Cigarette Smoking and Epidemic Influenza12

Finklea, John F.; Sandifer, Samuel H.; Smith, Douglas D.

doi:10.1093/oxfordjournals.aje.a121084

Cited by 83 publications

(42 citation statements)

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“…The effect of cigarette smoking on the immune response to influenza vaccination with a killed vaccine and on susceptibility to epidemic influenza have been reported previously (Finklea et al 1969;Finklea et al 1971b). It was observed that, before immunization with the killed vaccine, cigarette smokers showed significantly lower titres of HI antibody than non-smokers, but immediately after vaccination this antibody deficit was abolished and the immunological response did not differ significantly between the two groups.…”

Section: Discussionmentioning

confidence: 66%

“…However, the HI titres in the smokers had fallen behind their non-smoking counterparts within a few weeks, and by one year after vaccination the titres of humoral HI antibody of the smokers were much lower (Finklea et al 1971b). This may have contributed to the increased susceptibility of cigarette smokers to subsequent infection with epidemic influenza (Finklea et al 1969).…”

Section: Discussionmentioning

confidence: 99%

“…No difference in susceptibility could be demonstrated if smokers had prior immunity (titres of > 24), whether from vaccination or previous natural infection. In the study reported by Finklea et al (1969), the epidemic was caused by a novel influenza virus strain, A/Hong Kong/68, which had undergone a partial antigenic shift. Their subjects, therefore, would also have had little or no prior immunity.…”

Section: Discussionmentioning

confidence: 99%

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The effect of cigarette smoking on susceptibility to epidemic influenza and on serological responses to live attenuated and killed subunit influenza vaccines

Mackenzie

MacKenzie

Holt

1976

J. Hyg.

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SUMMARYThe effects of cigarette smoking on the incidence of epidemic influenza and on the serological response to influenza vaccination with killed subunit and live attenuated vaccines have been investigated during comparative vaccine trials in Western Australia. It was found that cigarette smokers with no pre-epidemic haemagglutination-inhibiting (HI) antibody (titres of < 12) were significantly more susceptible to epidemic influenza than non-smokers. Smokers were no more susceptible however, if they had possessed detectable pre-epidemic HI antibody. A significantly higher proportion of smokers sero-converted after receiving the live virus vaccine than their non-smoking counterparts, but this could not be correlated with pre-vaccination HI antibody titres. The longevity of the immune response to the subunit vaccine was severely depressed 50 weeks post-vaccination in smokers who had possessed little or no immunity before vaccination (titres of < 12). This antibody deficit was not observed in live virus vaccinees or subunit vaccinees with pre-vaccination HI antibody (titres of > 24). Post-vaccinal symptoms were similar regardless of vaccine group or smoking history.

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Section: Discussionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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The effect of cigarette smoking on susceptibility to epidemic influenza and on serological responses to live attenuated and killed subunit influenza vaccines

Mackenzie

MacKenzie

Holt

1976

J. Hyg.

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“…For example, a study of U.S. Army recruits found that smokers had a 50% higher risk of upper respiratory infections compared with nonsmokers ( Blake, Abell, & Stanley, 1988 ). Similar studies have found increased rates of infl uenza and an increased rate of complications from infl uenza related to cigarette smoking among otherwise healthy young adults ( Finklea, 1969 ;Kark & Lebiush, 1981 ;Kark, Lebiush, & Rannon, 1982 ).…”

