Schistosomiasis and the risk of bladder cancer in Alexandria, Egypt

The relationship between history of schistosomiasis and bladder cancer risk was investigated using data from a case-control study conducted between January 1994 and July 1996 in Alexandria, Egypt. Cases were 190 subjects with incident, histologically confirmed invasive cancer of the bladder, and controls were 187 subjects admitted to hospital for acute, non-neoplastic, non-urinary tract conditions. Eighty-six cases (45%) vs 69 controls (37%) reported a history of urinary schistosomiasis. The corresponding multivariate odds ratio (OR) of bladder cancer -- after allowance for age, sex, education, smoking, other urinary infections and high-risk occupations -- was 1.72 (95% confidence interval (CI) 1.0-2.9). The ORs were 0.22 (95% CI 0.1-0.4) for intestinal schistosomiasis and 0.32 (95% CI 0.1-1.9) for schistosomiasis of other types. The OR for urinary schistosomiasis was higher in subjects who were younger at first diagnosis (OR of 3.3 for <15 years) and in those with a long time since first diagnosis (OR of 3.0 for > or = 35 years). The ORs were 15.8 for male ever-smokers with a history of urinary schistosomiasis, compared with never-smokers without such a history, and 3.2 for men ever-infected with urinary Schistosoma haematobium and ever-employed in high-risk occupations, compared with those never-infected and with no high-risk occupational history. This study confirms that clinical history of urinary schistosomiasis is significantly, but modestly, associated with increased bladder cancer risk, explaining some 16% of bladder cancer cases in this Egyptian population.     

Prospective study of effect of switching from cigarettes to pipes or cigars on mortality from three smoking related diseases

OBJECTIVE: To estimate the extent to which cigarette smokers who switch to cigars or pipes alter their risk of dying of three-smoking related diseases-lung cancer, ischaemic heart disease, and chronic obstructive lung disease. DESIGN: A prospective study of 21520 men aged 35-64 years when recruited in 1975-82 with detailed history of smoking and measurement of carboxyhaemoglobin. MAIN OUTCOME MEASURES: Notification of deaths (to 1993) classified by cause. RESULTS: Pipe and cigar smokers who had switched from cigarettes over 20 years before entry to the study smoked less tobacco than cigarette smokers (8.1 g/day v 20 g/day), but they had the same consumption as pipe and cigar smokers who had never smoked cigarettes (8.1 g) and had higher carboxyhaemoglobin saturations (1.2% v 1.0%, P < 0.001), indicating that they inhaled tobacco smoke to a greater extent. They had a 51% higher risk of dying of the three smoking related diseases than pipe or cigar smokers who had never smoked cigarettes (relative risk 1.51; 95% confidence interval 0.96 to 2.38), a 68% higher risk than lifelong non-smokers (1.68; 1.16 to 2.45), a 57% higher risk than former cigarette smokers who gave up smoking over 20 years before entry (1.57; 1.04 to 2.38), and a 46% lower risk than continuing cigarette smokers (0.54; 0.38 to 0.77). CONCLUSION: Cigarette smokers who have difficulty in giving up smoking altogether are better off changing to cigars or pipes than continuing to smoke cigarettes. Much of the effect is due to the reduction in the quantity of tobacco smoked, and some is due to inhaling less. Men who switch do not, however, achieve the lower risk of pipe and cigar smokers who have never smoked cigarettes. All pipe and cigar smokers have a greater risk of lung cancer than lifelong non-smokers or former smokers.     

