Breast cancer: weighing the evidence for a promoting role of dietary fat.

It has been hypothesized that a high-fat diet promotes the development of postmenopausal breast cancer. This contention is supported by data showing high international correlations between fat intake and breast cancer rates, modest positive associations with a high-fat diet in case-control studies, and animal model studies that have consistently demonstrated that dietary fat influences mammary cancer development at several stages in the carcinogenic process. A number of plausible biologic mechanisms have been suggested that may explain such promotional effects. In contrast, dietary fat intake is unrelated to the risk of breast cancer in cohort studies. The conflicting findings from cohort studies have created uncertainty regarding nutritional recommendations and breast cancer prevention. After reviewing key scientific findings that are relevant to this issue, the following conclusion is drawn: In the absence of data from dietary intervention trials, the weight of available evidence suggests that the type and amount of fat in the diet is related to postmenopausal breast cancer and that the inability to detect associations within populations (cohort studies) is because of measurement error and the relative homogeneity of diets measured. It is expected that the results from intervention trials will clarify this issue.

Cigarette smoking, asbestos exposure, and malignant mesothelioma.

In a hospital-based case-control study of 124 (105 male and 19 female) histologically confirmed malignant mesothelioma cases and age- and sex-matched controls, the role of cigarette smoking and the risk of asbestos exposure was investigated. Exposure to asbestos for at least 1 year was likely for 78% of male cases and 16% of female cases, and 90% of males were possibly exposed. Male cases worked predominantly in the ship-building industry, construction, or insulation trades. Elevated risks were found for males employed in asbestos-related industries [odds ratio (OR) 8.1; 95% confidence interval (CI) 4.9-13.5], e.g., shipyards (OR 82.9, 95% CI 25.5-269.1), construction/maintenance (OR 8.3, 95% CI 4.6-14.8), and other asbestos-related jobs (OR 3.2, 95% CI 1.4-7.2), and for males who self-reported exposure to asbestos or insulation (OR 50.9, 95% CI 21.7-119.8). A statistically significant trend was found for the risk of mesothelioma with increasing years employed in non-shipyard asbestos-related occupations. Among women, only one case worked in an asbestos-related industry and two reported domestic contact with asbestos. No association between cigarette smoking and mesothelioma was found for either men or women. We also report the occurrence of mesothelioma in occupations which have not been previously reported.

Gender differences in smoking and risk for oral cancer.

Based on studies that show gender differences in cigarette smoking and lung cancer risk, we hypothesized that sex differences also exist in the risk for cancer of the oral cavity and pharynx. A hospital-based study of 1009 patients with oral neoplasia and 923 age-matched controls was conducted from 1981-1990. All subjects were interviewed directly with an extensive questionnaire containing items on tobacco smoking, alcohol consumption, and occupational exposures. Using a cumulative lifetime measure of exposure to cigarette tar, the adjusted odds ratio for men, according to increasing quartile of tar consumption and relative to never smokers, was 1.0 [95% confidence interval (CI), 0.6-1.6) for the lowest category, 0.9 (95% CI, 0.6-1.6) for the second category, 1.6 (95% CI, 1.0-2.5) for the third category, and 2.1 (95p5 CI, 1.4-3.2) for the highest category. Among women, the corresponding odds ratios were 1.8 (95% CI, 1.1-3.0), 2.8 (95% CI, 1.6-4.9), 3.2 (95% CI, 1.9-5.6), and 4.6 (95% CI, 2.5-8.7). The linear increase in risk was significantly higher for women than for men. Among nonsmoking cases, there was a significantly higher proportion of women than men over the age of 50 years. This was consistent for all subsites within the oral cavity. These findings support the hypothesis that there are gender differences in the smoking-related risks for oral cancer and in the risk for nonsmoking-related oral cancer as well. The role of nutrition in relation to these findings is discussed.

Comparison of GSTM polymorphisms and risk for oral cancer between African-Americans and Caucasians.