Section: Discussionmentioning

confidence: 89%

Symptoms of cough and shortness of breath among occasional young adult smokers

Berg

Klatt

et al. 2009

Nicotine &Amp; Tobacco Research

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Discussion:In conclusion, this cross-sectional study found that occasional smoking and ETS exposure were associated with an increase in the rate of respiratory symptoms (cough/sore throat and shortness of breath/fatigue) among young adults. IntroductionYoung adulthood is a critical transition period in cigarette use ( Bachman, Wadsworth, O'Malley, Johnston, & Schulenberg, 1997 ;Chen & Kandel, 1995 ). Whereas fi rst experimentation with cigarettes occurs early in life for the majority of individuals, increased frequency of smoking and establishment of regular or heavy cigarette use often occur during the young adult years . Encouraging smoking cessation early in life is crucial to help individuals avoid many of the harms related to smoking ( Doll, Peto, Boreham, & Sutherland, 2004 ;Orleans, 2007 ). Effective strategies targeting occasional or intermittent young adult smokers are needed to interrupt the progression of smoking behavior and the development of nicotine dependence.Efforts to encourage cessation often focus on communicating the negative consequences of cigarette use. This approach is based on well-recognized health behavior theories such as the health belief model ( Janz & Becker, 1984 ;Rosenstock, Strecher, & Becker, 1988 ) and the theory of reasoned action ( Ajzen & Fishbein, 1980 ;Fishbein & Ajzen, 1975 ). Several studies have identifi ed concerns over health consequences as an AbstractIntroduction: The perception of negative health consequences is a common motive for quitting smoking, but specifi c information on the immediate health effects of occasional smoking among young adults is limited.Method: To examine the relationship between cigarette use and symptoms of (a) cough or sore throat and (b) shortness of breath or fatigue after regular activities among young adults, we performed online health screening of a random sample of 25,000 college undergraduates. The screening survey assessed demographic characteristics, smoking and related health behaviors, and respiratory symptoms in the previous 30 days.

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“…(a) A direct consideration of this research may lead to the fact that elevated environmental chemical levels do in fact aggravate or they may alleviate viral infections. (b) It is known that cigarette smoking aggravates influenzal infection in man (1), and many chemicals have been shown to increase viral infections experimentally (2). (c) Insofar as lead poisoning and viral infection is concerned, possible synergism between lead poisoning and eastern encephalitis viral (EEV) infection was observed "naturally" in a dead calf in Florida wherein EEV was isolated from the brain, the calf had a viral type of encephalitis histologically, and 20 ppm lead was present in the kidney of the calf.…”

Section: Introductionmentioning

confidence: 99%

Lead Aggravates Viral Disease and Represses the Antiviral Activity of Interferon Inducers

Gainer¹

1974

Environ Health Perspect

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Lead acetate was administered continuously in the drinking water to CD-1 male mice beginning at 4 weeks of age. An LD,o02o of the lytic viruses or 300 plaque-forming units of RLV was inoculated intrapertioneally at 6 weeks of age. Lead increased the response of the mice to all classes of viruses against which it was tested: an RNA picornavirusencephalomyocarditis (EMCV), a DNA herpesvirus-pseudoribies, an RNA leukemiavirus-Rauscher leukemia (RLV), an RNA arbovirus B-St. Louis encephalitis, and an RNA arbovirus A-western encephalitis. Most studies were performed between lead and EMCV. Increases in EMCV mortality in lead treated mice over controls ranged from 2 X at a lead level of 0.004M to 7 x (100% mortality) at a 0.1M lead level. Splenomegaly with spleens 800 to 1100 mg in weight containing high titers of RLV occurred in lead (0.03M)-treated mice 3 and 6 weeks after RLV inoculation; spleens or RLV controls were normal in weight (200 mg) and were free of virus. Lead did not reduce the protective effect of mouse interferon (IF) against the lethal action of EMCV, but it did repress the EMCV antiviral effect of poly I/poly C (PIC) and of Newcastle disease virus (NDV) against EMCV mortality. These data indicate several new facts concerning adverse effects lead may have on an animal: (1) lead aggravates viral disease, most likely in part, through reduced IF synthesis; (2) lead represses the anti-EMCV protective effects of both PIC and of NDV, which, in other reports, were shown to induce IF in radioresistant macrophages (PIC) or in radiosensitive lymphocytes (NDV); (3) lead may then be said to repress IF induction in two kinds of cells; (4) however, lead does not inhibit IF action.

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Cigarette Smoking and Epidemic Influenza12

Cited by 83 publications

References 0 publications

The effect of cigarette smoking on susceptibility to epidemic influenza and on serological responses to live attenuated and killed subunit influenza vaccines

The effect of cigarette smoking on susceptibility to epidemic influenza and on serological responses to live attenuated and killed subunit influenza vaccines

Symptoms of cough and shortness of breath among occasional young adult smokers

Lead Aggravates Viral Disease and Represses the Antiviral Activity of Interferon Inducers

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