Co-expression of polyhydroxyalkanoate synthase and (R)-enoyl-CoA hydratase genes of Aeromonas caviae establishes copolyester biosynthesis pathway in Escherichia coli

Arylamine N-acetyltransferase 2 (NAT2) is involved in both the detoxification and bioactivation of carcinogenic arylamines and other mutagens. This enzyme is polymorphic, and the fast and slow phenotypes are thought to be risk factors for colon and bladder cancer, respectively. Here, we report on a case-control study of adenomatous and hyperplastic polyps, with particular attention to tobacco smoking, a known risk factor for adenomas, and polymorphisms of NAT2. All participants underwent complete colonoscopy and were subsequently divided into case and control groups on the basis of pathology. Cases were diagnosed with confirmed adenomas (n = 527) or hyperplastic polyps (n = 200); controls (n = 633) had no history of colonic neoplasia and no polyps at colonoscopy. NAT2 genotype was determined using an oligonucleotide ligation assay and fast, intermediate, or slow phenotype imputed. Multivariate-adjusted odds ratios (ORs) and 95% confidence intervals were computed using logistic regression adjusting for age, sex, nonsteroidal anti-inflammatory drug use, and hormone replacement therapy use. Smoking was associated with an increased risk of adenomas [current versus never smoking OR = 2.0 (95% confidence interval, 1.4-2.9)] and hyperplastic polyps [current versus never smoking OR = 4.1 (2.6-6.5)]. NAT2 status among adenomatous polyp patients and hyperplastic polyp patients, respectively, showed ORs of 1.1 (0.8-1.4) and 1.2 (0.8-1.6; intermediate versus slow) and 1.1 (0.6-1.9) and 0.9 (0.4-1.9; fast versus slow). There were no differences in risk when adenoma patients were stratified on multiplicity, size, or histopathological subtype of polyps. Never-smokers showed no variation in risk across acetylator status for either species of polyp, whereas current smokers showed ORs of 2.0 (1.2-3.2) and 2.3 (1.4-3.9) for adenomas and 3.9 (2.1-7.1) and 4.9 (2.6-9.4) for hyperplastic polyps for slow and intermediate/fast NAT2, respectively, compared with slow-NAT2 never-smokers. Risks of both multiple [OR = 4.3 (2.1-8.8)] and large [OR = 3.8 (1.9-7.5)] adenomas were somewhat elevated in current smokers with an intermediate/fast phenotype compared with smokers with a slow NAT2 phenotype, but the interaction was not statistically significant. Risk of hyperplastic polyps and adenomatous polyps is strongly related to smoking. There is little suggestion of interaction between NAT2 status and smoking and no relationship with NAT2 genotype alone.     

Case-control study of bladder cancer and water disinfection methods in Colorado

A population-based case-control study of bladder cancer and drinking water disinfection methods was conducted during 1990-1991 in Colorado. Surface water in Colorado has historically been disinfected with chlorine (chlorination) or with a combination of chlorine and ammonia (chloramination). A total of 327 histologically verified bladder cancer cases were frequency matched by age and sex to 261 other-cancer controls. Subjects were interviewed by telephone about residential and water source histories. This information was linked to data from water utility and Colorado Department of Health records to create a drinking water exposure profile. After adjustment for cigarette smoking, tap water and coffee consumption, and medical history factors by logistic regression, years of exposure to chlorinated surface water were significantly associated with risk for bladder cancer (p = 0.0007). The odds ratio for bladder cancer increased for longer durations of exposure to a level of 1.8 (95% confidence interval 1.1-2.9) for more than 30 years of exposure to chlorinated surface water compared with no exposure. The increased bladder cancer risk was similar for males and females and for nonsmokers and smokers. Levels of total trihalomethanes, nitrates, and residual chlorine were not associated with bladder cancer risk after controlling for years of exposure to chlorinated water.     

The surgical therapy of prostatic tumors]

A random sample of 26,000 Swedish women who were asked about their smoking habits in the early 1960s have now been followed for 26 years with respect to cancer incidence. Most findings regarding tobacco smoking and cancer from studies of men were confirmed also among the women. Elevated relative risk for current smokers compared with women who never smoked regularly were seen for cancers of the lung, upper aerodigestive sites, pancreas, bladder, cervix and all cancers combined, as well as a notably high relative risk for cancers of organs of the urinary tract other than kidney and bladder. Relative risk increased with dose, measured as grams of tobacco smoked per day, for cancers of the upper aerodigestive sites, lung, cervix, bladder, organs of the urinary tract other than kidney and bladder and all cancers combined. For cancers of the lung, bladder and cervix, there was an inverse relationship with age when starting to smoke tobacco. The reported inverse relationship between smoking and endometrial cancer could not be corroborated, nor was there any significant relationship between smoking and colorectal or breast cancer.     

