Passive Smoking In Childhood Research Articles

IMPACT OF HEAT–NOT–BURN CIGARETTE PASSIVE SMOKING ON CHILDREN‘S OXIDATIVE STRESS, ENDOTHELIAL AND PLATELET FUNCTION

IMPACT OF HEAT–NOT–BURN CIGARETTE PASSIVE SMOKING ON CHILDREN‘S OXIDATIVE STRESS, ENDOTHELIAL AND PLATELET FUNCTION

Mediating Effect of Tobacco Dependence on the Association Between Maternal Smoking During Pregnancy and Chronic Obstructive Pulmonary Disease: Case-Control Study.

Maternal smoking during pregnancy (MSDP) is a known risk factor for offspring developing chronic obstructive pulmonary disease (COPD), but the underlying mechanism remains unclear. This study aimed to explore whether the increased COPD risk associated with MSDP could be attributed to tobacco dependence (TD). This case-control study used data from the nationwide cross-sectional China Pulmonary Health study, with controls matched for age, sex, and smoking status. TD was defined as smoking within 30 minutes of waking, and the severity of TD was assessed using the Fagerstrom Test for Nicotine Dependence. COPD was diagnosed when the ratio of forced expiratory volume in 1 second to forced vital capacity was <0.7 in a postbronchodilator pulmonary function test according to the 2017 Global Initiative for Chronic Obstructive Lung Disease criteria. Logistic regression was used to examine the correlation between MSDP and COPD, adjusting for age, sex, BMI, educational attainment, place of residence, ethnic background, occupation, childhood passive smoking, residential fine particulate matter, history of childhood pneumonia or bronchitis, average annual household income, and medical history (coronary heart disease, hypertension, and diabetes). Mediation analysis examined TD as a potential mediator in the link between MSDP and COPD risk. The significance of the indirect effect was assessed through 1000 iterations of the "bootstrap" method. The study included 5943 participants (2991 with COPD and 2952 controls). Mothers of the COPD group had higher pregnancy smoking rates (COPD: n=305, 10.20%; controls: n=211, 7.10%; P<.001). TD was more prevalent in the COPD group (COPD: n=582, 40.40%; controls: n=478, 33.90%; P<.001). After adjusting for covariates, MSDP had a significant effect on COPD (β=.097; P<.001). There was an association between MSDP and TD (β=.074; P<.001) as well as between TD and COPD (β=.048; P=.007). Mediation analysis of TD in the MSDP-COPD association showed significant direct and indirect effects (direct: β=.094; P<.001 and indirect: β=.004; P=.03). The indirect effect remains present in the smoking population (direct: β=.120; P<.001 and indirect: β=.002; P=.03). This study highlighted the potential association between MSDP and the risk of COPD in offspring, revealing the mediating role of TD in this association. These findings contribute to a deeper understanding of the impact of prenatal tobacco exposure on lung health, laying the groundwork for the development of relevant prevention and treatment strategies.

Impact of heat-not-burn cigarette passive smoking on children's oxidative stress, endothelial and platelet function

Growing global use of heat-not-burn cigarettes (HNBC) prompts investigation. Prior studies assessed HNBC's effects on cardiovascular health, revealing heightened oxidative stress, platelet activation, and endothelial dysfunction. However, limited understanding exists regarding passive smoking's impact on children exposed to HNBC.This study aims to assess levels of oxidative stress, endothelial and platelet function among children exposed to passive smoke from HNBC, traditional tobacco (TT) cigarettes and unexposed subjects.Seventy-eight children (2–18 years) were divided into three groups: HNBC passive smokers (n = 26), TT cigarette exposed (n = 26), and control (CNT) group (n = 26, unexposed).Oxidative stress was evaluated by serum NADPH oxidase-2 (NOX2) activity, assessed by soluble Nox2-derived peptide (sNOX2-dp), isoprostanes, hydrogen peroxide (H2O2) production, hydrogen break-down activity (HBA) and NO bioavailability. Endothelial function was assessed by brachial flow-mediated dilation (FMD). Platelet function was evaluated by soluble CD40 ligand (sCD40L), soluble P-selectin (sP-selectin) and thrombus formation by T-TAS analysis.Passive smoking-exposed children (both HNBC and TT) exhibited significantly increased serum sNOX2-dp, isoprostanes, H2O2, sCD40L sP-selectin and thrombus formation versus controls. Conversely, exposed children displayed reduced brachial FMD and serum NO bioavailability. No significant differences were found between children exposed to passive smoking of HNBC vs TT.Multivariable regression linked sNOX2 (standardized coefficient β: 0.284; SE: 0.040; p = 0.01) and H2O2 (standardized coefficient β: 0.243; SE: 0.0; p = 0.02) as independent predictors of FMD, and isoprostanes (standardized coefficient β:0.388; SE: 0.022; p < 0.001) and serum cotinine (standardized coefficient β:0.270; SE: 0.048; p = 0.01) with sNOX2-dp levels.Exposure to HNBC smoke heightened oxidative stress, endothelial dysfunction, platelet activation, and thrombus formation in children. Findings suggest avenues for interventions to curb childhood passive smoking exposure.