Two members of the mu class of glutathione S-transferase (GST) genes, GSTM1 and GSTM3, have polymorphic alleles which have been associated with altered levels of GST mu protein expression and may be linked to increased risk for several tobacco-related cancers. Oral cancer is a tobacco-related disease that affects African-American men at a significantly higher incidence than Caucasian men. To examine the potential role of GSTM polymorphisms in risk for oral cancer in African-Americans and Caucasians, the prevalences of the GSTM1 null and GSTM3 intron 6 polymorphisms were examined in 63 African-American and 101 Caucasian patients with histologically confirmed primary oral cancer, as well as in 133 African-American and 213 Caucasian matched control subjects. In African-Americans, the odds ratio for oral cancer associated with the GSTM1 (0/0) genotype was 3.1 [95% confidence interval (CI) = 1.1-8.5], with the association between the GSTM1 (0/0) genotype and oral cancer risk strongest in heavy smokers [i.e. > 24 pack-years; odds ratio (OR) = 5.4, 95% CI = 1.2-24]. Using the potentially most protective GSTM1 [+]/GSTM3 (B/B) genotype as the reference group, increased risk for oral cancer was observed in African-Americans with the GSTM1 [+]/GSTM3 [(A/A) + (A/B)] (OR = 2.2, 95% CI = 0.82-6.0), GSTM1 (0/0)/GSTM3 (B/B) (OR = 4.3, 95% CI = 1.1-16), and GSTM1 (0/0)/GSTM3 [(A/A) + (A/B)] (OR = 6.6, 95% CI = 1.2-38) genotypes (P < 0.01, trend test). No significant associations were observed between GSTM genotype and oral cancer risk in Caucasians. These results suggest that the GSTM1 null and GSTM3 intron 6 polymorphisms play an important role in risk for oral cancer among African-Americans and implicates the mu class of GSTs as important tobacco carcinogen detoxifying enzymes in this population.

Smoking and pancreatic cancer in men and women.

Most studies of smoking and pancreatic cancer have used male subjects or combined men and women together in statistical analyses. There is little information on the relative risk of smoking and pancreatic cancer in women. Because of the high case-fatality rate, many of these studies were also based on information gathered from proxy respondents, in which smoking habits may not be recalled with certainty. A hospital-based study of 484 male and female patients with pancreatic cancer and 954 control subjects was conducted based on direct interviews of incident cases. Compared to never smokers, the odds ratio (OR) for current cigarette smokers was 1.6 [95% confidence interval (CI), 1.1-2.4] for men and 2.3 (95% CI, 1.4-3.5) for women. In women, but not in men, there was a trend in the ORs with years of daily cigarette consumption (P < 0.01). Filter cigarettes offered no protective advantage compared to nonfilter cigarettes. Among men, the OR was 2.1 (95% CI, 1.2-3.8) for pipe/ cigar smokers and 3.6 (95% CI, 1.0-12.8) for tobacco chewers. Tobacco smoke causes pancreatic cancer when inhaled into the lungs. Tobacco juice may also cause pancreatic cancer when ingested or absorbed through the oral cavity. These data suggest that smoking is a cause of pancreatic cancer in women and that the risks for female smokers are comparable to male smokers. Nevertheless, the causes of most pancreatic cancers are unknown.

Cigarette smoking and large cell carcinoma of the lung.

Large cell carcinoma is the fourth most common histological type of lung cancer in the United States. Cigarette smoking causes large cell lung cancer, but it is uncertain whether the effect varies with the amount and duration of smoking. This uncertainty stems from ambiguity in the histopathological classification of large cell cancer, especially before 1971, and the relatively infrequent occurrence of large cell cancer in epidemiological studies. The present case-control investigation demonstrates that the risk of large cell cancer increases with both the frequency and number of years of cigarette smoking. The odds ratio associated with smoking two or more packs/day was 37.0 (95% confidence interval, 16.4-83.2) in men and 72.9 (35.4-150.2) in women. It is concluded that cigarette smoking is the predominant cause of large cell lung cancer.

Breast cancer risk in relation to adipose concentrations of organochlorine pesticides and polychlorinated biphenyls in Long Island, New York.

