A cohort study conducted among California teachers observed an increased riskin the most highly exposed subgroup of postmenopausal women exposed in adulthood (age 20 years) (hazard ratio = 1.25, 95%CI = 1.01–1.56) . Another cohort study observed a 32% excess risk of breastcancer associated with the most extensive exposure to passivesmokingamong post- menopausal women who had never been active smokers . Other epidemiological studies also showed a statistically significant positive association between passivesmokingandbreastcancerriskin postmenopausal women [17, 19, 39, 43]. Consistent with these results, our study also pro- vided strong supporting evidence that passivesmoking was associated with an increased risk of breastcancerin postmenopausal women. One possible explanation for the positive association of passivesmoking with breastcancerin the postmenopausal only might be related to the anti- estrogenic effects of passivesmoking . Smokingwomen have an earlier menopause and thus fewer years of menstruation. And cigarette smoking alters estrogen metabolism [45,46], which may contribute to the absence of a positive association of passivesmoking with premenopausal breastcancer. However, some reports suggested that passivesmoking was associated with an in- creased risk of breastcanceramong premenopausal women [20, 47, 48] or both pre/post-meno- pausal women . Since this was a stratified analysis, chance findings might arise. More studies with a larger sample size might be needed to confirm this association.
A population-based casecontrolstudyin British Columbia reported an excess breastcancerriskamongwomen (pre- and post- menopausal ages combined) employed as crop and fruit and vegetable farmers, with a reason- ably likely exposure to numerous pesticides (Band et al., 2000). Occupational exposure to pesticides was also significantly associated with a 4-fold increase inbreastcancerriskin Serbia (Kocic et al., 1996), andrisk was also ele- vated among Chinese women with some prob- ability of high level pesticide exposure, al- though this finding was based on a small num- ber of exposed (Petralia et al., 1998). Female breastcancer mortality and incidence was not increased among Florida licensed pesticide users (Fleming et al., 1999a, 1999b), while a case-controlstudy on occupational risk of male breastcancer did not find an association with exposure to herbicides and other pesti- cides (Cocco et al., 1998). Also, agricultural oc- cupations were not included among high risk occupations for breastcancerin Swedish women (Pollan & Gustavsson, 1999). In most of these studies, exposure to pesticides was large- ly hypothetical, based on occupational titles or derived from working histories. Studies mea- suring pesticide residuals in body fluids or tis- sues as markers of internal dose of exposure are supposed to provide a more precise defini- tion of exposure. Besides, as stated above, ex- posure to pesticide mix, resulting from numer- ous different chemicals, which change rapidly on a yearly base, is the norm in agricultural set- tings, making it difficult to identify the poten- tial risk factor. On the other hand, by defini- tion, studies using markers of internal dose are aimed to identify associations with specific compounds or their derivatives, and only chemicals for which specific tests are available may be identified. Therefore, it is uncertain how to interpret contradictory findings, whether in relation to random variation in the response to the known chemical, or to changes in the as- sociated chemicals, or factors responsible for the increase inrisk. Most such reports focused on the association between organochlorines, particularly DDT derivatives, andbreast can- cer. A large number of such studies have been published, on the wave of few positive reports. Table 3 summarizes their results.
This study is the first attempt to identify and quantify risk factors associated with non-adherence to breastcancer screening among hospitalized women age 50–74 years. Using multivariable anal- ysis model accounting for both socio-demographic and clinical variables simultaneously, low income, current/ex-smoking status, and a history of stroke were each independently associated with non-adherence to breastcancer screening among hospitalized women. These results are not dissimilar from previous studies looking at other populations that reported screening disparities amongwomen with low socioeconomic status, and low levels of education who fail to engage in screening or preventive testing [8,21–26]. Because hospitalized women have been found to be amenable to breastcancer screening if offered during the hospitalization , and even willing to pay out of pocket to offset a part of the cost associated with inpatient mammography , the results of this current study may be helpful in identifying subgroups to target with initial inpa- tient screening interventions.
In 1989–1990, 32,826 participants provided blood samples , which were immediately processed upon arrival and aliquoted into cryotubes as plasma, buffy coat, and red blood cells. Among this cohort, multiple prospective nested case-control studies of cancers and CVD were conducted [28,29,30]. All of these case-control studies used the same design: for each incident case of a disease, a risk-set sampling scheme was used to select one to three controls from the remaining participants in the blood sub-cohort who were free of that disease when the case was diagnosed. All cases and controls were free of the specific disease of interest in each individual study when blood was drawn. In addition, cases and controls were matched for menopausal status and postmenopausal hormone use (except for the myocardial infarction case-controlstudy), age, and time of blood draw, as well as other factors that were carefully chosen for each individual study. In addition to these case-control studies, telomere length data were also available in a study of cognitive function . In total, the current analysis included data of 7,116 participants from nine studies (myocardial infarction, stroke, cognitive function, breastcancer, endometrial cancer, pancreatic cancer, and three skin cancer studies), in which LTL was measured. In published data based on some of these studies, shorter telomere length was not significantly associated with cancer risks [28,29,30], but weakly correlated with more cognitive decline .