Childhood and adulthood passive and active smoking, and the ABO group as risk factors for pancreatic cancer in women.

Active smoking and the A blood group are associated with pancreatic adenocarcinoma (PC) risk. However, potential interactions between those risk factors and the role of passive smoking have been little investigated. We aimed to explore specific and joint associations of passive and active smoking, and effect modification by the ABO blood group in French women. The study included 96,594 women from the E3N prospective cohort, mean age: 49years (SD 6.7). Information on active and passive smoking was reported at inclusion and throughout follow-up. Cases were classified according to the International Classification of Diseases 10. Associations with passive and active smoking and effect modification by the ABO blood group were investigated with multivariable Cox regression models to estimate hazard ratios (HR) and 95% confidence intervals (CI). During a 24-year median follow-up, 346 incident PC cases were identified. Current smoking compared with never and former smoking (HR 1.51 [95% CI 1.08-2.10]), and passive smoking in childhood compared with no childhood exposure (HR 1.47 [95% CI 1.08-2.00]) were associated with increased PC risk, but not passive exposure in adulthood (HR 1.16 [95% CI 0.91-1.47]). Exposure to both passive smoking in childhood and current smoking was associated with a stronger risk (HR 2.80 [95% CI 1.42-5.52]) than exposure to both current smoking and passive smoking only in adulthood (HR 1.68 [95% CI 1.10-2.57]) compared with neither passive nor active smoking. Associations between active smoking and PC risk were strongest in the O or B groups, while associations with passive smoking were strongest in the A or AB blood groups, but the interaction terms were not statistically significant. Both current smoking and passive smoking in childhood were associated with PC risk, with a maximal risk of current smokers exposed to passive smoking during childhood. Possible interactions between blood groups and active or passive smoking must be investigated in a larger series.

The Association Between Inflammatory Bowel Disease and Exposure to Tobacco Smoking: A Case-Control Study in Qatar.

This research investigated the association between childhood and adulthood tobacco smoking exposure with ulcerative colitis (UC) and Crohn's disease (CD) in Qatar. In this case-control study, CD and UC cases were matched to controls of the same age and sex. The associations between UC and CD and childhood passive smoking and adulthood active smoking were assessed using conditional multivariable logistic regression. A total of 89 CD cases, median age of 37 years (IQR 29-47), and 362 UC cases, median age of 35 years (IQR 28-44), and equal numbers of controls were included. After multivariable logistic regression, CD was associated with higher odds of being a current smoker (OR 2.51, 95% CI 0.85-7.37, p=0.095), with weak evidence against the null hypothesis. This association was more pronounced in women, where CD was associated with both adulthood current smoking (OR 42.71, 95% CI, 1.17-1559.57, p=0.041), and childhood smoking exposure (OR 8.23, 95% CI, 1.36-49.66, p=0.021). In males, no associations were observed between CD and the smoking exposures. No associations were observed between UC and both smoking variables. In Qatar, adulthood tobacco smoking appears to increase the odds of CD. Further, our findings suggest that both childhood and adulthood cigarette smoke exposure may possibly have a detrimental effect on the odds of CD in females but not in males, although further research is needed.

