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On the 30th anniversary of the U.S. Surgeon General's report Smoking and Health, we present updated results from one of the original cohort studies that comprised the groundbreaking document. A 26-year follow-up of 248,046 U.S. veterans evaluating the risks of cigarette smoking revealed strong dose-response effects between smoking and total cancer and a large number of cancer sites. Over 50% of cancer deaths among current smokers and 23% of cancer deaths among former smokers were attributable to cigarette smoking. These findings further demonstrate the large and unique role cigarette smoking plays in cancer etiology and the importance of smoking cessation to reduce this enormous public health burden.

Background : The lung cancer incidence in Chinese women is among the highest in the world, but tobacco smoking accounts for only a minority of the cancers. Epidemiologic investigations of lung cancer among Chinese women have implicated exposure to indoor air pollution from wok cooking, where the volatile emissions from unrefined cooking oils are mutagenic. Purpose : This study was conducted to identify and quantify the potentially mutagenic substances emitted from a variety of cooking oils heated to the temperatures typically used in wok cooking. Methods: Several cooking oils and fatty acids were heated in a wok to boiling, at temperatures (for the cooking oils) that ranged from 240 °C to 280 °C (typical cooking temperatures in Shanghai, China). The oils tested were unrefined Chinese rapeseed, refined U.S. rapeseed (known as canola), Chinese soybean, and Chinese peanut in addition to linolenic, linoleic, and erucic fatty acids. Condensates of the emissions were collected and tested in the Salmonella mutation assay (using Salmonella typhimurium tester strains TA98 and TA104). Volatile decomposition products also were subjected to gas chromatography and mass spectroscopy. Aldehydes were detected using high-performance liquid chromatography and UV spectroscopy. Results : 1,3-Butadiene, benzene, acrolein, formaldehyde, and other related compounds were qualitatively and quantitatively detected, with emissions tending to be highest for unrefined Chinese rapeseed oil and lowest for peanut oil. The emission of 1,3-butadiene and benzene was approximately 22-fold and 12-fold higher, respectively, from heated unrefined Chinese rapeseed oil than from heated peanut oil. Lowering the cooking temperatures or adding an antioxidant, such as butylated hydroxyanisole, before cooking decreased the amount of these volatile emissions. Among the individual fatty acids tested, heated linolenic acid produced the greatest quantities of 1,3-butadiene, benzene, and acrolein. Separately, the mutagenicity of individual volatile emission condensates was correlated with linolenic acid content (r =.83 ; P =.0004). Condensates from heated linolenic acid, but not linoleic or erucic acid, were highly mutagenic. Conclusions : These studies, combined with experimental and epidemiologic findings, suggest that high-temperature wok cooking with unrefined Chinese rapeseed oil may increase lung cancer risk. This study indicates methods that may reduce that risk. Implications : The common use of wok cooking in China might be an important but controllable risk factor in the etiology of lung cancer. In the United States, where cooking oils are usually refined for purity, additional studies should be conducted to further quantify the potential risks of such methods of cooking. [J Natl Cancer Inst 87 :836-841, 19951

A survey was made of second primary cancers among patients who were enrolled in a large case-control investigation of oral and pharyngeal cancer, hereafter called oral cancer, during 1984-1985 in four areas of the United States. Among the original 1090 patients with oral cancer (nearly all squamous cell carcinomas), 107 developed a second cancer (one-half of them squamous cell) by the end of follow-up in June 1989 (average follow-up 2.6 years), with 69% occurring in the oral cavity, pharynx, oesophagus, larynx or lung. Rates of second tumours varied by age and socioeconomic status, but not sex or race, and were higher among those whose initial cancer was localised, even after adjusting for their longer survival. Long-term survival was lower among those with second cancers. Conditional on surviving for 2 years, the survival at 5 years was under 50% and nearly 70%, respectively, for those with versus those without a second cancer in the first 2 years. These findings confirm the exceptionally high rate of second cancers (especially of the aerodigestive tract) following oral cancer, describe the clinical and pathological features of patients with multiple cancers and indicate the importance of preventive measures.

A case-control study of lung cancer involving interviews with 965 female patients and 959 controls in Shenyang and Harbin, two industrial cities which have among the highest rates of lung cancer in China, revealed that cigarette smoking is the main causal factor and accounted for about 35% of the tumours among women. Although the amount smoked was low (the cases averaged eight cigarettes per day), the percentage of smokers among women over age 50 in these cities was nearly double the national average. Air pollution from coal burning stoves was implicated, as risks of lung cancer increased in proportion to years of exposure to 'Kang' and other heating devices indigenous to the region. In addition, the number of meals cooked by deep frying and the frequency of smokiness during cooking were associated with risk of lung cancer. More cases than controls reported workplace exposures to coal dust and to smoke from burning fuel. Elevated risks were observed for smelter workers and decreased risks for textile workers. Prior chronic bronchitis/emphysema, pneumonia, and recent tuberculosis contributed significantly to lung cancer risk, as did a history of tuberculosis and lung cancer in family members. Higher intake of carotene-rich vegetables was not protective against lung cancer in this population. The findings were qualitatively similar across the major cell types of lung cancer, except that the associations with smoking and previous lung diseases were stronger for squamous/oat cell cancers than for adenocarcinoma of the lung.

