Smoking: additional burden on aging and death

Abstract Tobacco smoking is a major cause of lung cancer. It has been suggested that there is an approximately linear dose–response relationship between the number of cigarettes smoked per day and clinical outcome such as lung cancer mortality. It has also been proposed that there is a greater incre...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Watanabe, Masahiko [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	Cigarette smoking Smoking cessation Dose–response relationship Aging Cancer risk

Anmerkung:	© The Author(s) 2016

Übergeordnetes Werk:	Enthalten in: Genes and environment - [London] : BioMed Central, 2006, 38(2016), 1 vom: 22. Jan.
Übergeordnetes Werk:	volume:38 ; year:2016 ; number:1 ; day:22 ; month:01

Links:	Volltext

DOI / URN:	10.1186/s41021-016-0029-9

Katalog-ID:	SPR038062887

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allfields	10.1186/s41021-016-0029-9 doi (DE-627)SPR038062887 (SPR)s41021-016-0029-9-e DE-627 ger DE-627 rakwb eng Watanabe, Masahiko verfasserin aut Smoking: additional burden on aging and death 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 Abstract Tobacco smoking is a major cause of lung cancer. It has been suggested that there is an approximately linear dose–response relationship between the number of cigarettes smoked per day and clinical outcome such as lung cancer mortality. It has also been proposed that there is a greater increase in mortality at high doses when the dose is represented by the duration of the smoking habit rather than the number of cigarettes. The multistep carcinogenesis theory indicates that a greater increase in mortality rate at high doses is possible, as is the case between aging and cancer, even though each dose–response relationship between a carcinogenic factor and a carcinogenic step forward is linear. The high incidence of lung cancer after long-term smoking and the decreased relative risk after smoking cessation suggests a similarity between the effects of smoking and aging. Prediction of lung cancer risk in former smokers by simple integration of smoking effects with aging demonstrated a good correlation with that estimated from the relative risk of the period of smoking cessation. In contrast to the smoking period, there appears to be a linear relationship between smoking strength and cancer risk. This might arise if the dose–response relationship between smoking strength and each carcinogenic step is less than linear, or the effects become saturated with a large dose of daily smoking. Such a dose–response relationship could lead to relatively large clinical effects, such as cardiovascular mortality, by low-dose tobacco smoke exposure, e.g., second-hand smoking. Consideration of the dose–response of each effect is important to evaluate the risk arising from each carcinogenic factor. Cigarette smoking (dpeaa)DE-He213 Smoking cessation (dpeaa)DE-He213 Dose–response relationship (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Cancer risk (dpeaa)DE-He213 Enthalten in Genes and environment [London] : BioMed Central, 2006 38(2016), 1 vom: 22. Jan. (DE-627)52422742X (DE-600)2269162-5 1880-7062 nnns volume:38 year:2016 number:1 day:22 month:01 https://dx.doi.org/10.1186/s41021-016-0029-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 38 2016 1 22 01
spelling	10.1186/s41021-016-0029-9 doi (DE-627)SPR038062887 (SPR)s41021-016-0029-9-e DE-627 ger DE-627 rakwb eng Watanabe, Masahiko verfasserin aut Smoking: additional burden on aging and death 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 Abstract Tobacco smoking is a major cause of lung cancer. It has been suggested that there is an approximately linear dose–response relationship between the number of cigarettes smoked per day and clinical outcome such as lung cancer mortality. It has also been proposed that there is a greater increase in mortality at high doses when the dose is represented by the duration of the smoking habit rather than the number of cigarettes. The multistep carcinogenesis theory indicates that a greater increase in mortality rate at high doses is possible, as is the case between aging and cancer, even though each dose–response relationship between a carcinogenic factor and a carcinogenic step forward is linear. The high incidence of lung cancer after long-term smoking and the decreased relative risk after smoking cessation suggests a similarity between the effects of smoking and aging. Prediction of lung cancer risk in former smokers by simple integration of smoking effects with aging demonstrated a good correlation with that estimated from the relative risk of the period of smoking cessation. In contrast to the smoking period, there appears to be a linear relationship between smoking strength and cancer risk. This might arise if the dose–response relationship between smoking strength and each carcinogenic step is less than linear, or