Forward angle analyzing power in p

BACKGROUND: Independent carcinogenic effects of alcohol drinking and tobacco smoking as well as their interaction can be usefully studied in a population of heavy drinkers and smokers. METHODS: A hospital-based case-control study was conducted during 1972 to 1983 in a large Veterans hospital in East Orange, New Jersey. A total of 359 oral cavity-oropharynx cancer cases and 2280 controls were interviewed according to tobacco smoking, use of smokeless tobacco, alcoholic beverage, coffee and tea drinking, race, family origin, religion, and occupation as bartender. RESULTS: Odds ratio of oral cancer increased up to the level of 35 cigarettes per day and 21 whiskey equivalents per day: no further increase was found for higher level of exposure to either factor. A protective effect of quitting smoking was found, but the number of former smokers was small. No difference occurred in oral cancer risk according to type of alcoholic beverage drunk. An interaction effect compatible with a multiplicative model was found between the two exposures. Blacks were at lower risk than whites, and, in the latter group, individuals of Italian origin were at lower risk than individuals from northern or central European countries. CONCLUSIONS: Alcohol drinking and tobacco smoking were responsible for the majority of oral cancer cases in this population of US Veterans.     

Growth and development of twins compared with singletons at ages one and four years

To assess the relationship of smoking and coffee, tea, and alcohol intake to the risk of cancer of the exocrine pancreas, analyses were performed using data from a prospective cohort study of 33,976 postmenopausal Iowa women who responded to a mailed questionnaire in 1986 and were followed through 1994 for cancer incidence and total mortality. At baseline, information on cigarette smoking, consumption of tea, coffee, and alcoholic beverages, and other dietary and lifestyle factors was obtained. Age-adjusted relative risks of pancreatic cancer (n = 66 cases) showed a dose-response association with smoking. Those with fewer than 20 pack-years and those with 20 or more pack-years of smoking exposure were 1.14 (95% confidence interval, 0.53-2.45) and 1.92 (95% confidence interval, 1.12-2.30) times more likely, respectively, to develop pancreatic cancer than were nonsmokers. Current smokers were twice as likely as were nonsmokers to develop pancreatic cancer. Relative risks of pancreatic cancer increased with the amount of alcohol consumed (Ptrend = 0.11) after adjustment for age, smoking status, and pack-years of smoking. Relative risks of pancreatic cancer according to alcoholic beverage intake were as strong among never-smokers as they were in the total cohort. After the data were adjusted for age, smoking status, and pack-years of smoking, there was a statistically significant 2-fold (95% confidence interval, 1.08-4.30) elevated risk of pancreatic cancer for those who drank > 17.5 cups of coffee per week, compared to those who consumed < 7 cups/week; among never-smokers, the relative risks across coffee intake categories were still positive but were attenuated somewhat (P trend = 0.17). Tea intake was not related to cancer incidence. In summary, these findings provide evidence of an association of both alcoholic beverage and coffee consumption with pancreatic cancer incidence that is independent of age and cigarette smoking.     

Cell-mediated autoimmunity in paraneoplastic neurological syndromes with anti-Hu antibodies

The authors investigated the association of caffeinated coffee, decaffeinated coffee, and tea with myocardial infarction in a study of 340 cases and age-, sex-, and community-matched controls. The odds ratio for drinking > or = 4 cups/day of caffeinated coffee versus drinking < or = 1 cup/week was 0.84 (95% confidence interval (CI) 0.49-1.42) after adjustment for coronary risk factors (1 cup = 237 ml). The odds ratio for drinking > 1 cup/day of decaffeinated coffee versus nondrinkers was 1.25 (95% CI 0.76-2.04). For tea, the odds ratio for drinking > or = 1 cup/day versus nondrinkers was 0.56 (95% CI 0.35-0.90). In these data, only tea was associated with a lower risk of myocardial infarction.     