Background: The consumption of alcoholic beverages is a strong risk factor for cancers of the oral cavity and pharynx (oral cancers). Alcohol dehydrogenase type 3 (ADH 3 ) metabolizes ethanol to acetaldehyde, a carcinogen. We evaluated whether individuals homozygous for the fast-metabolizing ADH 3 1 allele (ADH 3 1-1 ) have a greater risk of developing oral cancer in the presence of alcoholic beverage consumption than those with the slow-metabolizing ADH 3 2 allele (ADH 3 1-2 and ADH 3 2-2 ). Methods: As part of a population-based study of oral cancer conducted in Puerto Rico, the ADH 3 genotypes of 137 patients with histologically confirmed oral cancer and of 146 control subjects (i.e., individuals with no history of oral cancer) were determined by molecular genetic analysis of oral epithelial cell samples. Risks were estimated by use of multiple logistic regression analyses. Results: Compared with nondrinkers with the ADH 3 1-1 genotype, consumers of at least 57 alcoholic drinks per week with the ADH 3 1-1 , ADH 2 , and ADH 3 2-2 genotypes had 40.1-fold (95% confidence interval [CI] = 5.4-296.0), 7.0-fold (95% CI = 1.4-35.0), and 4.4-fold (95% CI = 0.6-33.0) increased risks of oral cancer, respectively; the risk associated with the ADH 3 1-1 genotype, compared with the ADH 3 1-2 and ADH 3 2-2 genotypes combined, was 5.3 (95% CI = 1.0-28.8) among such drinkers. Considering all levels of alcohol consumption, the risk of oral cancer per additional alcoholic drink per week increased 3.6% (95% CI = 1.9%-5.4%) for subjects with the ADH 3 1-1 genotype and 2.0% (95% CI = 0.9%-3.0%) for subjects with the ADH 3 1-2 or ADH 3 2-2 genotype (two-sided P = .04). Conclusions: The ADH 3 1-1 genotype appears to substantially increase the risk of ethanol-related oral cancer, thus providing further evidence for the carcinogenicity of acetaldehyde.

We examined the relationship between a family history of cancer and risk of oral and pharyngeal cancer using epidemiological data from a large case-control investigation of these tumours. 487 (45.7%) of the cases and 485 (41.0%) of the controls reported cancer in a parent or a sibling. After controlling for age, race, sex, study location, respondent status and smoking and alcohol use, the OR associated with any cancer in the family was 1.1 [95% confidence interval (CI) 0.9-1.3]. Risks were non-significantly elevated among those with a history of cancers arising from the oral cavity/pharynx (OR = 1.2, 95% CI 0.7-2.3), oesophagus/larynx (OR = 1.6, 95% CI 0.7-3.8) and lung (OR = 1.2, 95% CI 0.8-1.8), with the excess risk primarily among those for whom a male relative, particularly a brother, was affected with these smoking-related cancers. In addition, an elevated risk of oral/pharynx cancer was found among those whose sisters developed other cancers (OR = 1.6, 95% CI 1.1-2.2). Subsite analyses revealed stronger elevated risks of smoking-related cancers in relatives of pharyngeal cancer cases (OR = 1.7, 95% CI 1.1-2.8) than of oral cancer patients. The data indicate that there is at most a weak familial aggregation of oral/pharynx cancers. Furthermore, since the excess familial risk of oral/pharynx cancer was associated with smoking-related cancers among male but not female relatives, it seems likely that environmental factors (notably smoking and drinking) contribute to the familial tendency observed in this study.(ABSTRACT TRUNCATED AT 250 WORDS)

Researchers from the US National Cancer Institute compared data on 25-49 year old US women who died of primary liver cancer between 1985 and 1986 with data on age matched controls who died of causes other than liver conditions or oral contraceptive (OC) related conditions to determine the association between primary liver cancer and parity. Women who had experienced at least 1 live birth wear 1.9 times more likely to have died of primary liver cancer than were nulliparous women. The association was not significant (p=.22), however. The highest risks were among children with at least 6 children (odds ratio [OR]=2.9) and with 2 children (2.1). Further the risks were greater when the parents or spouse completed the questionnaire and the association almost reached significance (p=.07). This may have been due to parents and spouse providing more complete information than a friend or neighbor. The risks of developing primary liver cancer were higher among women who had never used OCs than they were among those who ever did. For example, the OR for never users past parity 2 was 3.6 compared with 1.3 for ever OC users. There was a higher risk associated with parity among long term OC users (=or 5 years) than with short-term OC users, however. The researchers concluded that since parity was positively associated with increased risk of primary liver cancer in the US (a low risk country), endogenous hormones may contribute to liver cancer development. The following facts add to this plausibility. Estrogen profiles of parous women are different from those of nulliparous women. Estrogen levels rise considerably during pregnancy. Estrogens alter liver metabolism. Pregnancy makes the body more defenseless against hepatitis and its sequelae. In low risk countries, the risk of primary liver cancer rises among women using exogenous hormones.

A comparison of death certificate statements on occupation for 858 white males who lived in coastal Georgia counties and who died of lung cancer during 1961--74, and for 858 controls who were of the same age and county of residence revealed a twofold excess risk of lung cancer associated with the construction industry. No elevated risk of lung cancer was found for workers in the wood and paper industries in the urban areas of Savannah, Brunswick, or Waycross, but a threefold increase was uncovered for the remaining coastal counties where the wood and paper industry was the largest employer.

Average mortality-rates from lung cancer for White males and females in the U.S.A. 1950-69 were significantly increased in counties with copper, lead, or zinc smelting and refining industries, but not in counties where other non-ferrous ores are processed. The excess mortality was not attributed to differences in geographic region, population density, urbanisation, socioeconomic status, or other manufacturing processes. The findings suggest the influence of community air pollution from industrial emissions containing inorganic arsenic.