Tobacco Smoking In Relation Research Articles

Sex differences in the polygenic architecture of hearing problems in adults

BackgroundHearing problems (HP) in adults are common and are associated with several comorbid conditions. Its prevalence increases with age, reflecting the cumulative effect of environmental factors and genetic predisposition. Although several risk loci have been already identified, HP biology and epidemiology are still insufficiently investigated by large-scale genetic studies.MethodsLeveraging the UK Biobank, the Nurses’ Health Studies (I and II), the Health Professionals Follow-up Study, and the Million Veteran Program, we conducted a comprehensive genome-wide investigation of HP in 748,668 adult participants (discovery N = 501,825; replication N = 226,043; cross-ancestry replication N = 20,800). We leveraged the GWAS findings to characterize HP polygenic architecture, exploring sex differences, polygenic risk across ancestries, tissue-specific transcriptomic regulation, cause-effect relationships with genetically correlated traits, and gene interactions with HP environmental risk factors.ResultsWe identified 54 risk loci and demonstrated that HP polygenic risk is shared across ancestry groups. Our transcriptomic regulation analysis highlighted the potential role of the central nervous system in HP pathogenesis. The sex-stratified analyses showed several additional associations related to peripheral hormonally regulated tissues reflecting a potential role of estrogen in hearing function. This evidence was supported by the multivariate interaction analysis that showed how genes involved in brain development interact with sex, noise pollution, and tobacco smoking in relation to their HP associations. Additionally, the genetically informed causal inference analysis showed that HP is linked to many physical and mental health outcomes.ConclusionsThe results provide many novel insights into the biology and epidemiology of HP in adults. Our sex-specific analyses and transcriptomic associations highlighted molecular pathways that may be targeted for drug development or repurposing. Additionally, the potential causal relationships identified may support novel preventive screening programs to identify individuals at risk.

Life Course Tobacco Smoking and Risk of HPV-Negative Squamous Cell Carcinomas of Oral Cavity in Two Countries

BackgroundTobacco smoking remains one of the major risk factors for oral cavity cancers (OCC), a subgroup of head and neck cancer (HNC) less attributed to human papillomavirus (HPV) infection. Although a strong dose-dependent association between tobacco smoking and OCC exists, several important questions on the age-dependent effects of this habit remain unanswered. We investigated which life course hypothesis best describes the association between tobacco smoking and HPV-negative (HPV−ve) OCC in Canada and India.MethodsWe used data from the HeNCe Life study, a hospital-based case-control study conducted in Canada and India, using similar protocols. Cases were newly diagnosed subjects with primary squamous cell carcinomas of the head and neck region. Control subjects were patients with non-cancer selected from various outpatient clinics in a hospital located in the same catchment area as the cases and frequency-matched to cases according to age and sex. We collected information on an array of life course exposures using a structured questionnaire with the help of a life grid. Tobacco exposure (pack-years) during three life periods (≤ 30, 31−50, and >50 years of age) was calculated from the entire life course history of smoking. We used CDx brushes to collect oral exfoliated cells. Alpha HPV DNA detection and genotyping were performed for 36 HPV genotypes using the linear array. Participants who tested positive for HPV were excluded from the analysis. We used the Bayesian relevant life course exposure model (BRLM) to identify the life course hypothesis that best described the relationship between tobacco smoking and HPV−ve OCC.ResultsWe show evidence for a late-life sensitive period (>50 years of age) for tobacco smoking in relation to the risk of HPV−ve OCC in both Canada and India. An increase of 1 pack-year of tobacco smoking increased the risk of OCC by ~3% in both countries.ConclusionOur findings from the Canadian and Indian data suggest that smoking tobacco after 50 years of age may carry a higher risk of developing oral cancer than earlier in life. Further studies are warranted to confirm the results.