To assess a possible etiological role of organochlorine compounds in breast cancer development on Long Island, a high-risk region of New York State, concentrations of organochlorine pesticides and polychlorinated biphenyls (PCBs) were measured in the adipose tissue of 232 women with breast cancer and 323 hospital controls admitted to surgery for benign breast disease or non-breast-related conditions. Seven pesticide residues and 14 PCB congeners were assayed via a supercritical fluid extraction method followed by gas chromatography with electron capture detection. After adjustment for age and body mass index, which were strongly correlated with organochlorine levels, adipose concentrations of 1,1-dichloro-2,2-di(4-chlorophenyl)ethylene, total pesticides, and total polychlorinated biphenyls (PCBs) did not differ significantly between cases and controls. The relative abundance of individual pesticide species and PCB congeners was similar in cases and controls. Odds ratios adjusted for age, BMI, hospital, and race gave no evidence of a dose-response for 1,1-dichloro-2,2-di(4-chlorophenyl)ethylene, total pesticides, or total PCBs, whether stratified by estrogen receptor status or not. Breast cancer risk among Long Island residents was not elevated compared with residents of the adjacent New York City borough of Queens. We did not confirm a previously reported association between breast cancer risk and levels of PCB congener 118 (2,3',4,4',5-pentachlorobiphenyl), nor did we observe an association with the most abundant congener 153 (2,2',4,4',5,5'-hexachlorobiphenyl), a strong inducer of phase I enzymes that was reported recently to have estrogenic properties. Only PCB congener 183 (2,2',3,4,4',5',6-heptachlorobiphenyl), which is also an inducer, was significantly associated with risk, with an adjusted odds ratio of 2.0 (95% confidence interval, 1.2-3.4) in women with adipose levels >5.67 ng/g; the biological importance of this observation is unclear without confirmation in additional studies. Although neither the present nor other studies have provided convincing evidence of an association between body burden of 1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane and PCBs with cancer of the breast, these compounds are rated as "possible" and "probable" human carcinogens, respectively, by the International Agency for Research on Cancer. Investigations of associations with cancer at other sites should be carried out.

Differences in the urinary metabolites of the tobacco-specific lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in black and white smokers.

Incidence and mortality rates for lung cancer in the United States are significantly greater in blacks than in whites. This disparity cannot be explained by differences in smoking behavior. We hypothesize that the observed racial differences in risk may be due to differences in the metabolic activation or detoxification of the tobacco-specific lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). To test this, different biomarkers of NNK exposure and metabolism, including the urinary metabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and the presumed detoxification product [4-(methylnitrosamino)-1-(3-pyridyl)but-1-yl]-beta-O-D-glucosiduronic acid (NNAL-Gluc), were examined along with questionnaire data on lifestyle habits and diet in a metabolic epidemiological study of 34 black and 27 white healthy smokers. Results demonstrated that urinary NNAL-Gluc:NNAL ratios, a likely indicator of NNAL glucuronidation and detoxification, were significantly greater in whites than in blacks (P < 0.02). In addition, two phenotypes were apparent by probit analysis representing poor (ratio < 6) and extensive (ratio > or = 6) glucuronidation groups. The proportion of blacks falling into the former, potentially high-risk group was significantly greater than that of whites (P < 0.05). The absolute levels of urinary NNAL, NNAL-Gluc, and cotinine were also greater in blacks than in whites when adjusted for the number of cigarettes smoked. None of the observed racial differences could be explained by dissimilarities in exposure or other sociodemographic or dietary factors. Also, it is unlikely that the dissimilarities are due to racial differences in preference for mentholated cigarettes, because chronic administration of menthol to NNK-treated rats did not result in either increases in urinary total NNAL or decreases in NNAL-Gluc:NNAL ratios. Altogether, these results suggest that racial differences in NNAL glucuronidation, a putative detoxification pathway for NNK, may explain in part the observed differences in cancer risk.

CYP1A1 and GSTM1 polymorphisms and oral cancer risk.