Oral cancer risk in relation to sexual history and evidence of human papillomavirus infection

BACKGROUND: Experimental models and analyses of human tumors suggest that oncogenic, sexually transmittable human papillomaviruses (HPVs) are etiologic factors in the development of oral squamous cell carcinoma (SCC). We conducted a population-based, case-control study to determine whether the risk of this cancer is related to HPV infection and sexual history factors. METHODS: Case subjects (n = 284) were 18-65-year-old residents of three counties in western Washington State who were newly diagnosed with oral SCC from 1990 through 1995. Control subjects (n = 477) similar in age and sex were selected from the general population. Serum samples were tested for HPV type 16 capsid antibodies. Exfoliated oral tissue collected from case and control subjects and tumor tissue from case subjects were tested for HPV DNA. Odds ratios (ORs) were calculated after adjusting for age, sex, cigarette smoking, and alcohol consumption. RESULTS: Among males only, oral SCC risk increased with self-reported decreasing age at first intercourse, increasing number of sex partners, and a history of genital warts. Approximately 26% of the tumors in case subjects contained HPV DNA; 16.5% of the tumors contained HPV type 16 DNA. The prevalence of oncogenic HPV types in exfoliated oral tissue was similar in case and control subjects. The ORs for HPV type 16 capsid seropositivity were 2.3 (95% confidence interval [CI] = 1.6-3.3) for all oral SCCs and 6.8 (95% CI = 3.0-15.2) for oral SCCs containing HPV type 16 DNA. The joint association of cigarette smoking and HPV type 16 capsid seropositivity with oral SCC (OR = 8.5; 95% CI = 5.1-14.4) was stronger than predicted from the sum of individual associations with current smoking (OR = 3.2; 95% CI = 2.0-5.2) and seropositivity (OR = 1.7; 95% CI = 1.1-2.6). CONCLUSIONS: HPV type 16 infection may contribute to the development of a small proportion of oral SCCs in this population, most likely in combination with cigarette smoking.     

Cigarette smoking and the colorectal adenoma-carcinoma sequence: a hypothesis to explain the paradox

As recognized precursor lesions to colorectal cancer, colorectal adenomatous polyps have been studied to enhance knowledge of colorectal cancer etiology. Although most of the known risk factors for colorectal cancer are also associated with the occurrence of colorectal adenomas, cigarette smoking has had a strong, consistent relationship with colorectal adenomas but is generally not associated with colorectal cancer. The explanation for this paradox is unknown. With data collected in 1986-1988 during a large case-control study based on colonoscopy results in New York City, New York, the authors investigated the possibility that the paradox may arise because subjects with colorectal adenomas were included in the control group of cancer case-control studies. The authors found a statistically significant increased risk between heavy cigarette smoking (smokers with > or = 40 pack-years of smoking) and risk of adenoma (odds ratio (OR) = 1.61, 95% confidence interval (CI) 1.06-2.44). They saw no increased colorectal cancer risk from heavy cigarette smoking (OR = 1.02, 95% CI 0.52-1.99) using a "manufactured" control group to simulate a typical unscreened, population-based control group. When the authors compared these colorectal cancer cases with an adenoma-free control group examined by colonoscopy in a polytomous model with several case groups (newly diagnosed adenomas, carcinoma in situ, intramucosal carcinoma, and colorectal cancer), they found that the risk for 20-39 pack-years of smoking was elevated, although not statistically significant, and was similar for all four case groups. The risk for the highest smoking category (> or = 40 pack-years) was more strongly elevated in all four case groups, although it was statistically significant for only the newly diagnosed adenoma and the carcinoma in situ cases (adenomas, OR = 1.59, 95% CI 1.05-2.42; carcinoma in situ, OR = 2.05, 95% CI 1.01-4.15; intramucosal carcinoma, OR = 1.30, 95% CI 0.61-2.77; and colorectal cancer, OR = 1.30, 95% CI 0.64-2.65). While the authors' study is weakened by the lack of statistical significance concerning risk for colorectal cancer, these data offer some support for the hypothesis that the association between cigarette smoking and risk of colorectal cancer may have been masked by inclusion in the control group of subjects with adenomas. They also suggest that the major effect of smoking on the colorectal adenoma-carcinoma sequence occurs in the earlier stages of the formation of adenoma and the development of carcinoma in situ.     

