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Tobacco smoking is deleterious to reproduction. Benzo[a]pyrene (B[a]P) is a potent carcinogen in cigarette smoke. Its reactive metabolite induces DNA-adducts, which can cause mutations. We investigated whether B[a]P diol epoxide (BPDE) DNA adducts are detectable in preimplantation embryos in relation to parental smoking. A total of 17 couples were classified by their smoking habits: (i) both partners smoke; (ii) wife non-smoker, husband smokes; and (iii) both partners were non-smokers. Their 27 embryos were exposed to an anti-BPDE monoclonal antibody that recognizes BPDE-DNA adducts. Immunostaining was assessed in each embryo and an intensity score was calculated for embryos in each smoking group. The proportion of blastomeres which stained was higher for embryos of smokers than for non-smokers (0.723 versus 0.310). The mean intensity score was also higher for embryos of smokers (1.40+/-0.28) than for non-smokers (0.38+/-0.14; P = 0.015), but was similar for both types of smoking couples. The mean intensity score was positively correlated with the number of cigarettes smoked by fathers (P = 0.02). Increased mean immunostaining in embryos from smokers, relative to non-smokers, indicates a relationship with parental smoking. The similar levels of immunostaining in embryos from both types of smoking couples suggest that transmission of modified DNA is mainly through spermatozoa. We confirmed paternal transmission of modified DNA by detection of DNA adducts in spermatozoa of a smoker father and his embryo.

Objective: To detect immunoreactivity to cotinine protein, a major metabolite of nicotine, in granulosa-lutein cells from patients exposed to cigarette smoke, as measured by levels of cotinine in follicular fluid (FF) samples., Design: Controlled immunocytochemical study., Setting: Hospital IVF-ET program treating infertile patients., Patient(s): Twenty-eight women classified by self-reported smoking habits: active smokers (n = 17), passive smokers (n = 4), and nonsmokers (n = 7)., Intervention(s): Ovarian hyperstimulation., Main Outcome Measure(s): Grades of immunostaining intensity were assessed in granulosa-lutein cells. Patient scores of cell immunostaining were calculated and regressed on levels of FF cotinine., Result(s): Cotinine levels in FF were higher in active smokers than in passive smokers or nonsmokers. Cotinine immunostaining was visualized in the nucleus and cytoplasm of granulosa-lutein cells. Mean grades and mean scores of immunostaining intensity were higher in active smokers than in passive smokers or nonsmokers. There was a strong positive correlation between scores of cell immunostaining and FF cotinine levels., Conclusion(s): The association between cotinine expression in granulosa-lutein cells and FF cotinine provides reliable evidence for a dose-related effect. This constituent of cigarette smoke appears to interact directly with and incorporate into these ovarian cells. Our approach seems useful for monitoring ovarian exposure to environmental toxins.

Smoking of classic cigarettes has been well-established as a health risk factor, including cardiovascular, neurological, and pulmonary diseases. Adverse effects on human reproduction have also been shown. Smokers are assumed to have a significantly lower chance of pregnancy, however, the impact of smoking on medically assisted reproduction (MAR) treatment outcomes is controversial. Moreover, smoking habits have changed during the last decades since e-cigarettes and hookahs, or water pipes, have become very popular, yet little is known regarding vaping or hookah-smoking patients undergoing MAR treatments. This prospective study aimed to examine the presence of benzo[a]pyrene, nicotine, and its main metabolite, cotinine, in human follicular fluid (FF) in non-smoking, smoking, and vaping/hookah-smoking patients and to evaluate the impact on female fertility. Human FF samples were collected from 320 women subjected to intracytoplasmic sperm injection (ICSI) cycles due to male subfertility. Gas chromatography combined with mass spectrometry was used to analyse the presence of benzo[a]pyrene, nicotine, and cotinine. A questionnaire was provided to assess patient consumption behaviour and to identify (1) non-smoking patients, (2) patients who consumed cigarettes, and (3) patients with exclusive consumption of e-cigarettes or hookahs. Data were analysed using linear and logistic regression, Fisher's exact test, and the Mann–Whitney U Test. Nicotine was present in 22 (6.8%) and cotinine in 65 (20.3%) of the 320 samples. The nicotine and cotinine concentrations per sample ranged from 0 to 26.3 ng/ml and 0–363.0 ng/ml, respectively. Benzo[a]pyrene was not detectable in any of the samples analysed. Nicotine and cotinine were also present in the FF of patients with exclusive consumption of e-cigarettes or hookahs. The clinical pregnancy rate, fertilization and maturation rates, and number of oocytes per oocyte pick-up were not statistically significantly different between non-smoking, smoking, or vaping/hookah-smoking patients. Smoking and the accumulation of smoking toxins in the FF have no impact on the outcome of MAR treatments—neither the clinical pregnancy rate, maturation and fertilization rates, nor the number of retrieved oocytes were affected. For the first time, nicotine and cotinine were quantified in the FF of patients exclusively vaping e-cigarettes or smoking hookahs. Since vaping liquids and hookah tobaccos contain potentially harmful substances, other adverse effects cannot be excluded. Trial registration ClinicalTrials.gov Identifier: NCT03414567. [ABSTRACT FROM AUTHOR]