Abstract. Glutathione-S-transferases (GSTs) are a super- family of phase II metabolizing enzymes that catalyse the detoxification of a large range of endogenous and exogenous toxic compounds, playing an important role in protecting cells against damage, through glutathione conjugation with electrophilic substances. Polymorphic variation in these enzymes that affect its activity seems to be related to individual susceptibility to various human diseases, including cancer. Of the GST super-family, the alpha class GSTs have commonly been described as one of the most versatile class, since it is responsible for detoxification of compounds such as bilirubin, bile acids and penicillin, thyroid and steroid hormones, allowing its solubilization and storage in the liver. Among the alpha class, GSTA1 and GSTA2 isoforms are the most widely expressed in human tissues. Additionally, these enzymes can catalyse conjugation of the nitrogen mustard group of alkylating anticancer drugs, some heterocyclic amines and · ,ß-unsaturated aldehydes. Since some risk factors for increased breastcancerrisk could be related to high production of reactive oxygen species during the metabolism of estrogens by catechol estrogens, or to the exposure to genotoxic compounds, and some of these toxic compounds are usually metabolized by GSTA2, we carried out a hospital based case-controlstudyin a Caucasian Portuguese population (291 breastcancer patients without familiar history of breastcancerand 547 controls matched for age, sex and ethnicity) in order to evaluate the potential modifying role of three non-synonymous polymorphisms in
The use of hormonal therapies, including hormonal contraceptives (HC) and postmenopausal hormone replacement therapy (HRT) have been shown to influence breastcancer (BC) risk. However, the variations of these effects among populations and ethnic groups are not completely documented, especially among Hispanic women. We evaluated the association between HC and premenopausal BC risk, and between HRT and postmenopausal BC riskin Mexican women. Data from a Mexican multi-center population-based case–controlstudy ofwomen aged 35 to 69 years were analysed. A total of 1000 cases and 1074 matched controls were recruited between 2004 and 2007. Information on hormonal therapy was collected through a structured questionnaire. Results were analysed using conditional logistic regression models. Overall, HC were used by 422/891 (47.3%) premenopausal womenand HRT was used by 220/1117 (19.7%) postmenopausal women. For HC, odds ratios (ORs) for BC were 1.11 (95% confidence interval (CI): 0.82, 1.49) for current users and 1.68 (95% CI: 0.67, 4.21) for ever-users. No clear effect of duration of use was observed. For HRT, the OR for BC was significantly increased in ever users (OR: 1.45; 95% CI: 1.01, 2.08). A non-significant increased risk was observed for combined estrogen/progestin, (OR = 1.85; 95% CI: 0.84, 4.07) whereas no effect was observed for the use of estrogen alone (OR = 1.14; 95% CI: 0.68, 1.91). Our results indicate that, HC had a non-significant effect on the risk of pre-menopausal BC, but suggested that injected contraceptives may slightly increase the risk, whereas HRT had a significant effect on post-menopausal BC in this population. This study provides new information about the effects of HC and HRT on BC riskin a Mexican population, which may be of relevance for the population of Latin America as a whole.
) was based on height and weight at 10–15 weeks of pregnancy. We used logistic regression models to calculate odds ratios and corre- sponding 95% confidence intervals as measures of association, adjusting for potential con- founders and tested for additive and multiplicative interactions of body mass index andsmoking. Women’s body mass index during early pregnancy was positively associated with each hypertensive outcome. Compared with normal weight women, the multivariable adjusted odds ratio for any hypertensive disorder was 1.8 (95% confidence interval, 1.3– 2.3) for overweight womenand 3.1 (95% confidence interval, 2.2–4.3) for obese women. The odds ratio for any hypertensive disorder with obesity was 3.9 (95% confidence interval 1.8–8.6) among smokers and 3.0 (95% confidence interval 2.1–4.3) amongnon-smokers. The effect estimates for hypertensive disorders with high body mass index appeared more pronounced among smokers than non-smokers, although the observed difference was not statistically significant. Our findings may help elucidate the complicated interplay of these lifestyle-related factors with the hypertensive disorders during pregnancy.
