(1/187) Demographic variation in cancer in relation to industrial and environmental influence.

Mortality data (183,064 deaths in a 30-year period, 1940-1969) by sex and three ethnic groups (white excluding Spanish-surnamed, nonwhite, and Spanish-surnamed) in 15 regions within the city (Houston), grouped around the air pollution sample collection stations have been analyzed. Valid contrast studies were possible in only one region within the city for all three groups and in six regions for white excluding Spanish-surnamed and nonwhite. There is evidence that the environmental factors of exposure over time to air and industrial pollutants in Houston has had a demonstrable effect in increasing regional mortality from cancer of the respiratory tract as well as from all other diseases and conditions of the respiratory tract and heart disease. This study points out the need for mutually sustained collaboration of effort of the scientific and industrial communities to redirect their attention and research efforts to the exploration of the carcinogenic potential of the microchemical environment.  (+info)

(2/187) Effect of cigar smoking on the risk of cardiovascular disease, chronic obstructive pulmonary disease, and cancer in men.

BACKGROUND: The sale of cigars in the United States has been increasing for the past six years. Cigar smoking is a known risk factor for certain cancers and for chronic obstructive pulmonary disease (COPD). However, unlike the relation between cigarette smoking and cardiovascular disease, the association between cigar smoking and cardiovascular disease has not been clearly established. METHODS: We performed a cohort study among 17,774 men 30 to 85 years of age at base line (from 1964 through 1973) who were enrolled in the Kaiser Permanente health plan and who reported that they had never smoked cigarettes and did not currently smoke a pipe. Those who smoked cigars (1546 men) and those who did not (16,228) were followed from 1971 through the end of 1995 for a first hospitalization for or death from a major cardiovascular disease or COPD, and through the end of 1996 for a diagnosis of cancer. RESULTS: In multivariate analysis, cigar smokers, as compared with nonsmokers, were at higher risk for coronary heart disease (relative risk, 1.27; 95 percent confidence interval, 1.12 to 1.45), COPD (relative risk, 1.45; 95 percent confidence interval, 1.10 to 1.91), and cancers of the upper aerodigestive tract (relative risk, 2.02; 95 percent confidence interval, 1.01 to 4.06) and lung (relative risk, 2.14; 95 percent confidence interval, 1.12 to 4.11), with evidence of dose-response effects. There appeared to be a synergistic relation between cigar smoking and alcohol consumption with respect to the risk of oropharyngeal cancers and cancers of the upper aerodigestive tract. CONCLUSIONS: Independently of other risk factors, regular cigar smoking can increase the risk of coronary heart disease, COPD, and cancers of the upper aerodigestive tract and lung.  (+info)

(3/187) Nuclear retinoid acid receptor beta in bronchial epithelium of smokers before and during chemoprevention.

BACKGROUND: Retinoids can reverse neoplastic lesions and prevent second primary tumors in the aerodigestive tract. These effects are thought to be mediated by nuclear retinoic acid receptors (RARs) and retinoid X receptors (RXRs), each receptor group including three subtypes (alpha, beta, and gamma). Previously, we found that RARbeta expression was suppressed in lung cancer. In this study, we investigated whether expression of RARbeta is modulated by chemopreventive intervention. METHODS: Using in situ hybridization, we analyzed RARbeta messenger RNA (mRNA) expression in bronchial biopsy specimens from heavy smokers, at baseline and after 6 months of treatment with 13-cis-retinoic acid (13-cis-RA) or placebo. Since we had previously detected RARbeta expression in 90% of bronchial specimens from nonsmokers, we considered loss of RARbeta mRNA expression in at least one of six biopsy specimens at baseline in this study to be aberrant. RESULTS: RARbeta mRNA expression was aberrant in 30 (85.7%) of 35 subjects in the 13-cis-RA group and in 24 (72.7%) of 33 subjects in the placebo group. After 6 months of 13-cis-RA treatment, the number of subjects who were RARbeta positive in all six biopsy specimens increased from five of 35 to 13 of 35 (2.6-fold), so that the percentage of individuals with aberrant RARbeta expression decreased to 62.9% (22 of 35), which represents a statistically significant difference from baseline expression (two-sided P =.01). In the placebo group, no statistically significant difference in RARbeta expression was observed between baseline and 6 months. RARbeta expression was not related to current smoking status or reversal of squamous metaplasia. CONCLUSIONS: These results indicate that RARbeta is an independent marker of response to 13-cis-RA and may serve as an intermediate biomarker in chemoprevention trials of upper aerodigestive tract cancers.  (+info)

(4/187) Mortality patterns among workers exposed to acrylamide: 1994 follow up.