The importance of both the CYP1A1 exon 7 (ile:val) and GSTM1 (0/0) polymorphisms in oral cancer susceptibility was assessed by examining polymorphic prevalences in 135 patients with oral cancer and 135 noncancer controls frequency-matched by age at diagnosis (+/- 5 years), race, sex, and institute of patient recruitment. The prevalence of the GSTM1 (0/0) genotype was approximately 51% in both cases and controls. The prevalence of the CYP1A1 (ile:val) polymorphism [including both the (ile/val) and (val/val) genotypes] was significantly higher in cases as compared to controls (17.6% versus 7.6%, respectively; crude odds ratio, 2.6; confidence interval, 1.2-5.7). No association was observed between polymorphic prevalence and levels of smoking or alcohol consumption in cases. These results suggest that the GSTM1 null genotype is not associated with oral cancer risk. These results also suggest that individuals with the CYP1A1 exon 7 ile:val polymorphism are at increased risk for oral cancer, and that this risk may not be influenced by differences in exposure to tobacco smoke.

Relative abundance of organochlorine pesticides and polychlorinated biphenyls in adipose tissue and serum of women in Long Island, New York.

Some organochlorine pesticides (OCPs) and PCBs are under investigation as possible risk factors for breast cancer because of their estrogenic properties and widespread presence in the environment. It is important to know whether adipose tissue used by some investigators and serum assays used by others can provide comparable information on body burden. Concentrations of seven OCPs or their breakdown products as well as 14 PCB congeners were measured in the adipose tissue and serum of 293 women enrolled as controls in a case-control study of environmental factors for breast cancer in Long Island, New York, a high-risk region. Adipose OCP/PCB levels were measured using a supercritical fluid extraction method developed by the authors. 1,1-Dichloro-2,2-di(4-chlorophenyl)ethylene (p,p'-DDE) was detected in all adipose and serum samples; two chlordane derivatives, beta-hexachlorocyclohexane (a lindane isomer) and hexachlorobenzene, were detected in at least 92% of adipose samples. The di-ortho hexachlorinated PCB congeners 2,4,5,2',4',5'-hexachlorobiphenyl and 2,3,4,2',4',5'-hexachlorobiphenyl were detected in all adipose and over 98% of serum samples. 1,1-Dichloro-2,2-di(4-chlorophenyl)ethylene comprised 77% of total pesticide residues in adipose and 71% in serum. 2,4,5,2',4',5'-Hexachlorobiphenyl comprised 24% of adipose and 21% of serum PCBs. The relative concentration patterns of the 14 PCB congeners were similar to those reported in other human studies and were also typical of patterns reported in environmental samples from various biota, including mammals and birds, but differed substantially from patterns reported in occupationally exposed workers. All adipose-serum correlations for pesticides and most PCBs were statistically significant. Either serum or adipose OCP/PCB levels of a variety of environmental organochlorine compounds may serve as useful biomarkers of body burden.

Smoking and lung cancer risk in American and Japanese men: an international case-control study.

Rates of lung cancer in American men have greatly exceeded those in Japanese men for several decades despite the higher smoking prevalence in Japanese men. It is not known whether the relative risk of lung cancer associated with cigarette smoking is lower in Japanese men than American men and whether these risks vary by the amount and duration of smoking. To estimate smoking-specific relative risks for lung cancer in men, a multicentric case-control study was carried out in New York City, Washington, DC, and Nagoya, Japan from 1992 to 1998. A total of 371 cases and 373 age-matched controls were interviewed in United States hospitals and 410 cases and 252 hospital controls in Japanese hospitals; 411 Japanese age-matched healthy controls were also randomly selected from electoral rolls. The odds ratio (OR) for lung cancer in current United States smokers relative to nonsmokers was 40.4 [95% confidence interval (CI) = 21.8-79.6], which was >10 times higher than the OR of 3.5 for current smokers in Japanese relative to hospital controls (95% CI = 1.6-7.5) and six times higher than in Japanese relative to community controls (OR = 6.3; 95% CI = 3.7-10.9). There were no substantial differences in the mean number of years of smoking or average daily number of cigarettes smoked between United States and Japanese cases or between United States and Japanese controls, but American cases began smoking on average 2.5 years earlier than Japanese cases. The risk of lung cancer associated with cigarette smoking was substantially higher in United States than in Japanese males, consistent with population-based statistics on smoking prevalence and lung cancer incidence. Possible explanations for this difference in risk include a more toxic cigarette formulation of American manufactured cigarettes as evidenced by higher concentrations of tobacco-specific nitrosamines in both tobacco and mainstream smoke, the much wider use of activated charcoal in the filters of Japanese than in American cigarettes, as well as documented differences in genetic susceptibility and lifestyle factors other than smoking.