Multifocal occurrence of gastric carcinoma in patients with a family history of gastric carcinoma

BACKGROUND: Smoking and alcoholic beverage drinking habits as well as a family history of cancer are well known risk factors for the multifocal occurrence of squamous cell carcinoma of the esophagus and the head and neck region. However, the role of these risk factors in multiple gastric carcinoma remains to be clarified. The purpose of this study was to examine the risk factors for multiple gastric carcinoma. METHODS: The smoking and drinking habits as well as the family history of 157 patients with synchronous multiple gastric carcinoma and 157 patients with solitary gastric carcinoma who were similar with regard to gender, age, stage of the tumor, and year of admission were investigated. The risk of a multiple occurrence of gastric carcinoma also was elevated using the odds ratio (OR). RESULTS: The ORs of a multifocal occurrence of gastric carcinoma in patients who currently smoked and drank alcoholic beverages were 1.1 and 0.8, respectively, although the ORs were not related to the quantity of smoking or drinking. In patients with a close relative with gastric carcinoma the OR was 2.1 (95% confidence interval [CI], 1.3-3.7). In those patients with > or =2 close relatives with gastric carcinoma, the OR increased to 5.1 (95% CI, 1.2-21.1). Conversely, no significant elevation in the ORs was recognized regarding a family history of other cancers. CONCLUSIONS: In this study, a family history of gastric carcinoma was found to be clearly associated with the multifocal occurrence of gastric carcinoma; however, no significant correlation between the multifocal occurrence of gastric carcinoma in these patients and their smoking and drinking habits was recognized.     

Relation of cigarette smoking to non-Hodgkin's lymphoma among middle-aged men

Because of previous inconsistencies in the observed relation of cigarette smoking to non-Hodgkin's lymphoma, this association was investigated in the Selected Cancers Study, a population-based case-control study of 1,193 non-Hodgkin's lymphoma cases and 1,903 controls, conducted between 1984 and 1988. Study subjects were men, and the median age of non-Hodgkin's lymphoma cases was 50 years (range, 32-60 years). As compared with the risk among men who had never smoked cigarettes, the risk among ever smokers was not increased (odds ratio (OR) = 1.05, p approximately 0.50), but the risk was significantly elevated among men who reported smoking > or = 2 1/2 packs per day and among men who had smoked for 30-39 years (OR = 1.45 in each group, p < 0.05). The estimated odds ratio among the 350 heavy smokers (> or = 50 pack-years) was 1.41 (95% confidence interval 1.08-1.85) after controlling for educational achievement, various occupational and medical exposures, and other potential confounders. The observed associations, however, tended to vary by age, with the odds ratio among heavy smokers decreasing from 2.8 among 32- to 44-year-olds to 1.1 among men over 55 years of age. These age-related differences, which may account for some of the inconsistencies seen in previous studies of cigarette smoking and non-Hodgkin's lymphoma, should be considered in future investigations.     