Coffee consumption and risk of hospitalized miscarriage before 12 weeks of gestation

In order to analyse the association between drinking coffee in pregnancy and risk of spontaneous abortion, a case-controlled study was conducted in Milan, Northern Italy. Cases were 782 women with spontaneous abortion within the 12th week of gestation. The control group was recruited from women who gave birth at term (> 37 weeks gestation) to healthy infants on randomly selected days at the same hospitals where cases had been identified: 1543 controls were interviewed. A total of 561 (72%) cases of spontaneous abortion and 877 (57%) controls reported coffee drinking during the first trimester of the index pregnancy. The corresponding multivariate odds ratios of spontaneous abortion, in comparison with non-drinkers, were 1.2, 1.8 and 4.0, respectively, for drinkers of 1, 2 or 3, and 4 or more cups of coffee per day. No relationship emerged between maternal decaffeinated coffee, tea and cola drinking in pregnancy, as well as paternal coffee consumption, and risk of spontaneous abortion. With regard to duration in years of coffee drinking, the estimated multivariate odds ratios of spontaneous abortion were, in comparison with non-coffee drinkers, 1.1 (95% confidence interval (CI) 0.9-1.4) and 1.9 (95% CI 1.5-2.6) for women reporting a duration of coffee consumption < or = 10 or > 10 years. In conclusion, coffee drinking early in pregnancy was associated with an increased risk of abortion. This has biological implications, but epidemiological inference on the causality is difficult and still open to debate.     

Risk factors for renal cell carcinoma in Denmark. I. Role of socioeconomic status, tobacco use, beverages, and family history

Risk factors for renal cell carcinoma were examined in a population based case-control study in Denmark. A total of 368 cases and 396 age- and gender-matched controls were interviewed in their homes. Increased risk was associated with low socioeconomic status. For men, an increasing risk with decreasing socioeconomic status was seen (odds ratio [OR] = 2.2, 95 percent confidence interval [CI] = 1.0-4.6 for men in the lowest socioeconomic stratum cf the highest). For women, the risk was lower in the highest socioeconomic stratum compared with the rest (OR = 2.4, CI = 0.9-5.9 for the lowest strata cf the highest). Cigarette smoking was a risk factor in men with an OR = 2.3 (CI = 1.1-5.1) for cigarette smokers with a total consumption of more than 40 pack-years compared with nonsmokers. Family history of kidney cancer was associated with an increased risk in both genders (for men, OR = 4.1, CI = 1.1-14.9; for women, OR = 4.8, CI = 1.0-23). Observations were inconsistent regarding coffee and alcohol consumption, and we found no association with tea drinking. The association with socioeconomic status remained after adjustment for other factors.     

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.     

Dietary factors and lung cancer among men in west Sweden

BACKGROUND: Previous studies have reported an association between tea drinking and lung cancer. In view of these data, the relationship between tea drinking as well as other dietary factors and lung cancer was investigated in a case-control study in the west of Sweden. METHODS: Patients with suspected lung cancer were collected from pulmonary units at central hospitals in the area investigated, and population controls were matched for age. The material reported here comprises 308 male cases with a confirmed diagnosis of lung cancer and 504 controls. The participants were interviewed by specially trained nurses, using a questionnaire to assess smoking, dietary habits, occupational exposures and conditions in the residential area (local air pollution). This paper reports the results from dietary factors studied with a food frequency technique. RESULTS: The results demonstrated a strong protective effect of vegetables (odds ratio [OR] = 0.69, 95% confidence interval [CI]: 0.46-1.05, and OR = 0.37, 95% CI: 0.23-0.61 for intermediate and high consumption classes respectively). A low OR was consistent for all histological types of lung cancer. High consumption of fruits did not show any similar protective effect. Drinking milk was associated with a dose-response related risk increase after adjustment for smoking and vegetable consumption (P for trend = 0.07). Odds ratio was 1.73, 95% CI: 1.00-3.01 for high consumption of milk. CONCLUSIONS: High intake of vegetables had a strong protective effect among males. Diet is thus a potential confounding factor in studies on lung cancer and environmental factors and should thus be taken into consideration in the planning of such studies.     