Prevalence of second-hand tobacco smoke in relation to smoke-free legislation in the European Union

Exposure to second-hand smoke (SHS) is an important public health problem. We assessed SHS exposure in restaurants and bars across the European Union (EU) and studied associations with country-level smoke-free legislation.Data of Eurobarometer surveys 2014 and 2017 were used to estimate country-specific prevalence of observing smoking in restaurants and bars, which can be considered a marker of SHS exposure. Additionally, we used multilevel logistic regression models to study associations with comprehensiveness of national smoke-free regulations in restaurants and bars, which were derived from the Tobacco Control Scale.In total, 44,809 people from all 28 EU member states were included in the analysis. The results of the multilevel logistic analysis show that in countries with complete and extensive bans, respondents were less likely to have observed people smoking inside restaurants than in countries with partial bans, which represented the lowest level of smoke-free policy implementation (OR 0.24, 95%CI 0.10–0.57 for complete ban and OR 0.23, 95%CI 0.10–0.54 for incomplete but extensive ban). Also, the prevalence of seeing people smoking in a bar was lower in the countries with an extensive ban (OR 0.23 95%CI 0.11–0.45) and with a complete ban (OR 0.20 95%CI 0.10–0.40).Between 2014 and 2017, SHS exposure in restaurants and bars decreased significantly. Our results confirm that in countries with extensive or complete smoking bans, people were less exposed to SHS in restaurants and bars; and that partial bans are less effective in reducing SHS exposure.

Prevalence of second-hand tobacco smoke in relation to smoke-free legislation in the European Union

Abstract Background Second-hand smoke (SHS) is still an important public health problem. With joining the Framework Convention on Tobacco Control (FCTC), all parties acknowledged the health risks of SHS and agreed to implement policies to protect their populations from SHS in public places. The aim of this study was to explore the SHS exposure in restaurants and bars as well as its associations with smoke-free legislation in the European Union. Methods Data of Eurobarometer surveys 2014 and 2017 were used to estimate prevalence of SHS exposure. We also extracted data on individual confounders such as smoking status, gender, sex, age and information on social economic status. Additionally, we collected data on country specific data on smoking regulations in restaurants and bars from the Tobacco Control Scale to analyse associations with SHS exposure using multilevel logistic regression. Smoking regulations were categorized into the following three categories: partial ban, comprehensive ban with minor exceptions, and complete ban. Results Preliminary results on the prevalence of SHS in restaurants showed a decrease from 11.8% (95% confidence intervals (CI) 11.2-12.5) in 2014 to 8.8% (95% CI 8.3-9.3) in 2017. The crude multilevel model controlling only for smoking prevalence resulted in an odds ratio of 0.39 (95% CI 0.19-0.77) for comprehensive ban with minor exceptions and 0.28 (95% CI 0.16-0.50) for complete ban versus partial ban. Odds ratios remained at significant levels when controlling for all available confounders. Conclusions Between 2014 and 2017, SHS exposure in restaurants decreased significantly. Furthermore, strong associations with smoking regulations were observed suggesting a high compliance. Many tobacco control policies have been introduced during the last years but several countries need to strengthen their smoke-free tobacco control policies to further reduce SHS exposure preventing death, disease and disability. Key messages SHS exposure remains a significant public health challenge. The implementation of effective measures could be strengthened through a convergence of tobacco control strategies and policies among European Union member states.

Alcohol use and tobacco smoking in relation to ovarian response among egg donors

Alcohol use and tobacco smoking in relation to ovarian response among egg donors

Exposure to Environmental Tobacco Smoke in Relation to Behavioral, Emotional, Social and Health Indicators of Slovak School Children.

Environmental tobacco smoke (ETS) exposure has been shown in general as a major environmental risk factor and deserves attention in vulnerable population groups. The aim of the project is to analyze the relationships among the ETS and behavior and health in 6−15-year-old children in Slovakia. The status of physical and mental health of children in relation to exposure to tobacco smoke was examined in a representative group of 1478 school children. The methods used, included anonymous questionnaires filled in by parents, Columbia Impairment Scale (CIS), Behavior Problem Index (BPI) and anthropometry. The prevalence of ETS exposure is the highest in the capital (27%) and southern cities. A significant association was found between ETS and age, socio-economic status, incompleteness of the family, level of mother’s education and a higher prevalence of respiratory diseases (26.7%). The relationships of ETS with emotional (CIS scores ≥ 16) and behavioral functions (BPI score ≥ 14) were significant in children exposed to mother’s or father’s smoking at home. In the multivariate analysis these associations were not significant; the factors such as income and completeness of the family were dominant. The results showed mostly the predominant impact of social factors on the physical and mental health status of Slovak school children.