Autistic disorder: a review for the pediatric dentist

A combined analysis of two polymorphic enzymes, glutathione S-transferase mu (GST M1) and q (GST T1) and their implication as cancer risk factors was performed in a case-control study of lung and bladder cancers. Using a multiplex polymerase chain reaction (PCR) based method, the frequency of the homozygous deleted GSTM1 and GSTT1 genotypes was examined in 117 lung cancer patients, 67 urinary bladder cancer patients, and in a community-based sample of 248 healthy, unrelated individuals. In both cancer groups the frequency of the GSTM1 null genotype was higher in comparison with that of the control group (59% and 59.7% vs. 49.6%), but this increase did not reach statistical significance (p > 0.05). After grouping by the smoking status, among smokers in both cancer groups (62.1% in lung cancer and 71.4% in the bladder cancer group, respectively) there were statistically significantly (p < 0.05) increased frequencies of the GSTM1 deletion genotype as compared to the control group (49.6%). Smokers with absence of the GSTM1 gene were at an approximately 1.7-fold higher risk for lung cancer (odds ratio--OR = 1.67, 95% confidence interval--CI 95% = 1.0-2.7, p = 0.04) and an approximately 2.5-fold higher risk for bladder cancer (OR = 2.54, CI 95% = 1.2-5.5, p = 0.02). As related to GSTT1, our study demonstrated an overall GSTT1 effect on bladder cancer risk. Individuals with absence of the GSTT1 gene were at an approximately 2.5-fold higher risk of developing bladder cancer. In the lung cancer cases, the frequency of the putatively high risk GSTT1 null genotype was not increased as compared with controls. No effect of smoking was found on risk of lung and bladder cancer associated with the GSTT1 0/0 genotype. In combined analysis, the obtained results suggested that individuals who were both GSTM1 null and GSTT1 null may be at increased risk because they lack both enzymes. The findings suggest that the GSTM1 null genotype may be associated with susceptibility to lung and urinary bladder cancer in dependence on the exposure to carcinogens in cigarette smoke and that the GSTT1 null genotype is not a critical factor in mediating the risk of lung cancer, but may be associated with an increased susceptibility to bladder cancer.     

Glutathione S-transferase mu1 and N-acetyltransferase 2 genetic polymorphisms and exposure to tobacco smoke in nonsmoking and smoking lung cancer patients and population controls

We conducted a case-control study to assess the risk of lung cancer in relation to genetic polymorphisms of the detoxifying enzymes glutathione-S-transferase mu1 (GSTM1) and N-acetyl transferase 2 (NAT2), focusing on never-smokers, women, and older people. The study base consisted of persons > or =30 years of age in Stockholm County from 1992 to 1995. We recruited never-smoking lung cancer cases and a sex- and age-matched sample of ever-smoking cases at the three county hospitals mainly responsible for diagnosing and treating lung cancer. A total of 185 cases (25.4% men; 47.6% never-smokers) and 164 frequency-matched population controls (28.7% men; 48.2% never-smokers) supplied blood for genotyping. Detailed information was collected by interview on active and passive smoking, occupations, residences, and diet. The overall odds ratio (OR) for lung cancer associated with the GSTM1 null (GSTM1-) versus GSTM1+ genotype was 0.8 [95% confidence interval (CI), 0.5-1.2], with an OR close to unity among smokers, and lower ORs suggested among never-smokers. For NAT2 slow versus rapid acetylator genotypes, the OR was 1.0 (95% CI, 0.6-1.5) overall, which broke down into an increased risk for slow acetylators among never-smokers but an increased risk for rapid acetylators among smokers. Among never-smokers, a gene interaction was suggested, with combined slow acetylator and GSTM1+ genotype conferring particularly high risk (OR = 3.1; 95% CI, 1.1-8.6), but no clear pattern emerged among smokers. A detailed analysis among smokers showed no interaction between pack-years of smoking and the GSTM1 genotype but suggested a steeper increase in risk with increasing pack-years of smoking exposure for rapid than for slow acetylators. Our results do not support a major role for the GSTM1 genetic polymorphism as a risk factor for lung cancer among smokers or nonsmokers. There was, however, some suggestion that the slow acetylator genotype may confer an increased risk among never-smokers and that the rapid acetylator genotype interacts with pack-year dose to produce a steeper risk gradient among smokers.     

