Exercise induced bronchoconstriction (EIB) is a common complication of athletes and individuals who exercise regularly. It is estimated that about 90% of patients with underlying asthma experience EIB. Sex differences in the prevalence of asthma have been widely reported, with higher rates in boys vs. girls before puberty, and higher rates in women than men after puberty. Because atopy has been reported to occur at higher rates in athletes than in non-athletes, in this study we investigated sex differences in EIB and atopy in athletes. A systematic literature review identified 60 studies evaluating EIB and/or atopy in post-pubertal adult athletes (n=7501). Collectively, these studies reported: 1) a 23% prevalence of EIB in athletes; 2) a higher prevalence of atopy in male athletes vs. females; 3) a higher prevalence of atopy in athletes with EIB; and 4) a significantly higher rate of atopic EIB in male vs. female athletes. Our analysis indicates that the physiological changes that occur during exercise may differentially affect male and female athletes, and suggest an interaction between male sex, exercise, and atopic status in the course of EIB. Understanding these sex differences is important to provide personalized management plans to athletes with underlying asthma and/or atopy.

The practice of physical activity is an effective non-pharmacological strategy for preventing and treating chronic diseases. A large body of evidence has contributed to establishing a positive correlation between a physically active lifestyle and health benefits, including enhanced vaccination responses, lower numbers of senescent T-cells, increased T-cell proliferative capacity, lower levels of inflammatory cytokines, and improved neutrophil and macrophage function. While females are generally thought to exert more robust immune responses than males in response to a variety of challenges, and both male and female sex hormones have been suggested as mediators of immune function, research on this topic has not always been designed with a sex-specific lens. The goal of this review is to summarize the available experimental and clinical evidence linking exercise and immune function in male and female subjects, with an emphasis on sex differences and sex-specific mechanisms. Overall, the available evidence indicates that moderate exercise and physical activity improves immune function in both sexes, whereas prolonged and high-intensity exercise temporarily impairs immune responses at a higher degree in females. A role of male and female sex hormones in these sex-specific effects is also discussed.

Chronic obstructive pulmonary disease (COPD) is a multifactorial lung inflammatory disease affecting 174 million people worldwide, with a recently reported increased incidence in female patients. Patients with COPD are especially vulnerable to the detrimental effects of environmental exposures, especially from air particulate and gaseous pollutants. Exposure to air pollution severely influences COPD outcomes, resulting in acute exacerbations, hospitalizations, and death. In the current study, we conducted a review of the literature addressing air pollution induced acute exacerbations of COPD (AECOPD) in order to determine whether air pollution affects COPD patients in a sex-specific manner. We found that while the majority of studies enrolled both male and female patients, only a few reported results disaggregated by sex. Most studies had a higher enrollment of male patients, only four compared AECOPD outcomes between sexes, and only one study identified sex differences in AECOPD, with females displaying higher rates. Overall, our analysis of the literature confirmed that air pollution exposure is a trigger for AECOPD hospitalizations and revealed a significant gap in our knowledge of sex-specific effects of air pollutants on COPD outcomes, highlighting the need for more studies considering sex as a biological variable.

Air pollution has become the world’s single biggest environmental health risk of the past decade, causing about 7 million yearly deaths worldwide. One of the dominant air pollutants is fine particulate matter (PM2.5), a product of combustion. Exposure to PM2.5 has been associated with decreased lung function, impaired immunity, and exacerbations of lung disease. Accumulating evidence suggests that many of the adverse health effects of PM2.5 exposure are associated with lung inflammation and oxidative stress. While the physical structure and surface chemistry of PM2.5 are surrogate measures of particle oxidative potential, little is known about their contributions to negative health effects. In this study, we used functionalized carbon black particles as surrogates for atmospherically aged combustion formed soot to assess the effects of PM2.5 surface chemistry in lung cells. We exposed the BEAS-2B lung epithelial cell line to different soot at a range of concentrations, and assessed cell viability, inflammation, and oxidative stress. Our results indicate that exposure to soot with varying particle surface composition results in differential cell viability rates, expression of pro-inflammatory and oxidative stress genes, and protein carbonylation. We conclude that particle surface chemistry, specifically oxygen content, in soot modulates lung cell inflammatory and oxidative stress responses.

Bronchopulmonary dysplasia (BPD) is a form of chronic lung disease that develops in neonates as a consequence of preterm birth and arrested fetal lung development. The incidence of BPD remains on the rise, as a result of increasing survival of extremely preterm infants. Severe BPD contributes to significant health care costs and is associated with prolonged hospitalizations, respiratory infections, and neurodevelopmental deficits. In this study, we aimed to detect novel biomarkers of severe BPD. We collected tracheal aspirates (TA) from preterm babies with mild/moderate (n = 8) and severe (n = 17) BPD, and we profiled the expression of 1048 miRNAs using a PCR array. Associations with biological pathways were determined with the Ingenuity Pathway Analysis (IPA) software. We found 31 miRNAs differentially expressed between the two disease groups (2-fold change, FDR < 0.05). Of these, 4 miRNAs displayed significantly higher expression levels, and 27 miRNAs had significantly lower expression levels in the severe BPD vs. the mild/moderate BPD group. IPA identified cell signaling and inflammation pathways associated with miRNA signatures. We conclude that TAs of extreme premature infants contain miRNA signatures associated with severe BPD. These signatures may serve as biomarkers of disease severity in infants with BPD.