OBJECTIVE: To update the mortality experience of a cohort of 8508 workers with potential exposure to acrylamide at three plants in the United States from 1984-94. METHODS: Analyses of standardised mortality ratios (SMR) with national and local rates and relative risk (RR) regression modelling were performed to assess site specific cancer risks by demographic and work history factors, and exposure indicators for acrylamide and muriatic acid. RESULTS: For the 1925-94 study period, excess and deficit overall mortality risks were found for cancer sites of interest: brain and other central nervous system (CNS) (SMR 0.65, 95% confidence interval (95% CI) 0.36 to 1.09), thyroid gland (SMR 2.11, 95% CI 0.44 to 6.17), testis and other male genital organs (SMR 0.28, 95% CI 0.01 to 1.59), and cancer of the respiratory system (SMR 1.10, 95% CI 0.99 to 1.22); however, none was significant or associated with exposure to acrylamide. A previously reported excess mortality risk of cancer of the respiratory system at one plant remained increased among workers with potential exposure to muriatic acid (RR 1.50, 95% CI 0.86 to 2.59), but was only slightly increased among workers exposed or unexposed to acrylamide. In an exploratory exposure-response analysis of rectal, oesophageal, pancreatic, and kidney cancer, we found increased SMRs for some categories of exposure to acrylamide, but little evidence of an exposure-response relation. A significant 2.26-fold risk (95% CI 1.03 to 4.29) was found for pancreatic cancer among workers with cumulative exposure to acrylamide > 0.30 mg/m3.years; however, no consistent exposure-response relations were detected with the exposure measures considered when RR regression models were adjusted for time since first exposure to acrylamide. CONCLUSION: The contribution of 1115 additional deaths and nearly 60,000 person-years over the 11 year follow up period corroborate the original cohort study findings of little evidence for a causal relation between exposure to acrylamide and mortality from any cancer sites, including those of initial interest. This is the most definitive study of the human carcinogenic potential of exposure to acrylamide conducted to date.  (+info)

(5/187) Proliferative lesions in swimbladder of Japanese medaka Oryzias latipes and guppy Poecilia reticulata.

Thirteen cases of proliferative lesions of the swimbladder were encountered in Japanese medaka Oryzias latipes and guppy Poecilia reticulata from about 10,000 medaka and 5000 guppies used in carcinogenicity tests and histologically examined. Two of the 4 cases from medaka and 8 of the 9 from guppies occurred in untreated control specimens. The lesions affected the gas gland epithelium and included hyperplasia, adenoma, and adenocarcinoma. One medaka had hyperplasia of the gas gland epithelium and in 1 guppy the gland was enlarged with an increase in the number of epithelial layers. Gas gland adenomas, 3 cases in medaka and 1 in the guppy, were typically larger than the hyperplastic lesions, formed expansive masses up to 1 mm in greatest dimension, and exhibited a solid or glandular growth pattern and mild cellular pleomorphism. Adenocarcinoma was the most advanced lesion and all 7 cases occurred in guppies. Adenocarcinomas sometimes filled the entire swimbladder and measured up to 2.5 mm in diameter. Cells of adenocarcinomas were highly pleomorphic, with atypical nuclei, and an elevated mitotic activity. Because most of these tumors occurred in fish from control groups or in tests with noncarcinogenic compounds, the lesions observed here are probably spontaneous rather than chemically induced. Their rare occurrence, however, makes swimbladder proliferative lesions in small-fish carcinogenesis models sensitive indicators of compounds that might target cells of the gas gland.  (+info)

(6/187) Environmental exposure to tremolite and respiratory cancer in New Caledonia: a case-control study.