Passive smoking, active smoking, and education: their relationship to weight history in women in Geneva

OBJECTIVES: This study was undertaken to determine the relationship of education and tobacco smoke to lifetime weight history in women. METHODS: Information on passive smoking, active smoking, and weight history was collected from 928 women aged 29 to 74 years selected from the general population of Geneva, Switzerland. Multivariate analysis of variance was performed for weight, weight at age 20, and weight changes since age 20. RESULTS: Education was inversely related to weight at age 20, current weight, and weight gain since age 20. The least educated group had a current weight of 4 kg more than the most educated group. Differences across smoking categories were small: passive smokers had the highest current weight (63.4 kg) and former active smokers had the lowest (60.4 kg). Weight gain since age 20 tended to be smaller in former and current active smokers (5.5 to 7.2 kg) than in passive smokers (8.3 to 10.4 kg) and those never exposed (9.1 kg). CONCLUSIONS: In this sample, education was an important predictor of women's current weight and weight history. Passive and active smoking had little long-term effect on weight.     

Lifestyle factors and prostate cancer risk: a case-control study in Sweden

We examined associations between lifestyle factors and subsequent risk of prostate cancer in a population-based case-control study. Information on smoking and alcohol habits, socioeconomic factors, marital status, family history, and sexual habits were obtained from a questionnaire and a face-to-face interview with 256 (74.6%) eligible patients and 252 (76.6%) selected controls, frequency matched by age and screened for prostate cancer with negative findings. Unconditional logistic regression was used to estimate the odds ratios (ORs). Risk was elevated among current smokers of cigarettes (OR, 1.8) and current users of hard liquor (OR, 1.4); however, the lack of dose-response trend for both of these exposures argues against a causal association. We found tentative evidence that early first intercourse, a larger number of sexual partners, and other indices of high sexual activity are associated with increased risk. Similarly, adult height, an indicator of nutrition during childhood and adolescence, was weakly positively associated with risk, although larger studies are needed to establish this link. Unmarried men had a lower risk than married men (OR, 0.3), and socioeconomic status did not appear to be strongly associated with prostate cancer. Men with a father who had prostate cancer had a more than 2-fold increased risk of prostate cancer, whereas those with a brother affected had about a 5-folk risk.     

Body weight and risk of nonfatal acute myocardial infarction among women: a case-control study from northern Italy

BACKGROUND: The relationship between nonfatal acute myocardial infarction (AMI) and self-reported body weight and body mass index (BMI; Quetelet index, kg/m2) has been investigated. METHODS: A case-control study was conducted between 1983 and 1992 in northern Italy on 432 women with nonfatal AMI and 867 controls in hospital for acute, noncardiovascular, nonneoplastic, nondigestive, non-hormone-related conditions. Odds ratios (OR), with their 95% confidence intervals (CI), were computed by unconditional multiple logistic regression analysis, including terms for age, education, and smoking, plus history of selected diseases. RESULTS: Women with body weight and BMI in the highest quartile had an increased risk of AMI after allowance for age, education, and smoking status (OR 1.5, 95% CI 1.0 to 2.2, and OR 1.7, 95% CI 1.2 to 2.4, respectively). Compared with leaner women, the risk was higher among women with BMI above the median, in association with a history of diabetes (OR 5.2) or hyperlipidemia (OR 6.0). Hypertensive women had similar OR in the two strata of BMI (OR 5.1 and 4.8). The association of BMI with risk of AMI was apparently stronger among women younger than 50 years and among less educated women, but was similar among smokers and never smokers. CONCLUSIONS: The results of this study confirm that AMI among women is related to excess BMI, with a population attributable risk of 17%. The excess risk was substantial among overweight women with history of diabetes or hyperlipidemia, stressing the importance of controlling body weight among these women.     