Gastric emptying delay and gastric electrical derangement in IDDM

BACKGROUND: Attention has long been drawn to the potentially harmful effects of coffee on health, however recent epidemiological studies have suggested unexpected, possibly beneficial effects of coffee against the occurrence of alcoholic liver cirrhosis and upon serum liver enzyme levels. METHODS: We examined the potential inverse association between coffee drinking and serum concentrations of gamma-glutamyltransferase (GGT) and aminotransferases, with special reference to interaction with alcohol consumption, in a cross-sectional study involving 12687 health examinees (7398 men and 5289 women) aged 40-69 years from over 1000 workplaces in Nagano prefecture in central Japan. Those who had a history of liver disease and/or serum aminotransferases exceeding the normal range were excluded. Possible confounding effects of alcohol consumption, body mass index, cigarette smoking, and green tea consumption were controlled through multivariate analyses. RESULTS: Increased coffee consumption was strongly and independently associated with decreased GGT activity among males (P trend < 0.0001); the inverse association between coffee and serum GGT was more evident among heavier alcohol consumers (P < 0.0001), and was absent among non-alcohol drinkers. Among females, however, coffee was only weakly related to lower GGT level. Similar inverse associations with coffee and interactions between coffee and alcohol intake were observed for serum aspartate aminotransferase and alanine aminotransferase. Intake of green tea, another popular source of caffeine in Japan, did not materially influence the liver enzyme levels. CONCLUSIONS: Our results suggest that coffee may inhibit the induction of GGT in the liver by alcohol consumption, and may possibly protect against liver cell damage due to alcohol.     

Cigarette smoking, alcohol, tea and coffee consumption and pancreas cancer risk: a case-control study from Opole, Poland

A population-based, case-control study of pancreas cancer was undertaken in Opole, Poland, within the framework of the SEARCH Programme of the International Agency for Research on Cancer: this is the first aetiological study of pancreas cancer reported from Poland where the reported mortality rate has doubled since 1963. This study of pancreas cancer has provided some further supporting evidence of an association between increased pancreas risk with increasing levels of cigarette smoking. The risk rose with increasing lifetime cigarette consumption with a trend which was weakly significant (p = 0.061). Findings regarding lifetime tea and coffee consumption were not consistent with intake of either beverage increasing the risk of this disease. There was a strongly significant trend of decreasing risk with increasing lifetime consumption of tea (p < 0.001), which was also apparent when the analysis was restricted to subjects who were interviewed directly. For coffee consumption, which is low in Poland, there was also a negative association apparent in the data which was not statistically significant among the sub-set of subjects who were directly interviewed. The findings regarding alcoholic beverages were overall null, although the weakly positive trend in risk with spirits consumption (p = 0.71) may deserve further investigation in view of the special nature of the source of spirits (vodka) in Poland.     

Mortality of iron miners in Lorraine (France): relations between lung function and respiratory symptoms and subsequent mortality

An increased mortality from lung and stomach cancer was found in previous studies on Lorraine iron miners. A detailed analysis, however, was not possible due to the lack of data for survivors. In this study the cohort included 1178 workers selected at random from all the 5300 working miners aged between 35 and 55 at the start of the follow up period, which ranged from 1975 to 1985. Occupational exposures and tobacco consumption, lung function tests, and respiratory symptoms were assessed for each subject in 1975, 1980, and 1985. This study confirmed the excess of lung cancer (standardised mortality ratio (SMR) = 389, p < 0.001) and of stomach cancer (SMR = 273, p < 0.05). There was no excess of lung cancer in non-smokers and moderate smokers (< 20 pack-years) or the miners who worked only at the surface or underground for less than 20 years. A significant excess (SMR = 349, p < 0.001) was found in moderate smokers when they worked underground for between 20 and 29 years. Heavy smokers (over 30 pack-years) or subjects who worked underground for more than 30 years experienced a high risk: SMR = 478 (p < 0.001) for moderate smokers who worked underground for over 30 years; 588 (p < 0.001) for heavy smokers who worked underground for between 20 and 29 years; and 877 (p < 0.001) for heavy smokers who worked underground for over 30 years. This showed an interaction between smoking and occupational exposure. The excess mortality from lung cancer was because there were some subjects who died young (from 45 years old). Comparison with the results of a previous study showed that additional hazards produced by diesel engines and explosives increased the mortality from lung cancer. The SMR was higher than 400 (p < 0.001) from 45 years old instead of from 56 years. A relation was found between a decrease in vital capacity (VC), forced expiratory volume in one second (FEV1) and of FEV1/VC and mortality from all causes and from lung cancer in heavy smokers or men who had worked underground for more than 20 years. Respiratory symptoms were related to mortality from lung cancer among smokers (moderate and heavy) who worked underground for more than 20 years. It is considered that the risk of lung cancer in the Lorraine iron miners was mainly due to dust, diesel engines, and explosives although the role of low exposure to radon daughters could not be totally excluded.     

Toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin to several ecological receptor groups: a short review

The objective of this study was to examine the risks for lung cancer associated with lifestyle characteristics of smoking in a developing country where lung cancer is the first cause of mortality by cancer in men, tobacco propaganda is freely allowed, and there are no restrictions operating for smoking. The design was a case-control and hospital-based study. Two hundred men with lung cancer and 397 hospital controls were interviewed. Odds ratio (OR) for current smokers was 8.5, whereas former smokers displayed an OR of 5.3. The risk increased with duration of smoking and with the number of cigarettes smoked per day. The attributable risk for smoking was 85%. Smokers of black tobacco and more than 24 cigarettes/day showed a risk of 12.9 regarding non-smokers, and of 15.5 for 40 or more years duration of smoking. The proportion of cases diagnosed as adenocarcinoma was higher than the proportion of squamous cell carcinoma.     

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.     

Interpretation of Genetic Risk Feedback Among African American Smokers With Low Socioeconomic Status.

The authors report on factors related to interpretation of feedback on genetic susceptibility to lung cancer among 371 African American smokers receiving care in a community health clinic, with a focus on whether smokers were interpreting feedback consistent with a defensive processing or an accuracy orientation. Smokers were given feedback on the absence (indicating increased risk) or presence (indicating average risk) of the gene for the mu isoform of glutathione S-transferase . Smokers who were told they were at higher risk were more likely to inaccurately recall the result than those deemed at average risk. Smokers who inaccurately recalled the result, regardless of risk status, were most likely to misinterpret the meaning of the result. Perceived lung cancer risks and worries were not associated with comprehension of the test result. The authors suggest additional research is needed to develop more effective strategies for communicating genetic risk feedback to motivate smoking cessation. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Co-occurrent use of cigarettes, alcohol, and coffee in healthy, community-living men and women.

Compared the proportion of 226 male (aged 16–70 yrs) and 245 female (aged 16–69 yrs) healthy, community-living middle-class Americans identified as smokers (SMs), ex-smokers (XSMs), and nonsmokers (NSMs) that were categorized as users of more or less amounts of coffee and alcohol. Results indicate that for both sexes, SMs and XSMs were more likely than NSMs to drink greater amounts of alcohol and coffee. For all 3 groups, a majority of Ss who reported drinking more alcohol also reported drinking more coffee. The coffee and alcohol consumption levels of XSMs resembled those of SMs more than those of NSMs. XSMs also reported drinking more wine and decaffeinated coffee than either SMs or NSMs. The number of cigarettes smoked per day was positively related to total alcohol and coffee consumption in men but not in women. (24 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Degradation of weathered oil by mixed marine bacteria and the toxicity of accumulated water-soluble material to two marine crustacea

From 1982 to 1984, the authors conducted a population-based case-control study of lung cancer in men and women nonsmokers in New York State. In-person interviews were completed for 437 lung cancer cases (197 never smokers, 240 former smokers) and 437 matched population controls. Cases and controls were asked to report any history of physician-diagnosed nonmalignant lung disease; cases were more likely than controls to report such a history. Statistically significant associations were found for emphysema (odds ratio (OR) = 1.94, 95% confidence interval (CI) 1.10-3.43), chronic bronchitis (OR = 1.73, 95% CI 1.10-2.72), and the combined endpoint of emphysema, chronic bronchitis, or asthma (OR = 1.82, 95% CI 1.26-2.63). After adjustment for active and passive tobacco smoke exposure, emphysema, chronic bronchitis, and asthma (each condition and the combined endpoint) were significantly associated with lung cancer risk. The risk was more marked for squamous cell carcinomas and for subjects who were diagnosed at older ages, and it remained significant when surrogate interviews were excluded. These results are consistent with the hypothesis that certain prior lung conditions increase the risk of lung cancer in men and women nonsmokers.     

Immediate Antecedents of Cigarette Smoking in Smokers With and Without Posttraumatic Stress Disorder: A Preliminary Study.