Breastfeeding and infant acute otitis media: A comprehensive analytical study

Significance of the study acute otitis media (AOM) is an infection of the middle ear usually caused by a complication of viral infection in the upper respiratory tract 1. The interaction of virus and bacteria plays an important role in the development of AOM and in the latter case can be treated with antibiotics . Due to limited space in the middle ear and relatively poor drainage through the Eustachian tube, especially in young children, AOM is often accompanied by significant pain and other characteristics including fever, acute loss of hearing and general lethargy. The factors currently identified as associated with a reduced risk of AOM include breastfeeding, avoidance of in utero and childhood passive tobacco smoke exposure, and avoidance of indoor air pollution. Evidence from the literature supports a reduction in AOM risk from breastfeeding. However, there has been no recent comprehensive analytical review, particularly addressing issues related to the effect of duration and exclusivity of breastfeeding on the risk of AOM. Therefore, we aimed to study the relation between Breastfeeding and acute otitis media.

Passive smoking in childhood and adulthood and risk of rheumatoid arthritis in women: results from the French E3N cohort study

ObjectiveThe association between passive smoking exposure in childhood or in adulthood, and the risk of rheumatoid arthritis (RA) has been incompletely investigated. We aimed to assess the relationship between exposure...

The Association of Passive Smoking and Serum Urotensin-II Levels in Children.

Urotensin-II (UT-II) is the most powerful vasoconstrictor agent and is known to play a role in heart failure, diabetes, pulmonary hypertension and asthma. The effect of passive smoking on UT-II levels is unknown. The present study aims to evaluate serum UT-II levels in children exposed to passive smoke. The study included a total of 120 children; 47 children not exposed to passive smoke were included in Group 1 (control group), and 73 children exposed to passive smoke were included in Group 2. Serum samples of the participants were stored at -80 °C after centrifugation and were assessed at least two times with high-precision human ELISA kits. Serum UT-II levels were significantly higher in the children exposed to passive smoke than in the children not exposed. Furthermore, Group 2 was grouped according to the number of cigarettes smoked at home per day, type of passive smoking (second-hand smoke or third-hand smoke), and how many people in their family and/or living together smoked. There was a positive correlation between the number of cigarettes they were exposed to per day and serum UT-II levels. Passive smoking in childhood may be associated with high serum UT-II levels.

Passive smoking in childhood accelerates RA risk for smokers.

Passive smoking in childhood accelerates RA risk for smokers.

In Utero Exposure to Smoking and Alcohol, and Passive Smoking during Childhood: Effect on the Retinal Nerve Fibre Layer in Young Adulthood

ABSTRACT Purpose In utero exposure to cigarette smoke has been suggested to result in thinner retinal nerve fibre layer (RNFL). However, the potential cofounding effects of in utero alcohol exposure and passive smoking during childhood had not been considered. We explored RNFL thickness in young adults in relation to these early life factors. Methods In 1989–1991, pregnant women completed questionnaires on their current smoking and alcohol drinking patterns. Following the birth of their offspring, information on household smokers was obtained between the 1- and 13-year follow-ups. At the 20-year follow-up, these offspring underwent an eye examination including optical coherence tomography imaging of the RNFL. Results Participants (n = 1,287) were 19–22 years old at time of eye examination. Most participants (77%) had no in utero exposure to cigarette smoke; 1.3% were initially exposed but not after 18 weeks’ gestation, while 21% had continual in utero smoking exposure. Half of the mothers never consumed alcohol or only consumed alcohol once during their pregnancies. After correcting for potential confounders, including in utero alcohel exposure and childhood passive smoking, participants who had continued in utero exposure to >10 cigarettes/day and ≤10 cigarettes/day had thinner RNFLs by 6.6 (95% confidence interval [CI] = 4.4–8.7) and 3.7 µm (95%[CI] = 2.3–5.5), respectively, than those with no exposure (p < .001). In utero alcohol exposure and childhood passive smoking were not significantly associated with RNFL thickness after accounting for in utero exposure to smoking. Conclusions In utero exposure to cigarette smoke is associated with thinner RFNL in young adulthood, independent of other early life environmental factors.