Our objective was determining the effects of amniotic fluid (AF) and fetal cord blood (FCB) cotinine concentrations on pregnancy complications and the anthropometric measurements in the newborns whose mothers underwent amniocentesis. This study was conducted as a case-control study, in Turkey. A total of 250 pregnant women with amniocentesis indication were recruited into the study and the cotinine levels in the AF and FCB were determined. A smoking habit did not statistically affect the incidence of pregnancy complications (p>.05). The birth weights of the newborns were negatively correlated with the AF cotinine levels. The incidences of low birth weight, low Apgar scores and RDS were positively correlated with higher levels of cotinine in AF and FCB. It is important for healthcare staff to provide training and consultancy services for the health improvement of pregnant women and the prevention of smoking during pregnancy. Impact statement What is already known on this subject? The pre-pregnancy smoking habit usually continues during the pregnancy. A significant negative correlation was present between the foetal cord blood cotinine levels and the birth weight. What do the results of this study add? The anthropometric measurements of the newborns born from mothers with high AF cotinine levels were lower than newborns born from mothers with low amniotic fluid cotinine levels. Respiratory Distress syndrome is more often determined in newborns born from mothers with high AF cotinine levels. What are the implications of these findings for clinical practice and/or further research? Future studies should be performed to investigate the effects of cigarette smoking on the health problems, the growth characteristics and the neurological development of newborns and infants within the first year of life. [ABSTRACT FROM AUTHOR]

Introduction: The primary goal of nicotine replacement therapy (NRT) is to reduce smoking related harms by introducing low nicotine products. In spite of being a potential mode of NRT, there is lack of information on the risks and safety of long term oral nicotine usage on the female reproductive system.Methods: We evaluated the effects of 30 µg/mL oral nicotine consumption on the estrous cycle, circulating estradiol levels, and uterine and ovarian morphology after 2 or 7 weeks of intake by female Sprague-Dawley rats.Results: Estrous phase frequencies were similar between nicotine treated and control groups throughout the study, no changes were detected in nicotine-treated animals before and during the nicotine exposure period, and circulating estradiol levels were comparable between animals in both groups after 2 weeks of nicotine consumption. Histological examination of uteri from the nicotine group revealed a significant decrease in the height of uterine surface epithelium and an increase in the height of glandular epithelium compared to control animals; yet, the ovaries did not show attrition or changes in follicular appearance due to nicotine.Conclusions: These preclinical studies suggest that nicotine intake results in structural changes in uterine tissues without disrupting estrous cyclicity or estradiol hormone levels. Though oral nicotine may not be totally risk-free, continuing research on this mode of nicotine administration is worthwhile to determine optimal dosing and duration of consumption for its potential use as an NRT. [ABSTRACT FROM AUTHOR]

Many studies have reported that the contents of cigarette smoke negatively affect sperm parameters, seminal plasma, and various other fertility factors. Nevertheless, the actual effect of smoking on male fertility is not clear. The effect of smoking on semen parameters is based on the well-established biological finding that smoking increases the presence of reactive oxygen species, thereby resulting in oxidative stress (OS). OS has devastating effects on sperm parameters, such as viability and morphology, and impairs sperm function, hence reducing male fertility. However, not all studies have come to the same conclusions. This review sheds light upon the arguable association between smoking and male fertility and also assesses the impact of non-smoking routes of tobacco consumption on male infertility. It also highlights the evidence that links smoking with male infertility, including newly emerging genetic and epigenetic data, and discusses the clinical implications thereof. [ABSTRACT FROM AUTHOR]

Purpose: The majority of previous studies have observed an increased risk of mucinous ovarian tumors associated with cigarette smoking, but the association with other histological types is unclear. In a large pooled analysis, we examined the risk of epithelial ovarian cancer associated with multiple measures of cigarette smoking with a focus on characterizing risks according to tumor behavior and histology. Methods: We used data from 21 case-control studies of ovarian cancer (19,066 controls, 11,972 invasive and 2,752 borderline cases). Study-specific odds ratios (OR) and 95 % confidence intervals (CI) were obtained from logistic regression models and combined into a pooled odds ratio using a random effects model. Results: Current cigarette smoking increased the risk of invasive mucinous (OR = 1.31; 95 % CI: 1.03-1.65) and borderline mucinous ovarian tumors (OR = 1.83; 95 % CI: 1.39-2.41), while former smoking increased the risk of borderline serous ovarian tumors (OR = 1.30; 95 % CI: 1.12-1.50). For these histological types, consistent dose-response associations were observed. No convincing associations between smoking and risk of invasive serous and endometrioid ovarian cancer were observed, while our results provided some evidence of a decreased risk of invasive clear cell ovarian cancer. Conclusions: Our results revealed marked differences in the risk profiles of histological types of ovarian cancer with regard to cigarette smoking, although the magnitude of the observed associations was modest. Our findings, which may reflect different etiologies of the histological types, add to the fact that ovarian cancer is a heterogeneous disease. [ABSTRACT FROM AUTHOR]