Using ambulatory methods for 1 day of monitoring, the authors of this study investigated the association between smoking and situational cues in 63 smokers with posttraumatic stress disorder (PTSD) and 32 smokers without PTSD. Generalized estimating equations contrasted 682 smoking and 444 nonsmoking situations by group status. Smoking was strongly related to craving, positive and negative affect, PTSD symptoms, restlessness, and several situational variables among PTSD smokers. For non-PTSD smokers, the only significant antecedent variables for smoking were craving, drinking coffee, being alone, not being with family, not working, and being around others who were smoking. These results are consistent with previous ambulatory findings regarding mood in smokers but also underscore that, in certain populations, mood and symptom variables may be significantly associated with ad lib smoking. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

High-resolution microscopic determination of hepatic NADH fluorescence for in vivo monitoring of tissue oxygenation during hemorrhagic shock and resuscitation

Psychopharmacological studies using caffeinated beverages or caffeine have rarely considered temporal effects on psychological and physiological function or the specific contribution of caffeine, hot water, or beverage type to the observed effects. The effect of 400 ml hot tea, coffee, and water consumption on systolic and diastolic blood pressure (SBP and DBP), heart rate, skin conductance (a measure of sympathetic nervous system activation), skin temperature, salivary cortisol, and mood were monitored in 16 healthy caffeine-withdrawn (14 h) subjects in a complete crossover design. Beverages were ingested with/without 100 mg caffeine and milk (tea/coffee only). Hot beverage ingestion rapidly increased skin conductance and temperature (+1.7 degrees C) with peak effects observed only 10-30 min post-consumption. Caffeine in the beverage rapidly augmented skin conductance responses but, in contrast to the effect of hot water, reduced the skin temperature response and increased SBP (+2.8 mmHg) and DBP (+2.1 mmHg) 30-60 min post-consumption. Both caffeine and milk addition to beverages independently improved mood and reduced anxiety 30 and 60 min post-consumption. Milk addition had no other effects apart from attenuating the transient increase in physiological responses associated with the drinking phase. There were no effects of beverage consumption on salivary cortisol or of beverage vehicle on salivary caffeine levels, the latter indicating that caffeine pharmacokinetics was similar in both tea and coffee, and not different from caffeinated water. In keeping with this, the responses to tea and coffee ingestion were similar and largely accounted for by the effects of hot water and caffeine. However, tea potentiated the increase in skin temperature compared to coffee and water indicative of a greater vasodilatory response plausibly related to the presence of flavonoids in tea. We conclude that ingestion of hot caffeinated beverages stimulates physiological processes faster than hitherto described, primarily via the effects of hot water and caffeine, but with beverage type and milk playing important modulatory roles.     

Alpha-Tocopherol and beta-carotene supplements and lung cancer incidence in the alpha-tocopherol, beta-carotene cancer prevention study: effects of base-line characteristics and study compliance