Handheld cellular telephones and risk of acoustic neuroma.

The hypothesis that intracranial energy deposition from handheld cellular telephones causes acoustic neuroma was tested in an epidemiologic study of 90 patients and 86 control subjects. The relative risk was 0.9 (p = 0.07) and did not vary significantly by the frequency, duration, and lifetime hours of use. In patients who used cellular telephones, the tumor occurred more often on the contralateral than ipsilateral side of the head. Further efforts should focus on potentially longer induction periods.

Lung cancer pathology in smokers, ex-smokers and never smokers.

The histologic distribution of lung cancer is markedly different in smokers and non-smokers. It is not known whether the histology among former smokers varies according to the number of years since quitting. Using data from a large case-control study of lung cancer, we found that for both men and women, the proportion of adenocarcinomas increased with the number of years since quitting smoking. Among long-term quitters (> 25 years), the proportion of adenocarcinomas was similar to that in never smokers. These findings have implications for studies of environmental tobacco smoke and lung cancer.

The epidemiology of left-handedness in a hospital population.

PURPOSE: We evaluated the association between left-handedness (LH) and age, education, cigarette smoking, alcohol consumption, and disease status in a case-control study of 8801 hospitalized patients with cancer and those with other conditions. METHODS: Subjects were interviewed in person using a structured questionnaire that contained detailed sections of lifestyle behaviors. RESULTS: The overall prevalences of LH were 7.6% among men and 6.5% among women. Among both sexes LH declined with increasing age (P < 0.05). After adjustment for age, the following associations were observed. Men had a higher risk of LH than women. The prevalence of LH was lower in ever-married subjects compared with never-married subjects (odds ratio [OR] for men, 0.7; 95% confidence intervals [CI], 0.5-0.9; for women, OR, 0.5; 95% CI, 0.3-0.9). Among men, the prevalence of LH was not associated with race, years of education, smoking status, or levels of alcohol consumption. The risk of LH was elevated in men diagnosed with fractures as compared with all other male patients (OR, 2.4; 95% CI, 1.3-6.7). Among women, LH was not associated with race, smoking, or hormonal and reproductive factors, but LH was more common among female high-school and college graduates and among self-reported alcoholics. The odds ratio of LH was significantly lower in women with breast cancer (OR, 0.3; 95% CI, 0.1-0.7). CONCLUSIONS: The increased risk of serious injuries in LH is not a result of higher alcohol use. Handedness might be an important factor in the safe use of industrial equipment.

The changing epidemiology of smoking and lung cancer histology.