BACKGROUND: Germline mutations in BRCA1 and BRCA2 ( BRCA1/2) are related to an increased lifetime risk of developing breast and ovarian cancer. Although risk-reducing salpingo-oophorectomy reduces the risk of both cancers, loss of fertility is a major concern. A recent study suggested an association between BRCA1 mutation and occult primary ovarian insufficiency. The objective of the current study was to determine whether BRCA1/2 mutation carriers have an earlier onset of natural menopause compared with unaffected women. METHODS: White carriers of the BRCA1/2 gene (n = 382) were identified within the Breast Cancer Risk Program Registry at the University of California at San Francisco and compared with non-clinic-based white women in northern California (n = 765). The 2 groups were compared with regard to median age at the time of natural menopause before and after adjustment for known risk factors, and the role of smoking within each group was examined using the Kaplan-Meier approach for unadjusted analyses and Cox proportional hazards regression analyses for adjusted analyses. RESULTS: The median age at the time of natural menopause in the BRCA1/2 carriers was significantly younger than among the unaffected sample (50 years vs 53 years; P < .001). The unadjusted hazard ratio for natural menopause when comparing BRCA1/2 carriers with unaffected women was 4.06 (95% confidence interval, 3.03-5.45) and was 3.98 (95% confidence interval, 2.87-5.53) after adjusting for smoking, parity, and oral contraceptive use. For BRCA1/2 carriers who were current heavy smokers (smoking ≥ 20 cigarettes/day), the median age at natural menopause was 46 years versus 49 years for nonsmokers ( P = .027). CONCLUSIONS: The BRCA1/ 2 mutation was associated with a significantly earlier age at natural menopause, and heavy smoking compounded this risk. Because the relationship between menopause and the end of natural fertility is considered to be fixed, these findings suggest the risk of earlier infertility among BRCA1/ 2 carriers. Cancer 2013. © 2012 American Cancer Society. [ABSTRACT FROM AUTHOR]

The association between parental smoking and risk of childhood acute lymphoblastic leukemia (ALL) was investigated in an Australian population-based case-control study that included 388 cases and 868 controls aged <15 years, recruited from 2003 to 2006. Both of the child’s parents provided information about their smoking habits for each year from age 15 years to the child’s birth. Data were analyzed by logistic regression. Maternal smoking was not associated with risk of childhood ALL, but the odds ratio for paternal smoking of ≥15 cigarettes per day around the time of the child’s conception was 1.35 (95% confidence interval: 0.98, 1.86). The associations between parental smoking risk of childhood ALL did not differ substantially by immunophenotypic or cytogenetic subtype. Meta-analyses of paternal smoking, including results from the Australian Study of Causes of Acute Lymphoblastic Leukemia in Children and those of previous studies, produced summary odds ratios of 1.15 (95% confidence interval: 1.06, 1.24) for any paternal smoking around the time of the child’s conception and 1.44 (95% confidence interval: 1.24, 1.68) for smoking ≥20 cigarettes per day at that time. Study results suggest that heavier paternal smoking around the time of conception is a risk factor for childhood ALL. Men should be strongly encouraged to cease smoking, particularly when planning to start a family. [ABSTRACT FROM PUBLISHER]

To investigate the effect of age and smoking on the AMH levels in normal cycling healthy women with normal reproductive history. In 137 women, blood samples were taken on day 3 of a spontaneous cycle. Serum FSH, LH, E2, progesterone and AMH were measured in all blood samples. For the statistical analysis of the data, t test, Pearson’s correlation and linear regression analysis were performed. Of 137 women (43%), 59 were smokers. Age was positively correlated with serum FSH and LH levels ( r = 0.584, P < 0.001 and r = 0.330, P < 0.001, respectively) and negatively correlated with serum AMH levels ( r = −0.882, P < 0.001). There were no significant differences in FSH, LH, E2, progesterone and AMH levels between smokers and non-smokers. Multiple stepwise linear regression analysis showed that in both smokers and non-smokers, age was the most significant determinant of AMH levels ( r = −0.889, P < 0.001 and r = −0.944, P < 0.001, respectively), while smoking was not related to AMH levels. Aging significantly decreases AMH levels in women with normal cycles and normal reproductive history, while smoking does not seem to have significant effects on AMH levels. [ABSTRACT FROM AUTHOR]