Tobacco and tobacco smoke

Epidemiologic studies have demonstrated a causal relation between smoking of cigarettes and cancer of the lung in man. Women smokers, cigar, and pipe smokers also face an increased risk for lung cancer. Prospective and retrospective studies have found a correlation between smoking of cigarettes, cigars, and pipes and cancer of the oral cavity, larynx, and esophagus and for cigarette smokers increased risks to develop cancer of the pancreas, kidney, and urinary bladder. Dose responses have been established between number of cigarettes smoked and cancer of the respiratory and upper digestive tract. Tobacco chewers face an increased risk for cancer of the mouth and esophagus. Tobacco smoke has induced tumors of the lung in the dogs and of the larynx of hamsters. The particulate matter of the smoke is carcinogenic to the skin of mice and rabbits, and the bronchi and connective tissue of rats. In tobacco smoke were identified tumor initiators, tumor promoters, cocarcinogens and organ specific carcinogens. Chewing tobacco is a tumor promoting agent and contains traces of tobacco specific and carcinogenic nitrosamines. Ten to 15 yr after giving up smoking the ex-smoker faces the same low risk to develop cancer of the upper digestive tract, the lung, the pancreas, and the urinary tract as the nonsmoker. It should be our goal, therefore, to prevent young people from starting the smoking habit and to convince the smoker to quit smoking. So far, we can report no success in terms of decreasing smoking habits among younger people. On the other hand, we can take satisfaction from the fact that antismoking propaganda has had an effect on college educated males, that among the population as a whole, there is a considerable number of exsmokers; that smoking cessation clinics do prove cost effective and if they were to become part of every health care center, they could help a large number of heavy smokers who cannot seem to stop smoking on their own. We can also report that there has been a significant reduction in the tar yield of American cigarettes, a reduction which we hope will continue; that the tumorigenic activity of tobacco as measured in animal studies, has decreased; and that as a consequence of the above, the risk of lung cancer and other tobacco-related cancers among smokers of these cigarettes is lower than in years past. It is unlikely that man will ever be able to inhale smoke components as harmless as unpolluted air, but as long as we have a society which accepts this habit and as long as people find satisfaction in smoking, we must work towards the day when tobacco-related cancers and other diseases will be reduced to a minimum. With the world wide coperation of the scientific community, the Departments of Agriculture, and the tobacco industry, it is our hope that this goal will be achieved.     

Misclassification rates for current smokers misclassified as nonsmokers

OBJECTIVES: This paper provides misclassification rates for current cigarette smokers who report themselves as nonsmokers. Such rates are important in determining smoker misclassification bias in the estimation of relative risks in passive smoking studies. METHODS: True smoking status, either occasional or regular, was determined for individual current smokers in 3 existing studies of nonsmokers by inspecting the cotinine levels of body fluids. The new data, combined with an approximately equal amount in the 1992 Environmental Protection Agency (EPA) report on passive smoking and lung cancer, yielded misclassification rates that not only had lower standard errors but also were stratified by sex and US minority majority status. RESULTS: The misclassification rates for the important category of female smokers misclassified as never smokers were, respectively, 0.8%, 6.0%, 2.8%, and 15.3% for majority regular, majority occasional, US minority regular, and US minority occasional smokers. Misclassification rates for males were mostly somewhat higher. CONCLUSIONS: The new information supports EPA's conclusion that smoker misclassification bias is small. Also, investigators are advised to pay attention to minority/majority status of cohorts when correcting for smoker misclassification bias.     