In 1950, the first large-scale epidemiological studies demonstrated that lung cancer is causatively associated with cigarette smoking, a finding subsequently confirmed by the Royal College of Physicians in London, the U.S. Surgeon General, and the World Health Organization. Although cigarette consumption has gradually decreased in the United States from a high of about 3800 cigarettes per adult per year in 1965 to about 2800 cigarettes in 1993, death from lung cancer has reached a high among males at the rate of 74.9/100,000/year and among females at the rate of 28.5. However, in the younger cohorts, the lung cancer death rate is decreasing in both men and women. In this overview we discuss the steeper increase during recent decades of lung adenocarcinoma incidence compared with squamous cell carcinoma of the lung. In 1950, the ratio of these two major types of lung cancer in males was about 1:18; today it is about 1:1.2-1.4. This overview discusses two concepts that are regarded as contributors to this change in the histological types of lung cancer. One factor is the decrease in average nicotine and tar delivery of cigarettes from about 2.7 and 38 mg in 1955 to 1.0 and 13.5 mg in 1993, respectively. Other major factors for the reduced emission of smoke relate to changes in the composition of the cigarette tobacco blend and general acceptance of cigarettes with filter tips; the latter constitute 97% of all cigarettes currently sold. However, smokers of low-yield cigarettes compensate for the low delivery of nicotine by inhaling the smoke more deeply and by smoking more intensely; such smokers may be taking up to 5 puffs/min with puff volumes up to 55 ml. Under these conditions, the peripheral lung is exposed to increased amounts of smoke carcinogens that are suspected to lead to lung adenocarcinoma. Among the important changes in the composition of the tobacco blend of the U.S. cigarette is a significant increase in nitrate content (0.5% to 1.2-1.5%), which raises the yields of nitrogen oxides and N-nitrosamines in the smoke. Furthermore, the more intense smoking by the consumers of low-yield cigarettes increases N-nitrosamines in the smoke 2- to 3-fold. Among the N-nitrosamines is 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a powerful lung carcinogen in animals that is exclusively formed from nicotine. This organ-specific tobacco-specific nitrosamine (TSNA) induces adenocarcinoma of the lung. All of these factors, the more intense smoking, the deeper inhalation of the smoke, and the increased yields of N-nitrosamines in the smoke of low-yield cigarettes, are considered major contributors to the drastic increase in lung adenocarcinoma among cigarette smokers in recent years. This overview also discusses the differences in the major lung cancer types in female compared with male smokers as well as the likely underlying factors for increased lung cancer risk among African Americans compared with that among white Americans. Although the only sure way to prevent smoking-related diseases is giving up the tobacco habit, there must be a measure of protection for those who cannot accomplish this. Therefore, setting upper permissible limits of tar levels for the smoke of U.S. cigarettes, similar to strategies already taken in Western Europe, should be considered.

Diesel engine exhaust and lung cancer: an unproven association.

The risk of lung cancer associated with diesel exhaust has been calculated from 14 case-control or cohort studies. We evaluated the findings from these studies to determine whether there is sufficient evidence to implicate diesel exhaust as a human lung carcinogen. Four studies found increased risks associated with long-term exposure, although two of the four studies were based on the same cohort of railroad workers. Six studies were inconclusive due to missing information on smoking habits, internal inconsistencies, or inadequate characterization of diesel exposure. Four studies found no statistically significant associations. It can be concluded that short-term exposure to diesel engine exhaust (< 20 years) does not have a causative role in human lung cancer. There is statistical but not causal evidence that long-term exposure to diesel exhaust (> 20 years) increases the risk of lung cancer for locomotive engineers, brakemen, and diesel engine mechanics. There is inconsistent evidence on the effects of long-term exposure to diesel exhaust in the trucking industry. There is no evidence for a joint effect of diesel exhaust and cigarette smoking on lung cancer risk. Using common criteria for determining causal associations, the epidemiologic evidence is insufficient to establish diesel engine exhaust as a human lung carcinogen.

Carcinogenic effects of diesel emissions and lung cancer: the epidemiologic evidence is not causal.

The effects of diesel engine exhaust in lung carcinogenesis have been evaluated by several scientific organizations and government agencies. This complex issue has required a multidisciplinary approach including atmospheric measurements, toxicology, chemical carcinogenesis, epidemiology, and risk assessment. One important aspect of the epidemiological studies that deserves further attention is the confounding effects of cigarette smoking. Only some epidemiological studies have statistically adjusted for cigarette smoking, usually by years of smoking, cigarettes per day, or pack-years. Some studies obtained smoking information from proxy interviews. However, differences in "tar" intake, interpuff interval, depth of inhalation, and other smoking behavior patterns were not evaluated. These smoking parameters are rarely collected for occupational data analysis, yet the inability to adjust statistically for such parameters may result in a small degree of residual confounding. Because the highest odds ratios for lung cancer associated with diesel engine exhaust are usually less than 2 or 1.5, possible residual confounding effects of smoking may have resulted in spurious associations.