the effects become saturated with a large dose of daily smoking. Such a dose–response relationship could lead to relatively large clinical effects, such as cardiovascular mortality, by low-dose tobacco smoke exposure, e.g., second-hand smoking. Consideration of the dose–response of each effect is important to evaluate the risk arising from each carcinogenic factor. Cigarette smoking (dpeaa)DE-He213 Smoking cessation (dpeaa)DE-He213 Dose–response relationship (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Cancer risk (dpeaa)DE-He213 Enthalten in Genes and environment [London] : BioMed Central, 2006 38(2016), 1 vom: 22. Jan. (DE-627)52422742X (DE-600)2269162-5 1880-7062 nnns volume:38 year:2016 number:1 day:22 month:01 https://dx.doi.org/10.1186/s41021-016-0029-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 38 2016 1 22 01
allfields_unstemmed	10.1186/s41021-016-0029-9 doi (DE-627)SPR038062887 (SPR)s41021-016-0029-9-e DE-627 ger DE-627 rakwb eng Watanabe, Masahiko verfasserin aut Smoking: additional burden on aging and death 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 Abstract Tobacco smoking is a major cause of lung cancer. It has been suggested that there is an approximately linear dose–response relationship between the number of cigarettes smoked per day and clinical outcome such as lung cancer mortality. It has also been proposed that there is a greater increase in mortality at high doses when the dose is represented by the duration of the smoking habit rather than the number of cigarettes. The multistep carcinogenesis theory indicates that a greater increase in mortality rate at high doses is possible, as is the case between aging and cancer, even though each dose–response relationship between a carcinogenic factor and a carcinogenic step forward is linear. The high incidence of lung cancer after long-term smoking and the decreased relative risk after smoking cessation suggests a similarity between the effects of smoking and aging. Prediction of lung cancer risk in former smokers by simple integration of smoking effects with aging demonstrated a good correlation with that estimated from the relative risk of the period of smoking cessation. In contrast to the smoking period, there appears to be a linear relationship between smoking strength and cancer risk. This might arise if the dose–response relationship between smoking strength and each carcinogenic step is less than linear, or the effects become saturated with a large dose of daily smoking. Such a dose–response relationship could lead to relatively large clinical effects, such as cardiovascular mortality, by low-dose tobacco smoke exposure, e.g., second-hand smoking. Consideration of the dose–response of each effect is important to evaluate the risk arising from each carcinogenic factor. Cigarette smoking (dpeaa)DE-He213 Smoking cessation (dpeaa)DE-He213 Dose–response relationship (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Cancer risk (dpeaa)DE-He213 Enthalten in Genes and environment [London] : BioMed Central, 2006 38(2016), 1 vom: 22. Jan. (DE-627)52422742X (DE-600)2269162-5 1880-7062 nnns volume:38 year:2016 number:1 day:22 month:01 https://dx.doi.org/10.1186/s41021-016-0029-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 38 2016 1 22 01
allfieldsGer	10.1186/s41021-016-0029-9 doi (DE-627)SPR038062887 (SPR)s41021-016-0029-9-e DE-627 ger DE-627 rakwb eng Watanabe, Masahiko verfasserin aut Smoking: additional burden on aging and death 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 Abstract Tobacco smoking is a major cause of lung cancer. It has been suggested that there is an approximately linear dose–response relationship between the number of cigarettes smoked per day and clinical outcome such as lung cancer mortality. It has also been proposed that there is a greater increase in mortality at high doses when the dose is represented by the duration of the smoking habit rather than the number of cigarettes. The multistep carcinogenesis theory indicates that a greater increase in mortality rate at high doses is possible, as is the case between aging and cancer, even though each dose–response relationship between a carcinogenic factor and a carcinogenic step forward is linear. The high incidence of lung cancer after long-term smoking and the decreased relative risk after smoking cessation suggests a similarity between the effects of smoking and aging. Prediction of lung cancer risk in former smokers by simple integration of smoking effects with aging demonstrated a good correlation with that estimated from the relative risk of the period of smoking cessation. In contrast to the smoking period, there appears to be a linear relationship between smoking strength and cancer risk. This might arise if the dose–response relationship between smoking strength and each carcinogenic step is less than linear, or the effects become saturated with a large dose of daily