Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina 27709, USA.
Epigenetic modifications, such as DNA methylation, due to in utero exposures may play a critical role in early programming for childhood and adult illness. Maternal smoking is a major risk factor for multiple adverse health outcomes in children, but the underlying mechanisms are unclear.
We investigated epigenome-wide methylation in cord blood of newborns in relation to maternal smoking during pregnancy.
We examined maternal plasma cotinine (an objective biomarker of smoking) measured during pregnancy in relation to DNA methylation at 473,844 CpG sites (CpGs) in 1,062 newborn cord blood samples from the Norwegian Mother and Child Cohort Study (MoBa) using the Infinium HumanMethylation450 BeadChip (450K).
We found differential DNA methylation at epigenome-wide statistical significance (p-value
In the course of the "1998 Health and Social Survey", questions were included to verify the prevalence of chronic respiratory diseases and also of wheezing. The objectives of this study were 1) to verify the prevalence of wheezing and its validity as an indicator of chronic respiratory diseases in Québec; and 2) to examine the relationship between chronic respiratory diseases and some of their potential determinants. A total of 30,386 individuals participated in the study. For all ages, the prevalence of wheezing was 5.4%. It was associated with asthma, allergies, chronic bronchitis and emphysema. A low familial income and tobacco smoking were associated with wheezing, asthma, chronic bronchitis and emphysema. Passive smoking was associated with wheezing whereas the presence of carpets was associated with wheezing and asthma. Between 32 and 48% of families with an asthmatic or an allergic member modified their dwelling to alleviate respiratory problems. The prevalence of wheezing documented here was lower than in anglosaxon countries. This result could be explained by a cultural factor (the French translation or the perception of wheezing). This study emphasizes the role of reducing tobacco smoking in the prevention of chronic respiratory diseases.
The objective of this study was to evaluate the impact of the 2005 British Columbia Ministry of Health Smoking Cessation Mass Media Campaign on short-term smoking behavior.
National cross-sectional data are used with a quasi-experimental approach to test the impact of the campaign.
Findings indicate that prevalence and average number of cigarettes smoked per day deviated upward from trend for the rest of Canada (P = .08; P = .01) but not for British Columbia. They also indicate that British Columbia smokers in lower risk groups reduced their average daily consumption of cigarettes over and above the 1999-2004 trend (-2.23; P = .10), whereas smokers in the rest of Canada did not, and that British Columbia smokers in high-risk groups did not increase their average daily consumption of cigarettes over and above the 1999-2004 trend, whereas smokers in the rest of Canada did (2.97; P = .01).
The overall poorer performance of high-risk groups is attributed to high exposure to cigarette smoking, which reduces a smoker's chances of successful cessation. In particular, high-risk groups are by definition more likely to be exposed to smoking by peers, but are also less likely to work in workplaces with smoking bans, which are shown to have a substantial impact on prevalence. Results suggest that for mass media campaigns to be more effective with high-risk groups, they need to be combined with other incentives, and that more prolonged interventions should be considered.
To investigate the extent to which fecundability is associated with active smoking, time since smoking cessation, and passive smoking.
Prospective cohort study.
Denmark, 2007-2011.
A total of 3,773 female pregnancy planners aged 18-40 years.
None.
Self-reported pregnancy. Fecundability ratios (FRs) and 95% confidence intervals (CIs) were estimated using a proportional probabilities model that adjusted for menstrual cycle at risk and potential confounders.
Among current smokers, smoking duration of =10 years was associated with reduced fecundability compared with never smokers (FR, 0.85, 95% CI 0.72-1.00). Former smokers who had smoked =10 pack-years had reduced fecundability regardless of when they quit smoking (1-1.9 years FR, 0.83, 95% CI 0.54-1.27; =2 years FR, 0.73, 95% CI 0.53-1.02). Among never smokers, the FRs were 1.04 (95% CI 0.89-1.21) for passive smoking in early life and 0.92 (95% CI 0.82-1.03) for passive smoking in adulthood.
Among Danish pregnancy planners, cumulative exposure to active cigarette smoking was associated with delayed conception among current and former smokers. Time since smoking cessation and passive smoking were not appreciably associated with fecundability.
Surveillance and Risk Assessment Division, Centre for Chronic Disease Prevention and Control, Population and Public Health Branch, Health Canada, 120 Colonnade Road 6702A, AL: 6702A, Ottawa, Ontario, Canada K1A 0K9. jinfu_hu@hc-sc.gc.ca
This study aimed to assess the role of active and passive smoking in the development of renal cell carcinoma (RCC). Mailed questionnaires were completed by 1279 incident RCC cases and 5370 population controls between 1994 and 1997 in eight Canadian provinces. Data were collected on socio-economic status, smoking habits, diet and passive smoking status, as well as residential and occupational history. The study found an increased risk of RCC associated with active smoking. Elevated risk of RCC was also observed with passive smoking; compared with those never exposed to either passive or active smoking, men and women with 43 or more years of passive residential and/or occupational exposure had respective adjusted Odds Ratios (ORs) of 3.9 (95% Confidence Interval (CI) 1.4-10.6) and 1.8 (95% CI 1.0-3.3) (P=0.001 and P=0.09, respectively). Both active and passive smoking might play a role in the aetiology of RCC.