Childhood and Adulthood Passive Smoking and Nonalcoholic Fatty Liver in Midlife: A 31-year Cohort Study.

Identifying early life risk factors remains key to the prevention of nonalcoholic fatty liver (hereinafter "fatty liver") in adulthood. However, the longitudinal association of childhood passive smoking with adult fatty liver is not studied. We examined the association of childhood and adulthood passive smoking with fatty liver in midlife. This was a 31-year prospective cohort study of 1,315 participants. Information on childhood passive smoking (parental smoking) was collected in 1980 (aged 3-18 years) and 1983 and adulthood passive smoking in 2001, 2007, and 2011. Fatty liver was determined by ultrasound in 2011 (aged 34-49 years). The prevalence of fatty liver was 16.3%. Both childhood and adulthood passive smoking were associated with higher risk of fatty liver, adjusting for potential confounders such as age, sex, childhood socioeconomic status, and adulthood physical activity and alcohol consumption (relative risk = 1.41, 95% confidence interval: 1.01-1.97 for childhood; 1.35, 1.01-1.82 for adulthood). Individuals with persistent exposure to passive smoking between childhood and adulthood had the highest risk (relative risk = 1.99, 95% confidence interval: 1.14-3.45) compared with those without passive smoking in either childhood or adulthood. Passive smoking in both child and adult lives are associated with increased risk of adult fatty liver, suggesting that the prevention of passive smoking should start as early as possible and maintain throughout lifetime.

Abstract 15431: Childhood Passive Smoke Exposure is Associated With Subclinical Left Ventricular Dysfunction in Adulthood - Childhood Determinants of Adult Health Study

Introduction: Prolonged childhood passive smoke exposure may affect adult cardiovascular health but there are few studies of cardiac function. Subclinical left ventricular dysfunction detected by global longitudinal strain (GLS) is predictive of the subsequent development of heart failure. We investigated the association of passive smoke exposure during childhood with GLS in adults. Methods: Data were from the Childhood Determinants of Adult Health (CDAH) study 34-year follow-up (2014-19). Three measures of passive smoking (severity of exposure index [SEI], cumulative years of exposure [CYE], total household smokers [THS]) were derived retrospectively from a validated questionnaire. GLS was measured in clinics using a Siemens Acuson SC2000 ultrasound machine and 4V1c transducer with speckle tracking analysis. Linear regression adjusted for confounding factors (age, gender, childhood socioeconomic position, childhood smoking, adult smoking status, parental education level) examined the association between childhood passive smoke exposure and GLS in adulthood. Results: Among 781 participants (mean age 45.2 ± 2.5 SD years, 52.6% females, 54.2% exposed to passive smoking), GLS showed a decrease (β adjusted -0.17% 95% CI -0.32%, -0.02%) per SD of SEI (range: 0-318, mean 24.2 ± 35.8 SD). CYE (range: 0-106, mean 10.4 ± 13.9 SD) was associated with a decrease in GLS (β adjusted -0.18% 95% CI -0.33%, -0.05%) per SD of exposure. For each THS in childhood (range: 0-5, mean 0.9 ± 1.0 SD), there was a decrease in GLS (β adjusted -0.20% 95% CI -0.36%, -0.05%). Conclusion: Childhood passive smoke exposure, independent of own smoking, was associated with a reduction in GLS, a measure of subclinical cardiac dysfunction. Each 1% decrease in GLS has been associated with 12% higher risk of cardiovascular morbidity and mortality in low-risk general population. There are potential long-term consequences to cardiac function from childhood passive smoke exposure.