A case-control study on respiratory cancers was conducted in New Caledonia (South Pacific), where a high incidence of malignant pleural mesothelioma had been observed. The disease pattern suggested an environmental exposure to asbestos. The first results showed that, in some areas, tremolite asbestos derived from local outcroppings was used as whitewash (locally named "po"). All cases diagnosed between 1993 and 1995 (including 15 pleural mesotheliomas, 228 lung cancers, and 23 laryngeal cancers) and 305 controls were included in the study. Detailed information on past or present use of the whitewash, residential history, smoking, diet, and occupation was collected. The risk of mesothelioma was strongly associated with the use of the whitewash (odds ratio (OR) = 40.9; 95% confidence interval (CI): 5.15, 325). All Melanesian cases had been exposed. Among Melanesian women, exposure to the whitewash was associated with an increased risk of lung cancer (OR = 4.89; 95% CI: 1.13, 21.2), and smokers exposed to po had an approximately ninefold risk (OR = 9.26; 95% CI: 1.72, 49.7) compared with women who never smoked and had never used the whitewash. In contrast, no association was noted between exposure to po and lung cancer risk among Melanesian men, probably because of lower exposure levels. Among non-Melanesians, the numbers of exposed subjects were too small to assess the effect of exposure to po. There was no indication of elevated risks for the other cancer sites.  (+info)

(7/187) Respiratory cancer in a cohort of copper smelter workers: results from more than 50 years of follow-up.

Several studies have linked inhalation of airborne arsenic with increased risk of respiratory cancer, but few have analyzed the shape of the exposure-response curve. In addition, since inhaled airborne arsenic affects systemic levels of inhaled arsenic, there is concern that inhaled arsenic may be associated with cancers of the skin, bladder, kidney, and liver, which have been linked to ingested arsenic. The authors followed 8,014 white male workers who were employed for 12 months or more prior to 1957 at a Montana copper smelter from January 1, 1938 through December 31, 1989. A total of 4,930 (62%) were deceased, including 446 from respiratory cancer. Significantly increased standardized mortality ratios (SMRs) were found for all causes (SMR = 1.14), all cancers (SMR = 1.13), respiratory cancer (SMR = 1.55), diseases of the nervous system and sense organs (SMR = 1.31), nonmalignant respiratory diseases (SMR = 1.56), emphysema (SMR = 1.73), ill-defined conditions (SMR = 2.26), and external causes (SMR = 1.35). Internal analyses revealed a significant, linear increase in the excess relative risk of respiratory cancer with increasing exposure to inhaled airborne arsenic. The estimate of the excess relative risk per mg/m3-year was 0.21/(mg/m3-year) (95% confidence interval: 0.10, 0.46). No other cause of death was related to inhaled arsenic exposure.  (+info)

(8/187) Cancer incidence among male pulp and paper workers in Norway.

OBJECTIVES: The study investigated cancer incidence among 23,718 male pulp and paper workers employed continuously for at least 1 year between 1920 and 1993 in Norway. METHODS: The name, date of birth, personal identification number, dates of hire and termination for all employment periods, specific department, and job categories were registered for each worker. Six subcohorts were established (sulfite mill, sulfate mill, paper mill, maintenance department, administrative staff and other departments). Data on the cohort were linked with data in the Norwegian Cancer Register. The follow-up period for cancer incidence, date of death, or emigration was from 1953 through 1993. RESULTS: An excess incidence of lung cancer was found among both short- and long-term employees [standardized incidence ratio (SIR) 1.5, 95% confidence interval (95% CI) 1.13-2.03 and SIR 1.2, 95% CI 1.09-1.34, respectively], especially for workers with the longest latency (SIR 1.3, 95% CI 1.08-1.44) and for sulfite mill workers (SIR 1.5, 95% CI 1.09-1.99). The risk for pleural mesothelioma was also increased (SIR 2.4, 95% CI 1.45-3.75), especially among maintenance workers. The results also showed an increased risk for malignant melanoma (SIR 1.3, 95% CI 1.04-1.60), an unexpected finding. CONCLUSIONS: Almost all the increased risk for lung cancer can be explained by a combination of smoking habits and asbestos use. although an effect of other work-related exposures (sulfur and chloride compounds, wood dust) cannot be excluded. Most of the cases of pleural mesothelioma occurred in departments where asbestos was used. There is no clear explanation for the excess of malignant melanoma, and the finding may be a chance occurrence.  (+info)