Influenza and the Winter Increase in Mortality in the United States, 1959–1999
Identifieur interne : 000434 ( Istex/Curation ); précédent : 000433; suivant : 000435Influenza and the Winter Increase in Mortality in the United States, 1959–1999
Auteurs : Thomas A. Reichert ; Lone Simonsen ; Ashutosh Sharma ; Scott A. Pardo ; David S. Fedson [France] ; Mark A. MillerSource :
- American Journal of Epidemiology [ 0002-9262 ] ; 2004.
Abstract
In economically developed countries, mortality increases distinctly during winter. Many causes have been suggested, including light-dark cycles, temperature/weather, and infectious agents. The authors analyzed monthly mortality in the United States during the period 1959–1999 for four major disease classes. The authors isolated the seasonal component of mortality by removing trends and standardizing the time series. They evaluated four properties: coincidence in mortality peaks, autocorrelation structure and autoregressive integrated moving average (ARIMA) models, magnitude, and age distribution. Peak months of mortality for ischemic heart disease, cerebrovascular disease, and diabetes mellitus coincided appropriately with peaks in pneumonia and influenza, and coefficients of autocorrelation and ARIMA models were essentially indistinguishable. The magnitude of the seasonal component was highly correlated with traditional measures of excess mortality and was significantly larger in seasons dominated by influenza A(H2N2) and A(H3N2) viruses than in seasons dominated by A(H1N1) or B viruses. There was an age shift in mortality during and after the 1968/69 pandemic in each disease class, with features specific to influenza A(H3N2). These findings suggest that the cause of the winter increase in US mortality is singular and probably influenza. Weather and other factors may determine the timing and modulate the magnitude of the winter-season increase in mortality, but the primary determinant appears to be the influenza virus.
Url:
DOI: 10.1093/aje/kwh227
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Thomas A. Reichert<affiliation><mods:affiliation>Entropy Research Institute, Upper Saddle River, NJ.</mods:affiliation><wicri:noCountry code="subField">NJ.</wicri:noCountry></affiliation><affiliation><mods:affiliation>National Institute of Allergy and Infectious Diseases, Bethesda, MD.</mods:affiliation><wicri:noCountry code="subField">MD.</wicri:noCountry></affiliation><affiliation><mods:affiliation>Vyteris, Inc., Fairlawn, NJ.</mods:affiliation><wicri:noCountry code="subField">NJ.</wicri:noCountry></affiliation><affiliation><mods:affiliation>Becton Dickinson and Company, Inc., Franklin Lakes, NJ.</mods:affiliation><wicri:noCountry code="subField">NJ.</wicri:noCountry></affiliation><affiliation><mods:affiliation>Fogarty International Center, National Institutes of Health, Bethesda, MD.</mods:affiliation><wicri:noCountry code="subField">MD.</wicri:noCountry></affiliation>Le document en format XML
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Reichert</name><affiliation><mods:affiliation>Entropy Research Institute, Upper Saddle River, NJ.</mods:affiliation><wicri:noCountry code="subField">NJ.</wicri:noCountry></affiliation></author><author><name sortKey="Simonsen, Lone" sort="Simonsen, Lone" uniqKey="Simonsen L" first="Lone" last="Simonsen">Lone Simonsen</name><affiliation><mods:affiliation>National Institute of Allergy and Infectious Diseases, Bethesda, MD.</mods:affiliation><wicri:noCountry code="subField">MD.</wicri:noCountry></affiliation></author><author><name sortKey="Sharma, Ashutosh" sort="Sharma, Ashutosh" uniqKey="Sharma A" first="Ashutosh" last="Sharma">Ashutosh Sharma</name><affiliation><mods:affiliation>Vyteris, Inc., Fairlawn, NJ.</mods:affiliation><wicri:noCountry code="subField">NJ.</wicri:noCountry></affiliation></author><author><name sortKey="Pardo, Scott A" sort="Pardo, Scott A" uniqKey="Pardo S" first="Scott A." last="Pardo">Scott A. 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Epidemiol.</title><idno type="ISSN">0002-9262</idno><idno type="eISSN">1476-6256</idno><imprint><publisher>Oxford University Press</publisher><date when="2004-09-01">2004</date><biblScope unit="vol">160</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="492">492</biblScope><biblScope unit="page" to="502">502</biblScope></imprint><idno type="ISSN">0002-9262</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0002-9262</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In economically developed countries, mortality increases distinctly during winter. Many causes have been suggested, including light-dark cycles, temperature/weather, and infectious agents. The authors analyzed monthly mortality in the United States during the period 1959–1999 for four major disease classes. The authors isolated the seasonal component of mortality by removing trends and standardizing the time series. They evaluated four properties: coincidence in mortality peaks, autocorrelation structure and autoregressive integrated moving average (ARIMA) models, magnitude, and age distribution. Peak months of mortality for ischemic heart disease, cerebrovascular disease, and diabetes mellitus coincided appropriately with peaks in pneumonia and influenza, and coefficients of autocorrelation and ARIMA models were essentially indistinguishable. The magnitude of the seasonal component was highly correlated with traditional measures of excess mortality and was significantly larger in seasons dominated by influenza A(H2N2) and A(H3N2) viruses than in seasons dominated by A(H1N1) or B viruses. There was an age shift in mortality during and after the 1968/69 pandemic in each disease class, with features specific to influenza A(H3N2). These findings suggest that the cause of the winter increase in US mortality is singular and probably influenza. Weather and other factors may determine the timing and modulate the magnitude of the winter-season increase in mortality, but the primary determinant appears to be the influenza virus.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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