Tobacco smoking trends in Samoa over four decades: can continued globalization rectify that which it has wrought?

BackgroundThe island country of Samoa (population 188,000 in 2011) forms part of Polynesia in the South Pacific. Over the past several decades Samoa has experienced exceptional modernization and globalization of many sectors of society, with noncommunicable diseases (NCD) now the leading cause of morbidity and mortality. The evolution of risk factor prevalence underpinning the increase in NCDs, however, has not been well described, including tobacco smoking which is related to cardiovascular disease, lung cancer, and chronic obstructive pulmonary disease.MethodsThe present study examines tobacco smoking in relation to different forms and effects of globalization in Samoa using 7 population-based surveys (n = 9223) over 1978–2013.ResultsThe prevalence of daily tobacco smoking steadily decreased over 1978–2013 from 76% to 36% in men, and from 27% to 15% in women (p < 0.0001 both sexes). During 1991–2013, current tobacco smoking also steadily decreased from 64% to 40% in men (p < 0.0001), and from 21% to 17% in women (p < 0.05). Declines were similar in younger (25–44 years) and older (45–64 years) men and women. Colonial globalization facilitated the introduction and prolific spread of tobacco trade and consumption in the Pacific Islands from the sixteenth century, with many populations inexorably pulled into trade relations and links to the global economy. It has also been a different globalization which may have led to the decline in smoking prevalence in Samoa in recent decades, through global dissemination since the 1950s of information on the harmful effects of tobacco smoking derived from research studies in the USA and Europe.ConclusionsOver the past 35 years tobacco smoking has steadily declined among Samoan adults; the only NCD risk factor to demonstrate marked declines during this period. By 2013 tobacco smoking in women had decreased to levels similar to Australia and New Zealand (ANZ), however in men smoking prevalence remained more than three times higher than ANZ. The impact on smoking prevalence of the variety of tobacco control interventions that have been implemented so far in Samoa need to be evaluated in order to determine the most effective initiatives that should be prioritized and strengthened.

Active and passive exposure to tobacco smoke in relation to insulin sensitivity and pancreatic β-cell function in Japanese subjects

AimSeveral studies have suggested that cigarette-smoking affects insulin sensitivity in Western populations. The present study evaluated glucose tolerance, pancreatic β-cell function and insulin sensitivity in relation to active and passive smoking among the Japanese. MethodsA total of 411 men and 586 women were recruited into a community-based cross-sectional study in Gifu, Japan. Diabetes, impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) were screened for by a 75g oral glucose tolerance test. HOMA and insulinogenic (ΔI0−30/ΔG0−30) indexes were used to estimate insulin secretion and sensitivity. To assess the possible association of self-reported smoking status and parameters of glucose metabolism, logistic regression was applied after adjusting for potential confounders. ResultsCurrently smoking women were more likely to have diabetes, IGT or IFG compared with never-smoking women (OR: 2.26, 95% CI: 1.05–4.84). Heavy-smoking men (≥25 cigarettes/day) were likely to be in the lowest tertile group of ΔI0–30/ΔG0–30 compared with never-smoking men (OR: 2.64, 95% CI: 1.05–6.68, Ptrend=0.04). The number of cigarettes/day was borderline significantly associated with diabetes in men. Also with borderline significance, never-smoking women with smoking husbands were more likely to have diabetes, IGT or IFG (OR: 1.62, 95% CI: 1.00–2.62) and significantly more likely to have lower HOMA-β (OR: 2.17, 95% CI: 1.36–3.48) than those without smoking husbands. ConclusionThe greater the number of cigarettes smoked per day appears to be associated with diabetes among men whereas, among women, both active and passive smoking appear to be associated with diabetic states, including IGT and IFG. An association between smoking status and insulin secretion is also suggested, whereas no significant association was observed with HOMA-IR in this Japanese subjects, suggesting that the influence of smoking on glucose metabolism may differ among races.

THU0578-HPR Wide-Spread Pain and Pain Intensity in Patients with Early Rheumatoid Arthritis. A Comparison between Smokers and Non- Smokers. A Cross-Sectional Study

BackgroundPain is a frequent symptom in patients with rheumatoid arthritis (RA). In patients with established RA about 34% had wide-spread pain more than three months and pain was more likely...

