To quit or not: Vulnerability of women to smoking tobacco

Park, Se-Jung; Yi, B; Lee, Ho-Sun; Oh, Woo-Yeon; Na, Hyunkyung; Lee, Min‐Jeong; Yang, Mihi

doi:10.1080/10590501.2015.1131539

Cited by 9 publications

(12 citation statements)

References 127 publications

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“…Some studies have reported that duration of smoking is a much stronger risk factor than amount smoked [17,18,19,20]. Table 4 presents data of genetic frequencies for smokers stratified by smoking duration as a categorical variable (<20 YS/≥20 YS).…”

Section: Resultsmentioning

confidence: 99%

Effect of Genetic Polymorphisms and Long-Term Tobacco Exposure on the Risk of Breast Cancer

Verde

Santiago

Chicharro

et al. 2016

IJMS

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Introduction: Tobacco smoke contains many potentially harmful compounds that may act differently and at different stages in breast cancer development. The focus of this work was to assess the possible role of cigarette smoking (status, dose, duration or age at initiation) and polymorphisms in genes coding for enzymes involved in tobacco carcinogen metabolism (CYP1A1, CYP2A6) or in DNA repair (XRCC1, APEX1, XRCC3 and XPD) in breast cancer development. Methods: We designed a case control study with 297 patients, 217 histologically verified breast cancers (141 smokers and 76 non-smokers) and 80 healthy smokers in a cohort of Spanish women. Results: We found an association between smoking status and early age at diagnosis of breast cancer. Among smokers, invasive carcinoma subtype incidence increased with intensity and duration of smoking (all Ptrend < 0.05). When smokers were stratified by smoking duration, we only observed differences in long-term smokers, and the CYP1A1 Ile462Ile genotype was associated with increased risk of breast cancer (OR = 7.12 (1.98–25.59)). Conclusions: Our results support the main effect of CYP1A1 in estrogenic metabolism rather than in tobacco carcinogen activation in breast cancer patients and also confirmed the hypothesis that CYP1A1 Ile462Val, in association with long periods of active smoking, could be a breast cancer risk factor.

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Section: Resultsmentioning

confidence: 99%

Effect of Genetic Polymorphisms and Long-Term Tobacco Exposure on the Risk of Breast Cancer

Verde

Santiago

Chicharro

et al. 2016

IJMS

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“…Some authors have suggested that women tend to evolve from experimentation to addiction more quickly and have greater difficulty in quitting smoking [34,35]. Additionally, they are more susceptible due to hormonal differences [36]. Several studies providing evidence of gender influence on the genetic-smoking relationship are available [9,11,35].…”

Section: Discussionmentioning

confidence: 99%

CHRNA5/CHRNA3 polymorphisms and tobacco smoking risk in a Brazilian population sample

Mota

Mitri

Barata-Silva

et al. 2020

GSC Biol. and Pharm. Sci.

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Tobacco smoking is a major risk factor of several diseases such as lung cancer, stroke, chronic obstructive pulmonary disease and increases the susceptibility to infectious diseases. The understanding of smoking addiction requires phenotyping and genotyping studies. Variations in CHRNA5/CHRNA3 can alter receptor responses to nicotine and thus interfere with smoking behavior and risk. Therefore, this study aimed to investigate the association of CHRNA5 rs16969968 and CHRNA3 rs578776 with smoking behavior in a Brazilian population sample, comprising 449 subjects. Smoking data was obtained from a questionnaire. The polymorphisms were genotyped by Polymerase Chain Reaction (PCR). Associations were verified using logistic and linear regression analyses. We found that women with the variant AA genotype for CHRNA5 rs16969968 were at significantly increased risk of smoking, with an OR of 3.09 (95% CI: 1.09-8.76; p= 0.033). The variant TT genotype of CHRNA3 rs578776 showed protection against smoking and later smoking initiation in the overall population and in women, with an OR of 0.41 (95% CI: 0.19-0.88; p=0.022). In conclusion, CHRNA5 rs16969968 and CHRNA3 rs578776 were associated with increased risk and protective effect against smoking, respectively, in a Brazilian population sample. Gender and recessive homozygosis of the polymorphisms variants resulted in a significant effect regarding the results.

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“…This sex-based difference has been largely attributed to a bene cial protective role of female hormones on the cardiovascular system [16]. Contradictory reports have suggested that smoking women are more prone to develop worse adverse health outcome than smoking men [17]. This has been attributed to the combination of many factors.…”

Section: Introductionmentioning

confidence: 99%

“…Genetic and biological factors, hormonal factors, socioeconomic factors, occupational exposure, work stress, personal lifestyle, and secondhand smoke exposure may be responsible for adverse health outcomes in women [18]. This debate occurs along with the rising epidemic of smoking among women, while the prevalence of smoking among men is in slow decline [17].…”

Section: Introductionmentioning

confidence: 99%

Sex Differences in Cardiac Remodeling Post Myocardial Infarction with Acute Cigarette Smoking

Kaplan

Abidi

Diab

et al. 2022

Preprint

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Background. Whether cigarette smoking affects the heart post-myocardial infarction (MI) in a sex-dependent way remains controversial. Using a mouse model, we investigated cardiac remodeling under the influence of acute cigarette smoke (CS) exposure following ischemic injury in both sexes. Methods. Ten cigarettes were smoked twice daily for 2 weeks followed by MI and then 1 additional week post permanent LAD ligation. Cardiac function, histology, and infarct size were assessed, and inflammatory markers quantified by RT-PCR. Statistical comparisons were performed using an unpaired t-test or ANOVA followed by Tukey post hoc test. Results. We observed that cigarette smoking exacerbated both left and right ventricular remodeling only in males at an early stage of post-MI. Females did not display a significant structural and/or functional alteration within 7 days of cardiac remodeling post-MI upon CS exposure. Worsened right ventricular remodeling in males was independent of pulmonary congestion. CS-exposed males exhibited enhanced increases in left ventricular end systolic and diastolic volumes, as well as reductions in ejection fraction and fractional area changes of left ventricular base. At day 7, infarct size was increased by cigarette smoking in males only, which was accompanied by enhanced collagen deposition in both the infarcted and peri-infarcted areas. Both IL-6 and TNF-α mRNA expression significantly increased in CS-exposed MI male group only at day 7 post-MI suggestive of prolonged inflammation. Conclusions. These findings indicate that CS exposure worsens the progression of cardiac remodeling post-MI in male sex in a significant manner compared to female sex at least at early stages.

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To quit or not: Vulnerability of women to smoking tobacco

Cited by 9 publications

References 127 publications

Effect of Genetic Polymorphisms and Long-Term Tobacco Exposure on the Risk of Breast Cancer

Effect of Genetic Polymorphisms and Long-Term Tobacco Exposure on the Risk of Breast Cancer

CHRNA5/CHRNA3 polymorphisms and tobacco smoking risk in a Brazilian population sample

Sex Differences in Cardiac Remodeling Post Myocardial Infarction with Acute Cigarette Smoking

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