|Lai KY*, George WYN and Fanny FC|
|Department of Intensive Care, Queen Elizabeth Hospital, Hong Kong|
|Corresponding Author :||Lai KY
Department of Intensive Care
Queen Elizabeth Hospital, Hong Kong
E-mail: [email protected]
|Received November 27, 2014; Accepted December 02, 2014; Published December 05, 2014|
|Citation: Lai KY, et al. (2015) The 1918 Spanish Influenza Pandemic. J Pulm Respir Med 5:233. doi:10.4172/2161-105X.1000233|
|Copyright: ©2015 Lai KY, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
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Background: Majority of women living in rural areas use biomass fuels for production of domestic energy. Biomass fuel combustion causes indoor air pollution when used inside the dwellings. Combustion products may induce various effects on lung function.
Objective: Objective of this study was to compare the pulmonary functions in healthy non smoking rural women using biomass for cooking to those obtained in control group who were not exposed to biomass.
Methods: One hundred healthy non-smoking women were randomly selected within the age of 20-35 years for this study. The study group comprised of 50 subjects who cooked solely in biomass and 50 age matched subjects who were not exposed to biomass served as controls. A standardized respiratory questionnaire was administered to all the subjects and pulmonary function tests were evaluated by using Medspiror.
Results: The lung function parameters were significantly lesser in the study group, exposed to biomass fuel, than the controls FVC (p<0.01), FEF25-75%, (p<0.01), FEV1, (p<0.001), PEFR (p<0.01), FEV1/FVC% (p>0.05). The evaluation of PFT suggested both restrictive and early small airway obstructive type of pulmonary disease.
Conclusion: The reduction in the pulmonary function in the biomass exposed women could be due to high exposure of biomass pollutants with inadequate ventilation in cooking area leading to chronic pulmonary disease.
1918 H1N1 Spanish influenza pandemic virus (1918PV) killed 4 million people. The first wave of the 1918 H1N1 Spanish influenza pandemic had a mortality comparable to the usual seasonal influenza with a U-shaped mortality-age distribution that involved the very young and elderly. However, the second wave of the 1918 H1N1 Spanish influenza pandemic had a dramatic surge in mortality and a W-shaped mortality-age distribution that involved young adults with a distinct peak of death in individuals between 20 and 40 years of age (Figure a and b) .
Analysis of individual gene segment of the 1918PV isolated from archived samples of the 1918 H1N1 Spanish influenza pandemic’s second wave showed that the non-structural gene segment (NS) contributed to the virulence of 1918PV due to its ability to induce cytokine dysregulation and inhibit human inducible pre-transcriptional interferon-beta (IFN-β) production  and post-transcriptional maturation and nuclear export of host interferon-related mRNAs . The NS of the 1918PV entered the swine population in 1918 and re-emerged in the 2009 novel H1N1 pandemic virus (2009PV). The 2009PV is able to induce cytokine dysregulation and produced an enhanced mortality with a W-shaped mortality-age distribution that involved the young population. Adaptation in pigs has abolished the ability of the NS of 2009PV to block interferon production at the post-transcriptional level and may account for reduced mortality of 2009PV infection compared with the original 1918PV .
With new information from the 2009PV, the surge in mortality and the W-shaped mortality in the second wave of the 1918 Spanish influenza pandemic may be due to the reassortment of a potent cytokine inducing NS with the ability to suppress human interferon production at both the pre-transcriptional and post-transcriptional level into the 1918PV after the first wave (Figure b).
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