Smoking History in Relation to Survival after a Breast Cancer Diagnosis

Smoking History in Relation to Survival after a Breast Cancer Diagnosis

Exposure to ethanol and tobacco smoke in relation to level of PCNA antigen expression in pancreatic and hepatic rat cells

BackgroundPrevious results proved that simultaneous effect of tobacco smoke constituents and alcohol consumption may change toxicity of these substances and have a greater effect on hepatic and pancreatic disease and cancer risk. The aim of this study was to investigate hepatocyte and pancreatic cells regeneration after tobacco and/or ethanol treatment. MethodsIn the study, four groups of rats were used – alcohol non-addicted and addicted male and female rats. The animals from each group were exposed to tobacco smoke, to ethanol or tobacco smoke and ethanol. After the exposure, pancreas and liver were collected at two time-points - 5 and 24h. Biochemical methods were used to measure concentration of ethanol and cotinine in blood and plasma. Additionally, proliferating cell nuclear antigen labeling index (PCNA-LI), an S-phase marker was assessed by immunohistochemical staining and morphometric method. ResultsOur experimental results showed that the exposure of rats to tobacco smoke does not have influence on ethanol concentration in blood of non-addicted (male, female) and addicted (male and female) animals. The results also proved that alcohol addiction did not influence nicotine metabolism in all animals exposed to tobacco smoke. Morphological studies of tissues display significant damage in liver of addicted males, including fatty degradation, fibrosis and slight inflammatory infiltrate. Immunohistochemical studies revealed at first, significant increase of PCNA-LI and, thus, increased cell proliferation activity and damage in tissues were observed in hepatic and pancreatic cells of addicted males when compared with non-addicted males. Secondly, comparison between addicted males and addicted females revealed that PCNA-LI in females is significantly lower, both in hepatic and pancreatic tissues. And finally, animals exposed only to ethanol and to tobacco smoke plus ethanol were characterized by higher percentage of PCNA positive cells in relation to animals exposed only to tobacco smoke. ConclusionFrom the preliminary study one can conclude that the influence of ethanol and simultaneous influence of ethanol and tobacco smoke impairs liver and pancreatic functions to a greater degree than tobacco abuse.

Filaggrin gene mutation associations with peanut allergy persist despite variations in peanut allergy diagnostic criteria or asthma status

Filaggrin gene mutation associations with peanut allergy persist despite variations in peanut allergy diagnostic criteria or asthma status

Advances in adult asthma diagnosis and treatment in 2012: Potential therapeutics and gene-environment interactions

In the Journal of Allergy and Clinical Immunology in 2012, research reports related to asthma in adults clustered around mechanisms of disease, with a special focus on their potential for informing new therapies. There was also consideration of the effect of the environment on health from pollution, climate change, and epigenetic influences, underlining the importance of understanding gene-environment interactions in the pathogenesis of asthma and response to treatment.

Interaction between filaggrin null mutations and tobacco smoking in relation to asthma

The mechanisms underlying the association between filaggrin (FLG) deficiency and asthma are not known. It has been hypothesized that FLG deficiency leads to enhanced percutaneous exposure to environmental substances that might trigger immune responses. We hypothesized that interactions between FLG deficiency and environmental exposures play a role in asthma development. We sought to investigate possible interactions between FLG null mutations and tobacco smoking in relation to asthma. A total of 3471 adults from a general population sample participated in a health examination. Lung function and serum specific IgE levels to inhalant allergens were measured, and information on asthma and smoking was obtained by means of questionnaire. Participants were genotyped for the 2 most common FLG null mutations in white subjects: R501X and 2282del4. Another Danish population was used for replication. The FLG null mutation genotype was significantly associated with a higher prevalence of asthma and decreased FEV(1)/forced vital capacity ratio. In logistic regression analyses with asthma as the outcome, a significant interaction was found between FLG null mutations and smoking status (P= .02). This interaction was confirmed, although it was not statistically significant, in another Danish population study. Interactions between FLG genotype and cumulated smoking exposure were found in relation to asthma (P= .03) and decreased FEV(1)/forced vital capacity ratio (P= .03). A3-way interaction was found among FLG genotype, smoking, and asthma, suggesting that the FLG-smoking interaction mainly played a role in nonatopic subjects. FLG null mutations modified the effects of smoking on the risk of asthma. This finding might have implications for risk stratification of the population.

