**6. Conclusion**

**5.4. Pollution models of infection and pneumonia**

), ground level ozone (O<sup>3</sup>

18 Contemporary Topics of Pneumonia

(SO<sup>2</sup>

rodents [147].

NO<sup>2</sup>

mice after NO<sup>2</sup>

Air pollution has been shown to exacerbate respiratory diseases, such as pneumonia. Air pollutants that reach the respiratory tract are currently responsible for its genesis, especially particulate matter having an aerodynamic diameter equal to or less than 10 μm, sulfur dioxide

However, these pollutants may also increase the risk for pneumonia by altering the function of alveolar macrophages, epithelial cells, mucociliary clearance mechanisms, particle transport, and local immunity in the lungs [194]. Because of methodological difficulties and ethical issues, there are a limited number of studies on the effects of controlled pollutant exposure and infection in humans. It has now been almost 50 years since the "infectivity model" has been created. This model is based on the study of the effects of pollutants on pulmonary activity after pollutant exposure with disease and mortality as end-points in animals, particularly

The infectivity model is used by researchers to determine the amount and concentration of pollutants at which the immune system is compromised and disease is developed. This is accomplished by challenging animals with virulent agents either before or after exposure

challenge in mice show significantly higher death rates [195]. Moreover, mice infected with

ity, macrophage viability, systemic cell-mediated and humoral responses to viral infection in CD-1 mice inoculated intratracheally with murine cytomegalovirus [197]. Moreover, the number of viral particles capable of generating infection is lower in animals challenged with

than in animals exposed to filtered air. In addition, the risk of reinfection is higher in

exposure indicating damage in the development of virus-specific immunity

to different concentrations of the pollutant. Exposure to NO<sup>2</sup>

ity [196]. Exposure to varying concentrations of NO<sup>2</sup>

**Gene SNPs** C-reactive protein rs1205 Interleukin-1 beta rs16944

Interleukin-8 rs4073

Nitric oxide synthase 3 rs1799983 Toll-like receptor 2 rs5743708

Toll-like receptor 9 rs5743836

**Table 5.** Single nucleotide polymorphisms associated with pneumonia.

Interleukin-6 rs1800797, rs1800795

Toll-like receptor 4 rs4986790, rs4986791

Interleukin-10 rs1800896, rs1800871, rs1800872, rs5743629

*S. aureus* and then challenged with NO<sup>2</sup>

following a primary infection [198].

), and carbon monoxide (CO) [192, 193].

before and after infectious

affects respiratory tract susceptibil-

displayed a reduction in lung bactericidal capac-

), nitrogen dioxide (NO<sup>2</sup>

Regulation of the lung inflammatory response is critical to the successful outcome of pneumonia. Exposure to air pollutants has been linked to negative lung health outcomes, and sex hormones have been shown to mediate the lung immune response, especially during lung infection. The negative impact of air pollution on lung health, both in the short and long term, is now well accepted, and air quality indexes or scales are available to alert individuals when the air quality is at harmful levels. In this chapter, we have discussed experimental and epidemiological evidence on pneumonia infection incidence in different populations, influences of air pollution and environmental exposures, and sex-specific mechanisms involving male and female hormones in the context of lung immunity. This information could help researchers better explain the differences observed in pneumonia susceptibility and lung health outcomes in men versus women. Understanding the biological basis of these differences is critical for the development of more effective prevention and management strategies for pneumonia in men and women, and could help in the development of better treatment options for these patients.