Abstract P252: Passive Smoking in Childhood and Mortality From Coronary Heart Disease in Adulthood Among Japanese Men and Women: The Jacc Study

Background: Secondhand smoke exposure among adults is an established risk factor for cardiovascular disease, but little is known about the impact of passive smoking in childhood on risk of adverse cardiovascular outcome in adulthood. We examined whether childhood exposure to secondhand smoke is associated with mortality from coronary heart disease(CHD) in adulthood among Japanese men and women. Methods: We analyzed the data for 71,459 participants ( 31,027 men and 40,432 women) aged 40-79 years, with no history of CHD, stroke, or cancer at the baseline (1988-1990) and who completed a lifestyle questionnaire including the number of family members who smoked at home in childhood(0,1,2 and 3+ members) under the Japan Collaborative Cohort Study for Evaluation of Cancer Risk (JACC Study). Results: The sex-specific proportions of current smokers were 49.0% for 0 member, 54.3% for 1 member, 56.8% for 2 members and 59.3% for 3+members among men, and the respective proportions among women were 3.3%, 5.2%, 7.2%, and 11.2%.During the median follow-up of 18.9 years, a total of 955 (589 men and 366 women) deaths from CHD were reported. There was a dose-response relationship between the number of smoking family members at home and CHD mortality at adulthood among the middle aged (40-59 years); the multivariable HRs, adjusting for age, sex, history of hypertension and diabetes, body mass index, smoking status, alcohol consumption, hours of exercise and walking, perceived mental stress, educational level and employment status, were 1.05 (95% CI: 0.74, 1.48) for 1 family member, 1.27(0.83, 1.94) for 2 family members and 2.34(1.17, 4.68) for 3+ family members compared with no family member(p for trend=0.04). Such an association was not observed for the older persons aged 60-79 years.The excess CHD mortality associated with 3+ family members among the middle-aged was more evident among never or ex-smokers than among current smokers: the respective multivariable HRs were 3.74(1.40, 10.01) and 1.90(0.72, 5.06). Conclusions: Passive smoking exposure in childhood was associated with increased risk of mortality from CHD in adulthood, primarily for the middle aged men and non-current smokers.

Parental and life-course influences on symptomatic airflow obstruction.

Few studies have examined the contribution of life-course factors in explaining familial aggregation of chronic lung conditions. Using data from the 1958 British Birth Cohort, a life-course approach was used to examine whether, and how, exposure to risk factors through one's life explained the association between parental respiratory disease history and symptomatic airflow obstruction (AO). Cohort participants (n=6212) were characterised in terms of parental respiratory disease history and symptomatic AO at 45 years. Life-course factors (e.g. smoking, asthma and early-life factors) were operationalised as life period-specific and cumulative measures. Logistic regression and path analytic models predicting symptomatic AO adjusted for parental respiratory disease history were used to test different life-course models (critical period, accumulation- and chain-of-risks models). While some life-course factors (e.g. childhood passive smoking and occupational exposure) were individually associated with parental respiratory disease history and symptomatic AO, asthma (OR 6.44, 95% CI 5.01–8.27) and persistent smoking in adulthood (OR 5.42, 95% CI 4.19–7.01) had greater impact on the association between parental respiratory disease history and symptomatic AO. A critical period model provided a better model fit compared with an accumulation-of-risk model and explained 57% of the effect of parental respiratory disease history on symptomatic AO. Adulthood asthma and smoking status explained around half of the effect of parental respiratory disease history on chronic obstructive pulmonary disease. Beyond smoking history, the combination of parental respiratory disease history and adulthood asthma may provide an opportunity for early diagnosis and intervention.

Childhood Exposure to Passive Smoking and Bone Health in Adulthood: The Cardiovascular Risk in Young Finns Study.

Passive smoke exposure has been linked to the risk of osteoporosis in adults. We examined the independent effects of childhood passive smoke exposure on adult bone health. Longitudinal, the Cardiovascular Risk in Young Finns Study. The study cohort included 1422 individuals followed for 28 years since baseline in 1980 (age 3 to 18 years). Exposure to passive smoking was determined in childhood. In adulthood, peripheral bone traits were assessed with peripheral quantitative CT (pQCT) at the tibia and radius, and calcaneal mineral density was estimated with quantitative ultrasound. Fracture data were gathered by questionnaires. Parental smoking in childhood was associated with lower pQCT-derived bone sum index in adulthood (β± SE, -0.064 ± 0.023 per smoking parent; P = 0.004) in multivariate models adjusted for age, sex, active smoking, body mass index, serum 25-OH vitamin D concentration, physical activity, and parental socioeconomic position. Similarly, parental smoking was associated with lower heel ultrasound estimated bone mineral density in adulthood (β± SE, -0.097 ± 0.041 per smoking parent; P = 0.02). Parental smoking was also associated with the incidence of low-energy fractures (OR, 1.28; 95% CI, 1.01 to 1.62). Individuals with elevated cotinine levels (3 to 20 ng/mL) in childhood had lower bone sum index with pQCT (β± SE, -0.206 ± 0.057; P = 0.0003). Children whose parents smoked and had high cotinine levels (3 to 20 ng/mL) had significantly lower pQCT-derived bone sum index compared with those with smoking parents but had low cotinine levels (<3 ng/mL) (β± SE, -0.192 ± 0.072; P = 0.008). Children of parents who smoke have evidence of impaired bone health in adulthood.