CHILDREN’S HEALTH: Coal Fire Emissions Curb Children’s Growth

Putting more coal on the fire may help to keep off the chill, but it may not help your baby grow. New research found that the 3-year-old children of Czech families who reported using coal for indoor heating were shorter than those whose families used cleaner fuels.1 Similar to cigarette smoke, the smoke of burning coal contains fine particles, carbon monoxide, benzene, polycyclic aromatic hydrocarbons (PAHs), sulfur dioxide, arsenic, and other toxicants.2 “PAHs and particulate matter are associated with reduced intrauterine growth,” explains Irva Hertz-Picciotto, a professor of public health sciences at the University of California, Davis, and senior author of the study. “Air pollution has been linked to smaller length and head circumferences at birth, and there is evidence that secondhand [tobacco] smoke can affect the stature of children.” Putting the pieces together, she says she and her colleagues became interested in whether indoor coal burning—a common exposure scenario in many countries—might affect children’s early postnatal growth. To investigate this potential link, the researchers examined the height at 36 months of 1,105 Czech children whose mothers had been recruited into the Teplice Pregnancy Outcome Study launched by the Czech government with assistance from the U.S. Environmental Protection Agency. These families were then followed longitudinally in the Children’s Health and Air Pollution Study; information was obtained from pediatricians about the children’s health and growth at birth and at 36 months, and the children’s mothers responded to questionnaires to determine how families heated their homes, their children’s exposure to secondhand tobacco smoke, and other lifestyle variables. The researchers used the medical history data to determine height-for-age-and-sex z scores for the children in homes that did and did not use coal for indoor heating. “These scores reflect the difference between height-for-age-and-sex of a child compared with a reference population, with the units being standard deviations,” Hertz-Picciotto explains. “The growth of a child with a negative score is below the mean for the reference population, and the lower the score, the poorer the growth.” Indoor coal combustion was used to heat 10.2% of the children’s homes; of these, 77.6% used coal exclusively. The mean height-for-age-and-sex at 36 months for the children in these homes was significantly lower than that of children from non-coal-burning homes. In regression modeling, adjusting for confounders such as birth weight for gestational age and sex, maternal height, and maternal ethnicity, height-for-age-and-sex was found to be significantly associated with indoor coal combustion. Translating the z scores into absolute height differences, 3-year-old boys from indoor coal-burning homes were a mean 1.34 cm shorter, while the girls were a mean 1.3 cm shorter, says first author Rakesh Ghosh, a postdoctoral scholar at UC Davis. “The results showed the effect to be compounded if children were [also] exposed to secondhand cigarette smoke,” Ghosh says. The link between respiratory disease in children and the indoor burning of solid fuels (including coal, wood, and dung) has long been known in the developing world, where homes commonly have open hearths and no chimney. But this is the first time growth reduction has been associated with coal burning in the ventilated indoor hearths and furnaces of a developed country. Even with ventilated coal heaters, Hertz-Picciotto says there are two ways children can be exposed: first, when the coal is added, smoke and ash likely enter the room; and second, some fraction of the particles vented outdoors likely land nearby and circulate in areas near the house. The World Health Organization describes the emissions from solid fuels as the “killer in the kitchen,” claiming them responsible for 1.5 million respiratory illness–related deaths every year, mostly in Southeast Asia and sub-Saharan Africa and predominantly affecting women and children.3 Some research has also linked the use of such fuels to poorer growth in young children in developing countries,4,5 whereas other work has associated indoor coal use with increased lower respiratory tract illnesses.6 “The results provide an important public health warning for countries where coal is still burned indoors,” says study co-supervisor Radim Sram of the Institute of Experimental Medicine AS CR, Prague, Czech Republic. “Moving to cleaner heating systems should be a priority, yet indoor coal use in some countries, such as China, is increasing.” “It is difficult to disentangle the many influences on child development,” points out Martin McKee, a professor of European public health at the London School of Hygiene & Tropical Medicine, who was not involved with the study. “Many of them cluster together, so that families that are disadvantaged in one way may be exposed to many different hazards. As the authors note, they were unable to assess the extent to which children were exposed to coal smoke, [but nonetheless, this study] raises some important questions.”