Cigarette smoke has been linked to adult myeloid leukemia; however, the association between parental smoking and childhood leukemia remains unclear. Parental smoking and the risk of childhood leukemia were examined in the Northern California Childhood Leukemia Study, a case-control study, between 1995 and 2002. The present analysis included 327 acute childhood leukemia cases (281 acute lymphoblastic leukemia (ALL) and 46 acute myeloid leukemia (AML)) and 416 controls matched on age, sex, maternal race, and Hispanic ethnicity. Maternal smoking was not associated with an increased risk of either ALL or AML. Paternal preconception smoking was significantly associated with an increased risk of AML (odds ratio = 3.84, 95% confidence interval: 1.04, 14.17); an increased risk for ALL was suggestive for paternal preconception smoking (odds ratio = 1.32, 95% confidence interval: 0.86, 2.04). Greater risks of ALL were observed compared with the risk associated with paternal preconception smoking alone, when paternal preconception smoking was combined with maternal postnatal smoking (pinteraction = 0.004) or postnatal passive smoking exposure (pinteraction = 0.004). These results strongly suggest that exposure to paternal preconception smoking alone or in combination with postnatal passive smoking may be important in the risk of childhood leukemia. [ABSTRACT FROM AUTHOR]

The many studies into the relation between cigarette smoking and the risk of ovarian cancer have produced inconsistent results. Here we investigated this relation using data from the Japan Collaborative Cohort Study for Evaluation of Cancer Risk, initiated in 1988.A self-administered questionnaire on smoking habits and other risk factors for cancer was completed by 34 639 Japanese women. After 7.6 years of follow up, 39 cases of ovarian cancer were available for analyses. Cox proportional-hazards models were used to compute relative risks (RR) and to adjust for confounders.Relative to those who had never smoked, the RR of ovarian cancer were 1.63 (95% confidence interval[CI] = 0.21–12.50) for former smokers and 2.27 (95% CI = 0.85–6.08) for current smokers. Among current smokers, the RR were 1.48 (95% CI = 0.20–10.92), 5.56 (95% CI = 1.68–19.06), and 1.86 (95% CI = 0.25–14.30) among women who smoked<10, 10–19, and at least 20 pack-years ([number of cigarettes smoked per day/20] × number of years subject has smoked), respectively, relative to those who had never smoked. A test for trend was statistically significant (P = 0.044).These data indicate that cigarette smoking increases the risk of developing ovarian cancer in the Japanese population. [ABSTRACT FROM AUTHOR]

Presents a study to determine whether there is variation in levels of follicular fluid (FF) cotinine between the two ovaries of women undergoing in vitro fertilization (IVF), who are exposed to cigarette smoke. Information on the effect cigarette smoking has on the reproductive health of women; How cigarette smoke can be detected in body fluids; Materials and methods used in the study; Results of the study.

Background: Ovarian cancer (OC) is the seventh most common malignancy worldwide and the most lethal gynaecological malignancy. We aimed to explore global geographical patterns and temporal trends from 1973 to 2015 for 41 countries in OC incidence and especially to analyse the birth cohort effect to gain further insight into the underlying causal factors of OC and identify countries with increasing risk of OC.Methods: OC data were drawn from the Cancer Incidence in Five Continents databases and online databases published by governments. The joinpoint regression model was applied to detect changes in OC trends. The age-period-cohort model was applied to explore age and birth cohort effects.Results: The age-standardized rate of OC incidence ranged from 3.0 to 11.4 per 100,000 women worldwide in 2012. The highest age-standardized rate was observed in Central and Eastern Europe, with 11.4 per 100,000 women in 2012. For the most recent 10-year period, the increasing trends were mainly observed in Central and South America, Asia and Central and Eastern Europe. The largest significant increase was observed in Brazil, with an average annual percentage change of 4.4%. For recent birth cohorts, cohort-specific increases in risk were pronounced in Estonia, Finland, Iceland, Lithuania, the United Kingdom, Germany, the Netherlands, Italy, Malta, Slovenia, Bulgaria, Russia, Australia, New Zealand, Brazil, Costa Rica, Ecuador, India, Japan, the Philippines and Thailand.Conclusions: Disparities in the incidence and risk of OC persist worldwide. The increased risk of birth cohort in OC incidence was observed for most countries in Asia, Central and Eastern Europe, and Central and South America. The reason for the increasing OC risk for recent birth cohorts in these countries should be investigated with further epidemiology studies. [ABSTRACT FROM AUTHOR]