Editorial [Hot topic: Acute Health Effects of Passive Smoking (Guest Editor: Andreas D. Flouris)]

It is well known that passive smoking (PS) is a major threat to public health [1-4] as PS exposure is linked to an ever increasing frequency of diseases among children and adults, such as asthma, respiratory illness, vascular dysfunction, otitis media, sudden infant death syndrome, and predisposition towards cardiovascular disease and cancer [5-8] The majority of studies that have appeared on the unfavorable effects of PS have evaluated longitudinal epidemiological data, while exposure studies assessing the acute and short-term PS effects are limited [9]. However, as the latter is essential and of the utmost importance for elucidating the underlying physiological mechanisms involved in PS-induced system disruption [9, 10] research on the acute affects of PS has spread into different areas during the past 10 years and new scientific evidence continues to accumulate. The aim of the present Special Issue is to critically evaluate the existing biological evidence regarding the acute health effects of PS exposure. A variety of topics is included covering primarily the cardiovascular, the respiratory and the endocrine systems in human - both adults and children - and animal models.

Acting as the introduction to the Special Issue, the review by Faught et al. [11]. surveys the epidemiological literature examining the association between PS and cardiovascular disease (CVD). The various screening methods available in assessing smoking behavior and quantifying nicotine absorption are summarized while taking into consideration the natural history of those exposed to PS and the associated risk of CVD. Based on the presented evidence, the risk of developing an acute cardiac syndrome or chronic lifetime coronary events is >30% in individuals frequently exposed to PS, while a reduction in the incidence of a myocardial infarction decreases by nearly 50% in the absence of PS exposures. The review concludes that epidemiological research provides ample evidence to support a causal inference between PS exposure and increased risks of CVD morbidity and mortality among both men and women.

Continuing on the CVD topic, the review by Vardavas and Panagiotakos [12] focuses on the relationship between PS and inflammation on the development of CVD. Recent evidence has indicated that PS can lead to a 70-80% increase in the risk of coronary heart disease (CHD), nearly as much as light smoking. The authors describe the different mechanisms through which PS may induce an inflammatory response that may lead to the development of CVD, on a whole and through certain of its toxic constituents. Based on the presented evidence, the review concludes with effects suggesting a causal relationship between exposure to passive smoking and the development of cardiovascular disease.

The mechanisms contributing to the PS-induced increased CHD risk are complex and include endothelial dysfunction, lipoprotein modification, increased inflammation and platelet activation. Although the vascular effects of PS are well known, its effects on the heart have not been reviewed despite that recently several studies have shown that PS exposure can result in cardiac remodeling and compromised cardiac function. These issues are the primary focus of the review by Minicucci et al. [13]. which evaluates the recent findings as to the effects of PS in acute and chronic phases of vascular and cardiac remodeling.

Changing the theme from cardiovascular to respiratory, the review by Bergren [14] examines the link between PS exposure and airway hyperresponsiveness. Recent evidence suggested that PS is associated with changes in lung development and morphology, airway hyperresponsiveness and obstruction and development of asthma and its increased severity. However these PS-induced effects are not universally supported while we lack a complete understanding of PS effects on pulmonary function as well as its mechanism of action. The author addresses the respiratory effects of PS in human and animal models, particularly those with existing airway hyperresponsiveness, as well as the PS role as an adjuvant to airway hyperresponsiveness and its contribution to development of antigenic tolerance.

Several physiological systems, with the respiratory being the primary, are disrupted by PS and progressively deteriorate through chronic exposures. This is of particular importance in children, given that respiratory complications during childhood can be transferred to adulthood and leading to significantly inferior health profiles. In this light, the reviews by Metsios et al. [15] and Bakirtas [16] evaluate current evidence linking PS with asthma and allergy in children, particularly with regards to brief PS exposures. Data thus far suggest that the chemical and carcinogenic constituents of PS have profound effects on children's health as they may disrupt normal biological development. Children that are exposed to PS either in-utero or following birth demonstrate increased prevalence for allergies and asthma. Moreover, PS appears to have pronounced effects on respiratory parameters that promote asthma development and persistent wheezing rather than other allergies. Regarding asthma, PS seems to affect different aspects of disease control not only diurnal and nocturnal symptoms and exacerbations but also rescue medication use and lung functions as well as bronchial hyperreactivity, school absenteeism and quality of life. Acute PS effects in all these asthma parameters seem to be additive to those of chronic exposure.

Moving on to the endocrine system, growing evidence suggests that PS interferes with normal thyroid function, a topic that is reviewed in the paper by Carrillo et al. [17]. Toxic elements contained in PS such as thiocyanate may be partially responsible for impaired thyroid hormonogenesis. Moreover, a recently-discovered PS-induced inflammatory stress may impair thyroid hormonogenesis and iodine uptake initiating interleukin 6 production from thyroid epithelial cells which, in turn, stimulates the expression of molecules that exacerbate thyroid autoimmunity. Elevated inflammatory stress and thyroid hormone secretion in response to PS exposure initiates catabolic processes that alter body composition via lean body mass breakdown; translating to an elevation in resting energy expenditure of ∼10%. The combination of certain biological factors, such as sex and/or existing thyroid disease that may stimulate differential PS-induced effects on thyroid function is also reviewed.

The final review by Onozaki [18] evaluates etiological and biological aspects of PS in rheumatoid arthritis. Polycyclic aromatic hydrocarbons, constituents of cigarette smoke, and cigarette smoke extracts are able to induce proinflammatory cytokines from rheumatoid arthritis patient-derived fibroblast-like synoviocytes. Recent studies also suggest an important role of T helper 17 cells in rheumatoid arthritis and contribution of aryl hydrocarbon receptor to the induction and development of T helper 17 cells and rheumatoid arthritis. These new findings may lead to uncovering the basis for the etiological role of PS in rheumatoid arthritis.