Detrimental Effects of Environmental Tobacco Smoke in Relation to Asthma Severity

BackgroundEnvironmental tobacco smoke (ETS) has adverse effects on the health of asthmatics, however the harmful consequences of ETS in relation to asthma severity are unknown.MethodsIn a multicenter study of severe asthma, we assessed the impact of ETS exposure on morbidity, health care utilization and lung functions; and activity of systemic superoxide dismutase (SOD), a potential oxidative target of ETS that is negatively associated with asthma severity.FindingsFrom 2002–2006, 654 asthmatics (non-severe 366, severe 288) were enrolled, among whom 109 non-severe and 67 severe asthmatics were routinely exposed to ETS as ascertained by history and validated by urine cotinine levels. ETS-exposure was associated with lower quality of life scores; greater rescue inhaler use; lower lung function; greater bronchodilator responsiveness; and greater risk for emergency room visits, hospitalization and intensive care unit admission. ETS-exposure was associated with lower levels of serum SOD activity, particularly in asthmatic women of African heritage.InterpretationETS-exposure of asthmatic individuals is associated with worse lung function, higher acuity of exacerbations, more health care utilization, and greater bronchial hyperreactivity. The association of diminished systemic SOD activity to ETS exposure provides for the first time a specific oxidant mechanism by which ETS may adversely affect patients with asthma.

Environmental tobacco smoke in relation to bladder cancer risk--the Shanghai bladder cancer study [corrected

Environmental tobacco smoke (ETS) contains tobacco carcinogens. Hepatic cytochrome P450 (CYP) 1A2 and N-acetyltransferase (NAT2) are important isoenzymes in activation and detoxification, respectively, of tobacco carcinogens. Data on ETS and bladder cancer risk are sparse. We examined the effects of ETS alone and combined with NAT2/CYP1A2 on bladder cancer risk among lifelong-nonsmokers in a case-control study involving 195 patients and 261 controls in Shanghai, China. A comprehensive history of ETS exposure was determined through in-person interviews while CYP1A2 and NAT2 phenotypes by a caffeine-based urinary assay. ETS exposure was related to an overall statistically nonsignificant 38% increased bladder cancer risk. The risk increased with increasing number of cigarettes smoked by household members or number of hours per day at workplace where coworkers smoked. Compared with no ETS exposure, subjects living with smoking parents during childhood had an OR of 2.43 (95% CI = 0.99-5.96) for bladder cancer. When all ETS sources were combined, the risk increased with increasing total ETS score (P(trend) = 0.03). The OR for high versus nil ETS exposure was 3.00 (95% CI = 1.24-7.26). The increased risk with ETS was mainly seen among individuals possessing a CYP1A2 high efficiency and/or a NAT2 slow acetylation phenotype (P(trend) = 0.04). ETS was associated with an increased bladder cancer risk for lifelong-nonsmokers. The association was stronger for people possessing the at-risk phenotypes of CYP1A2 and/or NAT2. Reducing exposure to ETS for children and genetically more susceptible individuals could be more effective for bladder cancer prevention.

Abstract 4699: Environmental tobacco smoke in relation to bladder cancer risk: The Shanghai Bladder Cancer Study