Alcohol, smoking, and cataracts: the Blue Mountains Eye Study

OBJECTIVE: To investigate the associations between alcohol consumption, tobacco smoking, and cataract. DESIGN: A population-based, cross-sectional study. SETTING: An urban community in the Blue Mountains, close to Sydney, Australia. PARTICIPANTS: Three thousand six hundred fifty-four people aged 49 to 97 years. The participation rate was 82%. MAIN OUTCOME MEASURES: Smoking history and details of current alcohol consumption were assessed by questionnaire. Lens photographs were taken and graded for presence and severity of cortical, nuclear, and posterior subcapsular cataracts. RESULTS: After adjusting for multiple potential confounders, people who had ever smoked cigarettes had a higher prevalence than nonsmokers of more severe nuclear (adjusted odds ratio [OR], 1.3; 95% confidence interval [CI], 1.1-1.6) and posterior subcapsular (adjusted OR, 1.5; 95% CI, 1.1-2.1) cataracts. The association between pipe smoking and nuclear cataract (adjusted OR, 3.1; 95% CI, 1.5-8.2) was stronger than the association with cigarette smoking. Alcohol consumption was associated with a reduced prevalence of cortical cataract: compared with people who did not drink, the adjusted OR for cortical cataract among people who drank at least 1 drink a day was 0.7 (95% CI, 0.6-0.9). Heavy alcohol consumption (> or =4 drinks a day) was associated with nuclear cataract in current smokers (adjusted OR compared with nondrinkers, 3.9; 95% CI, 0.9-16.6) but not in never smokers. CONCLUSIONS: Consistent with other studies, smoking was associated with a higher prevalence of nuclear and posterior subcapsular cataracts. The only adverse effect of alcohol was among smokers: people who smoked and drank heavily had an increased prevalence of nuclear cataract.     

Departmental audit in surgical anatomical pathology

Chronic obstructive pulmonary disease (COPD) is the result of many years of accelerated decline in lung function in susceptible cigarette smokers. Although risk factors for the susceptibility of smokers to COPD have been established, there are still large gaps in our knowledge of the biological basis for these risk factors and of how to identify individuals at risk. COPD is the fourth leading cause of death and, in contrast to other major chronic diseases in the United States, has not shown declines in mortality over the past 20 years. Mortality trends reflect patterns of initiation of cigarette smoking that occurred 30 to 50 years previously. Current mortality trends indicate that COPD mortality may be leveling off among white males, but will continue to increase among women, African-Americans, and the elderly. Recent studies indicate that early identification of individuals with airflow obstruction and smoking intervention can halt the progression of COPD, but widespread screening and intervention programs have not yet been established.     

Stroke and use of low-dose oral contraceptives in young women: a pooled analysis of two US studies

BACKGROUND AND PURPOSE: The available data on low-dose oral contraceptive pill (OCP) use and stroke risk in US women are limited by small numbers. We sought more precise estimates by conducting a pooled analysis of data from 2 US population-based case-control studies. METHODS: We analyzed interview data from 175 ischemic stroke cases, 198 hemorrhagic stroke cases, and 1191 control subjects 18 to 44 years of age. RESULTS: For ischemic stroke, the pooled odds ratio (pOR) adjusted for stroke risk factors for current use of low-dose OCPs compared with women who had never used OCP (never users) was 0.66 (95% confidence interval [CI], 0.29 to 1.47) and compared with women not currently using OCPs (nonusers) the pOR was 1.09 (95% CI, 0.54 to 2.21). For hemorrhagic stroke, the pOR for current use of low-dose OCPs compared with never users was 0.95 (95% CI, 0.46 to 1.93) and compared with nonusers the pOR was 1.11 (95% CI, 0.61 to 2.01). The pORs for current low-dose OCP use and either stroke type were not elevated among women who were >/=35 years, cigarette smokers, obese, or not receiving medical therapy for hypertension. pORs for current low-dose OCP use were 2.08 (95% CI, 1. 19 to 3.65) for ischemic stroke and 2.15 (95% CI, 0.85 to 5.45) for hemorrhagic stroke among women reporting a history of migraine but were not elevated among women without such a history. Past OCP use (irrespective of formulation) was inversely related to ischemic stroke but unrelated to hemorrhagic stroke. CONCLUSIONS: Women who use low-dose OCPs are, in the aggregate, not at increased risk of stroke. Studies are needed to clarify the risk of stroke among users who may be susceptible on the basis of age, smoking, obesity, hypertension, or migraine history.