BACKGROUND: Experimental and epidemiologic investigations suggest that alpha-tocopherol (the most prevalent chemical form of vitamin E found in vegetable oils, seeds, grains, nuts, and other foods) and beta-carotene (a plant pigment and major precursor of vitamin A found in many yellow, orange, and dark-green, leafy vegetables and some fruit) might reduce the risk of cancer, particularly lung cancer. The initial findings of the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC Study) indicated, however, that lung cancer incidence was increased among participants who received beta-carotene as a supplement. Similar results were recently reported by the Beta-Carotene and Retinol Efficacy Trial (CARET), which tested a combination of beta-carotene and vitamin A. PURPOSE: We examined the effects of alpha-tocopherol and beta-carotene supplementation on the incidence of lung cancer across subgroups of participants in the ATBC Study defined by base-line characteristics (e.g., age, number of cigarettes smoked, dietary or serum vitamin status, and alcohol consumption), by study compliance, and in relation to clinical factors, such as disease stage and histologic type. Our primary purpose was to determine whether the pattern of intervention effects across subgroups could facilitate further interpretation of the main ATBC Study results and shed light on potential mechanisms of action and relevance to other populations. METHODS: A total of 29,133 men aged 50-69 years who smoked five or more cigarettes daily were randomly assigned to receive alpha-tocopherol (50 mg), beta-carotene (20 mg), alpha-tocopherol and beta-carotene, or a placebo daily for 5-8 years (median, 6.1 years). Data regarding smoking and other risk factors for lung cancer and dietary factors were obtained at study entry, along with measurements of serum levels of alpha-tocopherol and beta-carotene. Incident cases of lung cancer (n = 894) were identified through the Finnish Cancer Registry and death certificates. Each lung cancer diagnosis was independently confirmed, and histology or cytology was available for 94% of the cases. Intervention effects were evaluated by use of survival analysis and proportional hazards models. All P values were derived from two-sided statistical tests. RESULTS: No overall effect was observed for lung cancer from alpha-tocopherol supplementation (relative risk [RR] = 0.99; 95% confidence interval [CI] = 0.87-1.13; P = .86, logrank test). beta-Carotene supplementation was associated with increased lung cancer risk (RR = 1.16; 95% CI = 1.02-1.33; P = .02, logrank test). The beta-carotene effect appeared stronger, but not substantially different, in participants who smoked at least 20 cigarettes daily (RR = 1.25; 95% CI = 1.07-1.46) compared with those who smoked five to 19 cigarettes daily (RR = 0.97; 95% CI = 0.76-1.23) and in those with a higher alcohol intake (> or = 11 g of ethanol/day [just under one drink per day]; RR = 1.35; 95% CI = 1.01-1.81) compared with those with a lower intake (RR = 1.03; 95% CI = 0.85-1.24). CONCLUSIONS: Supplementation with alpha-tocopherol or beta-carotene does not prevent lung cancer in older men who smoke. beta-Carotene supplementation at pharmacologic levels may modestly increase lung cancer incidence in cigarette smokers, and this effect may be associated with heavier smoking and higher alcohol intake. IMPLICATIONS: While the most direct way to reduce lung cancer risk is not to smoke tobacco, smokers should avoid high-dose beta-carotene supplementation.     

A model for the effect of cigarette smoking on lung cancer incidence in Connecticut

Population based data on smoking history derived from NCHS surveys were used to develop a model for lung cancer incidence in Connecticut. Trends in smoking prevalence suggest that, while the prevalence in men increased earlier than women, more male smokers have quit than their female counterparts. These trends in smoking prevalence suggest striking gender differences in a period effect for the smoking prevalence. Estimates of the proportion of current smokers, ex-smokers, and the mean duration of smoking were used in a model for the lung cancer incidence rates. The form for the relationship between smoking history and the incidence rate for these subgroups was based on information from cohort studies. The models represented a mixture of the smoking subgroups where the effect of smoking was considered to be either a multiplicative effect on the underlying age distribution, or a separate effect in which the level of exposure was the sole contribution to risk among smokers. The multiplicative model explained more than 80 per cent of the deviance for the period and cohort effects, while the non-multiplicative model could only account for trends in females. Hence, these results suggest that a sizeable portion of the period and cohort contributions to the lung cancer incidence trends in Connecticut can be attributed to the multiplicative model that utilizes this smoking information, although the lack of more detailed information is a limiting factor in developing the model.     

Dietary fats and lung cancer risk among women: the Missouri Women's Health Study (United States)

In a population-based case-control study of women in Missouri (United States), most of whom were smokers, we obtained information on adult diet to evaluate the effects of dietary fats in relation to lung cancer risk. All newly diagnosed, primary lung cancer cases among women 35 to 84 years of age reported to the Missouri Cancer Registry from 1 January 1993 to 31 January 1994 were invited to participate, as were population-based controls. The analysis focused on interviews obtained from 624 controls and 587 cases. In-person interviews were obtained from 99.0 percent of controls and 60.6 percent of cases. Age and energy-adjusted relative risks suggested a direct relation between risk of lung cancer and intake of dietary fats (e.g., total fat, saturated fat) and frequency of meat consumption. After adjusting for confounders, dietary fats were no longer associated with risk, but the adverse effect of frequent consumption of meat persisted. Risk was elevated about 90 percent (95 percent confidence interval = 1.2-3.0) among women in the highest quintile of red meat intake compared with those in the lowest quintile. Risk estimates associated with red meat consumption, however, were dependent on interview status; the effect was restricted to cases whose dietary information was provided by proxy. In summary, after adjusting for potential confounders and removing data obtained from proxy respondents, dietary fats and consumption of red meat were not associated with lung cancer risk among women in Missouri.