Abstract Tobacco use is an established risk factor for bladder cancer. However, data on exposure to environmental tobacco smoke (ETS) are sparse. Given the important roles of hepatic cytochrome P450 (CYP1A2) in activation and N-acetyltransferase (NAT2) in detoxification of tobacco carcinogens, we examined ETS and bladder cancer risk association among lifelong nonsmokers and for subgroups stratified by CYP1A2/NAT2 phenotype status. As part of the Shanghai Bladder Cancer Study, a population based case-control study in Shanghai, China, we enrolled 202 case patients (101 women) who were lifelong nonsmokers aged 25-74 at diagnosis in 1995-1998 and 268 lifelong nonsmoking control subjects (130 women) who were comparable to cases in gender-age distributions. An in-person interview was administered. In addition to lifestyle factors, subjects were asked about smoking history (number of cigarettes/day and number of years of living together) of their mother, father, spouse, other relatives in the household and smoking habits of coworkers at workplace. CYP1A2 and NAT2 phenotype status were determined by ratios of specific caffeine metabolites in overnight urine samples collected from each subject after ingestion of 70mg of caffeine. Odds ratios (ORs) and 95% confidence intervals (CIs) for bladder cancer were calculated using unconditional logistic regression methods. Exposure to ETS was related to a statistically non-significant 20-30% increased bladder cancer risk in all lifelong nonsmokers. The positive ETS-bladder cancer association varied according to the source of ETS, and primarily was confined to women. Living with a smoking mother during childhood was associated with an OR of 1.59 (95% CI=0.79-3.21, P=0.19) in all lifelong nonsmokers and an OR of 2.02 (95% CI=0.71-5.78, P=0.19) in women only. Among all lifelong nonsmokers, bladder cancer risk increased with increasing number of cigarettes/day (OR=2.92, 95% CI=0.95-8.96, P=0.06, for more than 10 cigarettes/day), number of years of smoking (OR=2.47, 95% CI=0.94-6.46, P=0.07, for more than 10 years), and pack-years of smoking (OR=3.51, 95% CI=1.08-11.35, P&amp;lt;0.01 for more than 10 pack-years) by mothers who smoked. When all lifelong nonsmokers were stratified by CYP1A2 (below or above median in all controls) and NAT2 (slow or rapid) phenotype status, ORs (95% CI) of bladder cancer for ETS vs. non-ETS exposure were 0.98 (0.56-1.73, P=0.95) for subjects possessing both a low CYP1A2 and a rapid NAT2 phenotypes, 1.36 (0.78-2.32, P=0.26) for subjects with either a low CYP1A2 or a rapid NAT2 phenotypes, and 2.07 (0.98-4.38, P=0.06) among those possessing both a high CYP1A2 and a slow NAT2 acetylation phenotypes (P for trend=0.04). Exposure to ETS, especially during childhood, was associated with an increased risk of bladder cancer among lifelong nonsmokers. CYP1A2 and NAT2 acetylation phenotypes exert a moderate modifying effect on the ETS-bladder cancer association. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4699.

Polymorphisms in inflammation genes, tobacco smoke and furred pets and wheeze in children

Persistent wheeze in childhood is associated with airway inflammation. The present study investigated relationships between polymorphisms in inflammatory genes, exposure to tobacco smoke and furred pets and risk of recurrent wheeze in children. Within a birth cohort of 101,042 children we identified 1111 eighteen month old cases with recurrent wheeze and 735 wheeze-free controls among 11942 children recruited in the Copenhagen area. Polymorphisms in IL-4R, IL-8, IL-13, SPINK5, and CD14 were genotyped. Interviews at gestational wks 12 and 30, and at age 6 and 18 months included questions on number of episodes with wheeze (18 months), exposure to tobacco smoke and pet-keeping. Recurrent wheeze was defined as at least four episodes of wheeze before the child was 18 months old. There was a statistically significant association between the IL-13 Arg144Gln polymorphism and risk of recurrent wheeze (p = 0.01). Furthermore, there was a statistically significant interaction between this polymorphism and exposure to tobacco smoke during pregnancy, though this was probably a chance finding. There were no other statistically significant effects of the polymorphisms or interactions with exposure to tobacco smoke in relation to the risk of recurrent wheeze. Polymorphisms in IL-8 affected the association between pet-keeping and risk of wheeze. Polymorphisms in inflammation genes might affect the association between environmental exposures and risk of recurrent wheeze in early childhood.

Hookah, opium and tobacco smoking in relation to oesophageal squamous cell carcinoma

Sir, Nasrollahzadeh et al (2008) report that the regular use of hookah in Iran ‘may involve exposure to large amounts of tobacco combustion products' and that the intensity of hookah use (not duration, unlike nass) was associated with ESCC (oesophageal squamous cell carcinoma) risk. Certainly one feature of hookah use in countries, such as Iran, India and Pakistan, is the great related amount of tobacco; the weight equivalent of up to 60 cigarettes in the bowl (chilam) for one session (Sajid et al, 2008). In these conditions, the authors are right to assume that this practise might entail a risk factor for ESCC. However, in the light of recent studies on hookah smoking and cancer, a confusion factor may not have been taken into account. It deals with the fact that opium is also smoked, not only in the dedicated opium-only pipes described in detail by Nasrollahzadeh et al (2008), but, also, in the hookahs themselves, mixed or not with tobacco.