Passive smoking in childhood increases the risk of developing rheumatoid arthritis.

To investigate the link between smoking status, including childhood and adult passive exposure, and the risk of incident RA. The French E3N cohort includes 98 995 female volunteers prospectively followed since 1990. Self-administered questionnaires sent every 2-3 years collected medical events, general, lifestyle and environmental characteristics. RA diagnoses were collected in three successive questionnaires and confirmed if women received reimbursement for an RA-specific medication. The risk of incident RA was estimated using an age-adjusted Cox model that considers smoking status as a time-dependent variable. Among 71 248 women, 371 incident RA cases were confirmed. Ever-smokers not exposed to passive smoking had an increased risk of RA [1.38 (95% CI 1.10, 1.74)]. In never-smokers, passive smoking exposure during childhood was associated with a borderline increased risk of RA in the same range as active smoking in adults, with an hazard ratio (HR) of 1.43 (95% CI 0.97, 2.11). Ever-smokers who also had childhood passive smoking exposure had a higher risk of RA than smokers not exposed during childhood [HR 1.67 (95% CI 1.17, 2.39)], but without a significant difference (P = 0.30). RA began earlier in smokers exposed to childhood passive smoking. This study confirms that active smoking is associated with an increased risk of RA. It suggests for the first time that passive exposure to tobacco during childhood might also increase the risk of RA in future light smokers and probably non-smokers. Our results highlight the importance of avoiding any tobacco environment in children, especially in those with a family history of RA.

The Influence of Second-Hand Cigarette Smoke Exposure during Childhood and Active Cigarette Smoking on Crohn's Disease Phenotype Defined by the Montreal Classification Scheme in a Western Cape Population, South Africa.

BackgroundSmoking may worsen the disease outcomes in patients with Crohn’s disease (CD), however the effect of exposure to second-hand cigarette smoke during childhood is unclear. In South Africa, no such literature exists. The aim of this study was to investigate whether disease phenotype, at time of diagnosis of CD, was associated with exposure to second-hand cigarette during childhood and active cigarette smoking habits.MethodsA cross sectional examination of all consecutive CD patients seen during the period September 2011-January 2013 at 2 large inflammatory bowel disease centers in the Western Cape, South Africa was performed. Data were collected via review of patient case notes, interviewer-administered questionnaire and clinical examination by the attending gastroenterologist. Disease phenotype (behavior and location) was evaluated at time of diagnosis, according to the Montreal Classification scheme. In addition, disease behavior was stratified as ‘complicated’ or ‘uncomplicated’, using predefined definitions. Passive cigarette smoke exposure was evaluated during 3 age intervals: 0–5, 6–10, and 11–18 years.ResultsOne hundred and ninety four CD patients were identified. Cigarette smoking during the 6 months prior to, or at time of diagnosis was significantly associated with ileo-colonic (L3) disease (RRR = 3.63; 95%CI, 1.32–9.98, p = 0.012) and ileal (L1) disease (RRR = 3.54; 95%CI, 1.06–11.83, p = 0.040) compared with colonic disease. In smokers, childhood passive cigarette smoke exposure during the 0–5 years age interval was significantly associated with ileo-colonic CD location (RRR = 21.3; 95%CI, 1.16–391.55, p = 0.040). No significant association between smoking habits and disease behavior at diagnosis, whether defined by the Montreal scheme, or stratified as ‘complicated’ vs ‘uncomplicated’, was observed.ConclusionSmoking habits were associated with ileo-colonic (L3) and ileal (L1) disease at time of diagnosis in a South African cohort.

