: Inflammatory Response and Effects on the Lung's Vasculature

Abstract

Particulates from air pollution are implicated in causing or exacerbating respiratory and systemic cardiovascular diseases and are thought to be among the leading causes of morbidity and mortality. However, the contribution of ambient particulate matter to diseases affecting the pulmonary circulation, the right heart, and especially pulmonary hypertension is much less documented. Our own work and that of other groups has demonstrated that prolonged exposure to antigens via the airways can cause severe pulmonary arterial remodeling. In addition, vascular changes have been well documented in a typical disease of the airways, asthma. These experimental and clinical findings link responses in the airways with responses in the lung's vasculature. It follows that particulate air pollution could cause, or exacerbate, diseases in the pulmonary circulation and associated pulmonary hypertension. This perspective details the literature for support of this concept. Data regarding the health effects of particulate matter from air pollution on the lung's vasculature, with emphasis on the lung's inflammatory responses to particulate matter deposition and pulmonary hypertension, are discussed. A deeper understanding of the health implications of exposure to ambient particulate matter will improve our knowledge of how to improve the management of lung diseases, including diseases of the pulmonary circulation. As man-made ambient particulate air pollution is typically linked to economic growth, a better understanding of the health effects of exposure to particulate air pollution is expected to integrate the global goal of achieving healthy living for all.

Interleukin 13– and Interleukin 17A–Induced Pulmonary Hypertension Phenotype Due to Inhalation of Antigen and Fine Particles from Air Pollution

“…Exposure to antigen and PM induces increased RVSP and circumferential pulmonary arterial muscularization via IL-13 and IL-17A To understand the mechanism by which exposure to a weak antigen (OVA) and ambient PM 2.5 induced this phenotype, 18 groups of mice were given neutralizing anti-IL-13…”

“…The dose chosen was at half the concentration of the dose reported to induce significant airway inflammation using PM 2.5 sampled in New York City, 35 Beijing, 36 and Baltimore. Antigen immunization and exposure to antigen and PM Animals were primed and challenged with antigen as described elsewhere 17,18 and schematically presented in Figure 2A. ), and when antigen exposure was combined with PM, significant increases in right ventricular systolic pressures (RVSPs) were measured.…”

“…), and when antigen exposure was combined with PM, significant increases in right ventricular systolic pressures (RVSPs) were measured. 18 To verify that the anti- gen and PM delivery elicited the expected inflammation and that the PM dose used for the study did not induce microscopic signs of inflammation when given alone, the lungs were scored for airway and interstitial (alveolar) inflammation (Fig. 2B, 2C ) Functional evaluation and tissue collection RVSP was measured after inserting a catheter via the jugular vein in anaesthetized, spontaneously breathing mice.…”

Impact of the Airborne Particulate Matter onthe Human Health

“…Consequently PM can cause, or exacerbate, diseases in the pulmonary circulation. Evidences on the PM health effects on the lung's vasculature with emphasis on the lung's inflammatory responses to the particle deposition and pulmonary hypertension have been described (Grunig et al, 2014). The American Thoracic Society (Leary et al, 2013) has demonstrated that living in proximity to roadways, where exposure to high PM 2.5 levels and NO x is very high, is associated with a greater right ventricular mass and changes in right ventricular function.…”

Safety and Efficacy of Immunoadsorption as an Add-On to Medical Treatment in Patients with Severe Idiopathic Pulmonary Arterial Hypertension

“…A pathologic immune response is a major constituent of the molecular pathogenesis of PAH [2,3] . This has been demonstrated not only in connective tissue disease-associated PAH but also in pulmonary hypertension (PH) due to infectious diseases or pollution [4] . An increased autoimmune response has also been shown in idiopathic [5] or heritable [6] PAH and in PH due to lung disease [7] or left heart failure [8] .…”