smoking. Such a dose–response relationship could lead to relatively large clinical effects, such as cardiovascular mortality, by low-dose tobacco smoke exposure, e.g., second-hand smoking. Consideration of the dose–response of each effect is important to evaluate the risk arising from each carcinogenic factor. Cigarette smoking (dpeaa)DE-He213 Smoking cessation (dpeaa)DE-He213 Dose–response relationship (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Cancer risk (dpeaa)DE-He213 Enthalten in Genes and environment [London] : BioMed Central, 2006 38(2016), 1 vom: 22. Jan. (DE-627)52422742X (DE-600)2269162-5 1880-7062 nnns volume:38 year:2016 number:1 day:22 month:01 https://dx.doi.org/10.1186/s41021-016-0029-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 38 2016 1 22 01
allfieldsSound	10.1186/s41021-016-0029-9 doi (DE-627)SPR038062887 (SPR)s41021-016-0029-9-e DE-627 ger DE-627 rakwb eng Watanabe, Masahiko verfasserin aut Smoking: additional burden on aging and death 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 Abstract Tobacco smoking is a major cause of lung cancer. It has been suggested that there is an approximately linear dose–response relationship between the number of cigarettes smoked per day and clinical outcome such as lung cancer mortality. It has also been proposed that there is a greater increase in mortality at high doses when the dose is represented by the duration of the smoking habit rather than the number of cigarettes. The multistep carcinogenesis theory indicates that a greater increase in mortality rate at high doses is possible, as is the case between aging and cancer, even though each dose–response relationship between a carcinogenic factor and a carcinogenic step forward is linear. The high incidence of lung cancer after long-term smoking and the decreased relative risk after smoking cessation suggests a similarity between the effects of smoking and aging. Prediction of lung cancer risk in former smokers by simple integration of smoking effects with aging demonstrated a good correlation with that estimated from the relative risk of the period of smoking cessation. In contrast to the smoking period, there appears to be a linear relationship between smoking strength and cancer risk. This might arise if the dose–response relationship between smoking strength and each carcinogenic step is less than linear, or the effects become saturated with a large dose of daily smoking. Such a dose–response relationship could lead to relatively large clinical effects, such as cardiovascular mortality, by low-dose tobacco smoke exposure, e.g., second-hand smoking. Consideration of the dose–response of each effect is important to evaluate the risk arising from each carcinogenic factor. Cigarette smoking (dpeaa)DE-He213 Smoking cessation (dpeaa)DE-He213 Dose–response relationship (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Cancer risk (dpeaa)DE-He213 Enthalten in Genes and environment [London] : BioMed Central, 2006 38(2016), 1 vom: 22. Jan. (DE-627)52422742X (DE-600)2269162-5 1880-7062 nnns volume:38 year:2016 number:1 day:22 month:01 https://dx.doi.org/10.1186/s41021-016-0029-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 38 2016 1 22 01
language	English
source	Enthalten in Genes and environment 38(2016), 1 vom: 22. Jan. volume:38 year:2016 number:1 day:22 month:01
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container_title	Genes and environment
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author	Watanabe, Masahiko
spellingShingle	Watanabe, Masahiko misc Cigarette smoking misc Smoking cessation misc Dose–response relationship misc Aging misc Cancer risk Smoking: additional burden on aging and death
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topic_title	Smoking: additional burden on aging and death Cigarette smoking (dpeaa)DE-He213 Smoking cessation (dpeaa)DE-He213 Dose–response relationship (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Cancer risk (dpeaa)DE-He213
topic	misc Cigarette smoking misc Smoking cessation misc Dose–response relationship misc Aging misc Cancer risk
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title	Smoking: additional burden on aging and death
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title_full	Smoking: additional burden on aging and death
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title_sort	smoking: additional burden on aging and death
title_auth	Smoking: additional burden on aging and death