Active smoking is a well-established risk factor for myocardial infarction, but less is known about the impact of passive smoking, and possible sex differences in risk related to passive smoking. We investigated active and passive smoking as risk factors for myocardial infarction in an 11-year follow-up of 11,762 men and 13,206 women included in the Tromsø Study. There were a total of 769 and 453 incident cases of myocardial infarction in men and women, respectively. We found linear age-adjusted relationships between both active and passive smoking and myocardial infarction incidence in both sexes. The relationships seem to be stronger for women than for men. Age-adjusted analyses indicated a stronger relationship with passive smoking in ever-smokers than in never-smokers. After adjustment for important confounders (body mass index, blood pressure, total cholesterol, HDL cholesterol and physical activity) the associations with active and passive smoking were still statistically significant. Adjusting for active smoking when assessing the effect of passive smoking and vice versa, indicated that the effect of passive smoking in men may be explained by their own active smoking. In women, living with a smoker =30 years after the age of 20 increased the myocardial infarction risk by 40 %, even after adjusting for active smoking. Passive smoking is a risk factor for myocardial infarction on its own, but whereas the effect for men seems to be explained by their own active smoking, the effect in females remains statistically significant.
Surveillance & Risk Assessment, Centre for Chronic Disease Prevention and Control, Population and Public Health Branch, Health Canada, Tunney's Pasture AL0601C1, Ottawa, Ontario K1A 0L2, Canada. Yang_Mao@hc-sc.gc.ca
This study assessed the influence of active and passive smoking on the risk of stomach cancer by subsite. Mailed questionnaires were used to obtain information on 1171 newly diagnosed histologically confirmed stomach cancer cases and 2207 population controls between 1994 and 1997 in eight Canadian provinces. Data were collected on socio-economic status, lifestyle and passive smoking status. Odds ratios (OR) and 95% confidence intervals (95% CI) were derived by logistic regression. Compared with those who had never smoked, there was strongly increased risk for ex- and current smokers among subjects with cardial stomach cancer. For men with cardial cancer, the adjusted ORs were 1.9 (95% CI 1.2-3.0) and 2.6 (95% CI 1.6-4.3) for ex-smokers and current smokers, respectively, with a similar pattern among women. Among men, the adjusted ORs were lower for subsites of stomach cancer other than cardia. These findings suggest that active and passive smoking may play an important role in the development of cardial stomach cancer.
Active smoking and secondhand smoke increase breast cancer risk: the report of the Canadian Expert Panel on Tobacco Smoke and Breast Cancer Risk (2009).
Science Integration Division, Centre for Chronic Disease Prevention and Control, Public Health Agency of Canada, 785 Carling Avenue, Ottawa K1A0K9, Canada. ken_lcdc_johnson@phac-aspc.gc.ca
Four authoritative reviews of active smoking and breast cancer have been published since 2000, but only one considered data after 2002 and conclusions varied. Three reviews of secondhand smoke (SHS) and breast cancer (2004-2006) each came to different conclusions. With 30 new studies since 2002, further review was deemed desirable. An Expert Panel was convened by four Canadian agencies, the Ontario Tobacco Research Unit, the Public Health Agency of Canada, Physicians for a Smoke-Free Canada and the Canadian Partnership Against Cancer to comprehensively examine the weight of evidence from epidemiological and toxicological studies and understanding of biological mechanisms regarding the relationship between tobacco smoke and breast cancer. This article summarises the panel's full report (http://www.otru.org/pdf/special/expert_panel_tobacco_breast_cancer.pdf). There are 20 known or suspected mammary carcinogens in tobacco smoke, and recognised biological mechanisms that explain how exposure to these carcinogens could lead to breast cancer. Results from the nine cohort studies reporting exposure metrics more detailed than ever/never and ex/current smoker show that early age of smoking commencement, higher pack-years and longer duration of smoking increase breast cancer risk 15% to 40%. Three meta-analyses report 35% to 50% increases in breast cancer risk for long-term smokers with N-acetyltransferase 2 gene (NAT2) slow acetylation genotypes. The active smoking evidence bolsters support for three meta-analyses that each reported about a 65% increase in premenopausal breast cancer risk among never smokers exposed to SHS. The Panel concluded that: 1) the association between active smoking and breast cancer is consistent with causality and 2) the association between SHS and breast cancer among younger, primarily premenopausal women who have never smoked is consistent with causality.
The effects of pre- or postnatal passive smoking on the adult incidence of asthma have not been reported previously. Between 1985 and 1996/1997, we conducted an 11-year community cohort study on the incidence of asthma and respiratory symptoms in Western Norway. The cohort included 3,786 subjects aged 15 to 70 years, of which 2,819 were responders at both baseline and follow-up. The incidence of asthma and five respiratory symptoms by self-reported exposure to maternal smoking in utero and in childhood, as well as smoking by other household members in childhood, was examined. After adjustment for sex, age, education, hay fever, personal smoking, and occupational exposure, maternal smoking was associated with asthma, phlegm cough, chronic cough, dyspnea grade 2, attacks of dyspnea, and wheezing, with odds ratios (95% confidence intervals [CI]) of 3.0 (1.6, 5.6), 1.7 (1.1, 2.6), 1.9 (1.2, 3.0), 1.9 (1.2, 3.0), 2.0 (1.3, 3.0), and 1.4 (0.9, 2.2), respectively. The adjusted attributable fractions (95% CI) of the adult incidence of asthma were 17.3% (5.2, 27.9) caused by maternal smoking and 9.3% (95% CI, -23.2, 33.2) caused by smoking by other household members. Exposure to pre- and postnatal smoking carries a substantial risk for developing adult asthma and respiratory symptoms.