DBA/2J mice (Jackson Labs; male; age 12–14 weeks; n = 2–3 per group) were exposed to ambient air or cigarette smoke as previously described by Schweitzer et al . These mice have been shown to be susceptible to cigarette smoke-induced emphysema-like disease following at least 4 months of exposure [18,19], also demonstrated in this mouse cohort by increased mean linear intercepts (Figure S1). Briefly, mice were exposed 5 hours per day, 5 days a week to 11% mainstream and 89% side- stream smoke from reference cigarettes (3R4F; Tobacco Research Institute, Kentucky) using a Teague 10E whole body exposure apparatus (Teague Enterprise, CA) with monitored suspended particulates (average 90 mg/m 3 ) and carbon monoxide (average 350 ppm). Five groups of mice were analyzed: 1) ambient air-only exposed at four or six months (controls, n = 3), 2) cigarette smoke- exposed for 4 months (CS-4mo, n = 2), 3) cigarette smoke-exposed for 6 months (CS-6mo, n = 3), and 4) cigarette smoke-exposed for 4 months followed by 2 months in ambient air (CS-cessation, n = 3). At the end of experiments, the mice were euthanized and the plasma was collected by cardiac puncture and then snap- frozen in liquid nitrogen and stored at 280uC.
ABSTRACT: Introduction: Cerebrovascular disease is the third most common cause of death in the developed world after cancerand ischemic heart disease. In India, community surveys have shown a crude prevalence rate of 200 per 100000 population for hemiplegia. Aims and objectives: Identification of risk factors for cerebrovascular disease. Materials and Methods: Inclusion Criteria: Cases of acute stroke admitted in S.V.R.R.G.G.H, Tirupati were taken for the study. Exclusion Criteria: Head injury cases, neoplasm cases producing cerebrovascular disease were excluded. Results: Stroke was more common in male, 54% patients were male 46% were female. It was more common in 6 th and 7 th decade. More common risk factors were hypertension
RESULTS: Among the children, 51% had had respiratory infections during the preceding 3 months and 25.7% were asthmatic, of whom 52.1% had had one or more asthma attacks during the preceding 3 months. Children exposed to passivesmoking did not have more respiratory infections or asthma attacks in comparison with those not exposed. We observed a significant association between atopic disorders in parents and children who were not exposed to passivesmoking. There were also associations between atopic disorders in parents and asthma attacks in their infants, and between such disorders and a higher incidence of respiratory infections in the infants during the preceding 3 months. However, the presence of two or more positive skin tests for allergies did not have a correlation with respiratory infections and asthma attacks in this sample. In addition to this, children who studied full time at school did not have a higher occurrence of respiratory infections and asthma attacks.
Between the 1970s and the 1990s in the United States, the tobacco industry consolidated its position as a major sponsor of female athletes, especially tennis players, and tennis player Martina Navratilova represented the Virginia Slims brand (Phillip Morris) during the Wimbledon tournament. In the 1980s, political and ethnic minority organizations in the United States also received financial support from the tobacco industry. In 1987, Phillip Morris sponsored, in the city of New York, training programs for female leaders in African- American and Hispanic-American society, having contributed large sums of money. (4,5)
The sample size was small in this case-controlstudy. The amount of alcohol in grams/day was very low to have influenced the heart rate or other parameters. However, the exact number of cigarettes smoked, alcohol frequency and amount consumed were based on self-report. The consumption of caffeinated drinks and the exact level of physical activity were not assessed, which may have influenced the results. Use of spirometer is strongly recommended to assess the lung function for more specific lung volume and capacities. ECG recording would have brought more objectivity and reliability to this study, which was not performed. An overnight cessation of smoking influences the autonomic nervous system and increase activity to the vascular system. This effect is reduced in the afternoon after a continuous nicotinic impregnation. So these diurnal variations should be considered for future studies.
Strategies to combat smoking should include prohibiting the tobacco industry from sponsoring events of any nature, such as sporting events, corporate events, and even those involving the judiciary; prohibiting advertising in places where tobacco products are sold; awareness-raising campaigns aiming to avoid household smoking, which is one of the principal causes of exposure of womenand children to environmental tobacco smoke; compulsory dissemination of informative and preventive measures against smoking by all vehicles of communication operating under public concession; increasing the scope of the policy for raising cigarette taxes, submitting the tobacco industry to strict inspection; promoting a discussion of the theme of smoking prevention in schools, which can be achieved by implementing training programs for teachers; and training all health care workers in the public health care network, especially those who work in family health programs, which are aimed at rural populations, low-income nicotine replacement therapy and 7-13% quit
cervical malignant lesions, such as HPV-38, 44, 53, and 70, which may be underestimated, as the available kits for the detection of HPV are based on genotypes considered of high risk for anogenital lesions. Equally interesting is the possibility of carcinogenic action without the occurrence of viral integration, veriied by the high E6 and E7 mRNA expression, of high-risk genotypes, in whose cases the virus was in its episomal form. All these pieces of evidence reinforce the thesis of HPV participation in the genesis of oral carcinomas, while warn about the possible unexpected viral behaviors that, sometimes, are not noticed or understood due to the technological limitation of the time and the shortage of studies with the adequate approach. From now on, it is fundamental to develop appropriate research designs, with emphasis on case- control studies that may bring more consistent information about the cause-effect relationship between HPV and OSCC.