abstract	Abstract Tobacco smoking is a major cause of lung cancer. It has been suggested that there is an approximately linear dose–response relationship between the number of cigarettes smoked per day and clinical outcome such as lung cancer mortality. It has also been proposed that there is a greater increase in mortality at high doses when the dose is represented by the duration of the smoking habit rather than the number of cigarettes. The multistep carcinogenesis theory indicates that a greater increase in mortality rate at high doses is possible, as is the case between aging and cancer, even though each dose–response relationship between a carcinogenic factor and a carcinogenic step forward is linear. The high incidence of lung cancer after long-term smoking and the decreased relative risk after smoking cessation suggests a similarity between the effects of smoking and aging. Prediction of lung cancer risk in former smokers by simple integration of smoking effects with aging demonstrated a good correlation with that estimated from the relative risk of the period of smoking cessation. In contrast to the smoking period, there appears to be a linear relationship between smoking strength and cancer risk. This might arise if the dose–response relationship between smoking strength and each carcinogenic step is less than linear, or the effects become saturated with a large dose of daily smoking. Such a dose–response relationship could lead to relatively large clinical effects, such as cardiovascular mortality, by low-dose tobacco smoke exposure, e.g., second-hand smoking. Consideration of the dose–response of each effect is important to evaluate the risk arising from each carcinogenic factor. © The Author(s) 2016
abstractGer	Abstract Tobacco smoking is a major cause of lung cancer. It has been suggested that there is an approximately linear dose–response relationship between the number of cigarettes smoked per day and clinical outcome such as lung cancer mortality. It has also been proposed that there is a greater increase in mortality at high doses when the dose is represented by the duration of the smoking habit rather than the number of cigarettes. The multistep carcinogenesis theory indicates that a greater increase in mortality rate at high doses is possible, as is the case between aging and cancer, even though each dose–response relationship between a carcinogenic factor and a carcinogenic step forward is linear. The high incidence of lung cancer after long-term smoking and the decreased relative risk after smoking cessation suggests a similarity between the effects of smoking and aging. Prediction of lung cancer risk in former smokers by simple integration of smoking effects with aging demonstrated a good correlation with that estimated from the relative risk of the period of smoking cessation. In contrast to the smoking period, there appears to be a linear relationship between smoking strength and cancer risk. This might arise if the dose–response relationship between smoking strength and each carcinogenic step is less than linear, or the effects become saturated with a large dose of daily smoking. Such a dose–response relationship could lead to relatively large clinical effects, such as cardiovascular mortality, by low-dose tobacco smoke exposure, e.g., second-hand smoking. Consideration of the dose–response of each effect is important to evaluate the risk arising from each carcinogenic factor. © The Author(s) 2016
abstract_unstemmed	Abstract Tobacco smoking is a major cause of lung cancer. It has been suggested that there is an approximately linear dose–response relationship between the number of cigarettes smoked per day and clinical outcome such as lung cancer mortality. It has also been proposed that there is a greater increase in mortality at high doses when the dose is represented by the duration of the smoking habit rather than the number of cigarettes. The multistep carcinogenesis theory indicates that a greater increase in mortality rate at high doses is possible, as is the case between aging and cancer, even though each dose–response relationship between a carcinogenic factor and a carcinogenic step forward is linear. The high incidence of lung cancer after long-term smoking and the decreased relative risk after smoking cessation suggests a similarity between the effects of smoking and aging. Prediction of lung cancer risk in former smokers by simple integration of smoking effects with aging demonstrated a good correlation with that estimated from the relative risk of the period of smoking cessation. In contrast to the smoking period, there appears to be a linear relationship between smoking strength and cancer risk. This might arise if the dose–response relationship between smoking strength and each carcinogenic step is less than linear, or the effects become saturated with a large dose of daily smoking. Such a dose–response relationship could lead to relatively large clinical effects, such as cardiovascular mortality, by low-dose tobacco smoke exposure, e.g., second-hand smoking. Consideration of the dose–response of each effect is important to evaluate the risk arising from each carcinogenic factor. © The Author(s) 2016
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title_short	Smoking: additional burden on aging and death
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