Childhood Passive Smoking Exposure and Age at Menarche in Chinese Women Who Had Never Smoked: The Guangzhou Biobank Cohort Study.

ObjectiveWe examined the associations between childhood passive smoking exposure and age at menarche in women who had never smoked in southern China.MethodsAmong 30,518 participants in Guangzhou Biobank Cohort Study (GBCS) from 2003-2008, 20,061 women who had never smoked and had complete outcome data were included. Childhood passive smoking exposure was defined as living with 1 or more smokers in the same household during childhood. Data on the number of smokers in the household and frequency of exposure (density and frequency) were also obtained. Age at menarche was measured as a continuous variable.Results11,379 (56.7%) participants were exposed to passive smoking during childhood. Compared to those with no passive smoking exposure during childhood, those with exposure ≥5 days/week had menarche 0.19 year (95% confidence interval (CI): 0.13-0.25) earlier on average. Those exposed to more than two smokers had menarche 0.38 year earlier (95% CI: 0.29-0.47). Childhood exposure was associated with early age at menarche (≤13 vs. >13 years), with an adjusted odds ratio of 1.34 (95% CI: 1.21-1.48) for high density, and 1.17 (95% CI: 1.09-1.26) for high frequency of exposure.ConclusionChildhood passive smoking exposure was associated with earlier age at menarche, with a dose-response relationship in Chinese women who had never smoked. If causal, the results support the promotion of smoking cessation in families with children, particularly young girls.

Correlation between Abortion and Infertility among Nonsmoking Women with a History of Passive Smoking in Childhood and Adolescence.

The aim of this study is to evaluate the correlation of exposing to the cigarette smoke in childhood and adolescence with infertility and abortion in women. This case-control study evaluated 178 women who had been attended to at the Amir-al-Momenin Hospital in Tehran in 2012-2013. Seventy-eight women with chief complaint of abortion, infertility, and missed abortion and 100 healthy women were considered as case and control groups, respectively. The tool was a questionnaire with two parts. In the first part demographic information was gathered and in the second part the information regarding the history of passive smoking in childhood and adolescence period, abortion, and infertility was gathered. The mean age in case and control groups was 26.24 ± 3.1 and 27.3 ± 4.2 years, respectively. The mean body mass index (BMI) was 25.74 ± 1.38 Kg/m2. Abortion rates among passive smoker and nonpassive smoker patients were statistically significant (P = 0.036). Based on findings of this study, the experience of being a passive smoker in childhood and adolescence in women will increase the risk of abortion and infertility in the future, which could be the reason to encourage the society to step back from smoking cigarettes.

Childhood passive smoke exposure is associated with adult head and neck cancer

Introduction: Passive smoke is carcinogenic but its association with head and neck squamous cell carcinoma (HNSCC) is uncertain. Methods: We conducted a case-control study of childhood passive smoke exposure (CPSE) and HNSCC in 858 cases and 806 frequency-matched controls using an interviewer-administered questionnaire. Odds ratios (OR) and 95% confidence intervals (CI) were estimated with logistic regression controlling for adult smoking in the total study population, and in never-smokers only (184 cases and 415 controls). CPSE was also studied in oropharyngeal separately from other HNSCC using polytomous logistic regression. Results: CPSE was associated with HNSCC (OR, 1.28; 95% CI, 1.01–1.63) after controlling for adult smoking and other factors. This association was similar in magnitude, although not statistically significant, among subjects who never smoked as adults (OR, 1.19, 95% CI, 0.80–1.76). CPSE was associated more strongly with oropharyngeal cancer (a HNSCC subtype commonly associated with human papillomavirus (HPV) infection) than with HNSCC at non-oropharyngeal sites (OR, 2.02; 95% CI, 1.01–4.06, N=52 cases vs. OR, 1.04; 95% CI, 0.68–1.60, N=132 cases; P-for-heterogeneity=0.08). Conclusions: Data from this large US-based case control study suggest a role for CPSE in HNSCC etiology.