The human papillomavirus (HPV) is an epitheliotropic agent whose high-risk genotypes have a well-established link with the development of cervical cancer. Although the relation of HPV to the oral squamous cell carcinoma (OSCC) has been studied since the beginning of the 1980s, its role in the oral carcinogenesis and the probable underlying molecular mechanisms are still not fully elucidated. We performed a systematic review of the worldwide scientiic literature, published until the preparation of the present paper, concerning the association of HPV with OSCC, scrutinizing the samples, prevalence levels, the techniques utilized and relevant indings of the studies. The results showed that HPV is associated with approximately one quarter of OSCCs. Another interesting feature is the distinct pattern of infection in these oral tumors, including the participation of genotypes that are uncommon in cervical malignant lesions, such as HPV-38, 44, 53 and 70. Equally interesting is the possibility of carcinogenic action without the occurrence of viral integration, veriied by the high expression of messenger ribonucleic acid (mRNA) of E6 and E7 from high-risk genotypes in cases whose virus remain in the episomal form. These indings support the assumption of HPV involvement in the genesis of OSCC, whereas warn about the possibility of unexpected viral behaviors that sometimes are not perceived or understood due to the technological limitations of the time and to the shortage of studies with the adequate approaches.
Between January and June of 2008, a ques- tionnaire regarding attitudes toward smoking was sent, via the Internet, to all physicians who were members in good standing of the Brazilian Thoracic Association (BTA). The questionnaire consisted of 11 questions regarding demographic data and physician attitudes toward smokers. Physicians who answered and returned the questionnaire participated in a drawing to win free transportation and accommodation for the XXXIV Brazilian Pulmonology Conference, which was held in the national capital of Brazil (Brasília) in November of the same year. The drawing was a means to encourage BTA member physicians Similar to diabetes and systemic arterial
Based on the public HapMap SNP database (phase II Nov 08, on NCBI B36 assembly, dbSNP b126), we selected tagging SNPs for the region approximately 277 kb from 120.7 to 121.1 Mb at 1p11.2 (the LD block where the marker SNP rs11249433 located) with MAF $ 0.05 in Chinese Han population (CHB). Six SNPs (rs2580520, rs4844616, rs12033387, rs6600745, rs4259688, rs12743918) were selected based on an r 2 threshold of 0.8 by the Haploview software. Using UCSC Genome Browser (http:// genome.ucsc.edu/cgi-bin/hgGateway), there were two different locations (Feb.2009, GRCh37/hg19, dbSNP 132) of rs2580520, referring to 1p11.2 and 1q32.1. We designed the primers and probes for rs2580520 at 1p11.2. In addition, the previously reported SNP rs11249433 which was significantly associated with breastcancerriskin Caucasian and with MAF of 0.022 in CHB was directly included in our study.
to complete and return the questionnaire. By the deadline for returning the questionnaires via the Internet, we had received 587 valid ques- tionnaires, which corresponded to 21% of the pulmonologists enrolled in the BTA. For the analysis of the data (but not for the drawing), we excluded the questionnaires of 15 pedi- atric pulmonologists, 8 thoracic surgeons and 3 general practitioners. The number of question- naires received from each region of the country, as well as the answers to questions regarding attitudes toward smoking, can be seen in Table 1. When asked whether they considered smoking to be a medical condition, 3.2% of the respond- ents said no, and, although only 14.7% said that they treated smoking, 32.4% stated that they referred smokers to another professional for treatment. These data show that pulmon- ologists in Brazil do not recognize smoking as a medical condition. This is in contrast with their peers in other countries. For example, in Poland, 87.4% of pulmonologists always advise their patients to stop smoking cessation and 48% offer pharmacological or other types of support. (3) In contrast, 64% of the Chinese
Recently, lung cancer screening has acquired a position of central interest among the sci- entiic community. Many risk factors for non-small-cell lung cancer (NSCLC) susceptibility have already been identiied, such as tobacco exposure, occupational exposure, random expo- sure, silicosis andpassivesmoking. 1,2 his knowledge has raised certain questions: Is there any