Exposure to environmental tobacco smoke and the risk of heart attack.

BACKGROUND: Environmental tobacco smoke (ETS) increases the risk of heart disease in several epidemiological studies although the methods of assessing exposure have been incomplete. We determined the prevalence of ETS from various sources, and examined the association between ETS and the risk of myocardial infarction. METHODS: A hospital-based case-control study of myocardial infarction was conducted from 1980 to 1990 by interviewing 114 case patients and 158 control subjects. RESULTS: Among controls, the sources of ETS were the workplace (56%), childhood exposure (66%), home adult exposure (48%), car exposure (20%) and from trains or other surface transportation (4%). Compared to never smokers, the odds ratio (OR) for exposure to ETS during childhood was 0.97 (95% confidence intervals [Cl]: 0.53-1.46) for men and 0.92 (95% Cl: 0.5-1.86) for women. The adjusted OR associated with adult exposure was 1.5 (95% Cl: 0.9-2.6), although no trend was observed with the number of years of exposure. Women who were exposed to ETS in automobiles had an increased but non-significant risk (OR = 2.8, 95% Cl: 0.9-8.0). CONCLUSION: Exposure to ETS comes from a variety of sources besides the spouse including parents, workplace employees and motorists. Exposure to ETS during childhood is not associated with an increased risk of heart disease. However, ETS exposure during adulthood increased the risk of myocardial infarction approximately 50% in this data although the findings were not statistically significant.

Cancer mortality in the United States and Germany.

PURPOSE: The USA and Germany are currently two of the world's leading industrial nations with comparable standards of living and considerable similarities in lifestyle. Fifty years ago, i.e., in the years following the Second World War, the living conditions in the two countries were completely different. If it is true that the major part of cancer occurrence is lifestyle-related, we should see corresponding discrepancies and assimilations on the level of cancer occurrence. METHODS: As an exercise in descriptive epidemiology, we compare the time trends in German and US cancer mortality in order to examine whether they parallel indeed the differences and changes in lifestyle factors of the two countries. RESULTS: Overall, we found the cancer mortality of the two countries converging to rather similar rates. However, in detail, the data indicate various inconsistencies between the patterns of lifestyle factors and cancer mortality in the two countries: similar lung cancer rates, despite rather different patterns of cigarette consumption, or decreasing rectal cancer mortality, despite increasing prevalence of risk factors, are examples. CONCLUSIONS: Promising changes with regard to relevant risk factors indicate that the recent decline of cancer mortality in both countries will continue. Nevertheless, vigorous action towards primary prevention in Germany and more effective screening programs in both countries appear recommendable.

Cholesterol screening in a community health promotion program: epidemiologic results from a biracial population.

The prevalence and interrelationship of high blood cholesterol levels with other cardiovascular disease risk factors were studied in a biracial suburb of New York City. Participants in community-based screenings to determine blood cholesterol levels have been predominantly white women in older age groups, highly educated and nonsmokers. To reach a more representative segment of a local population and promote healthy lifestyle behaviors, cholesterol screenings were conducted within an ongoing health promotion program in Mount Vernon, NY. Plasma cholesterol levels were determined for 5,011 participants, including 2,308 whites and 1,778 blacks. Of the men, 29 percent had high cholesterol levels; among women, it was 27 percent. Of the men with high levels, half had levels greater than 200 milligrams per deciliter, as did 55 percent of the women. After statistical adjustments were made for age and other risk factors for high blood cholesterol, mean cholesterol levels were higher for whites than blacks. The level for white men was 204 milligrams per deciliter; for women, 212. For black men, the level was 199 milligrams per deciliter; for women, 208, P < .10. Hispanic men had levels of 199, P < .10. The levels for Hispanic women (203 milligrams per deciliter) were significantly lower than that of white women. Among whites who smoked more than 1 pack of cigarettes per day, mean cholesterol levels were 11 milligrams per deciliter higher than for those who never smoked or were light smokers (0, 1-20 cigarettes per day, P < .10). There were too few who smoked more than 1 pack to test this association adequately among blacks. The mean cholesterol levels for hypertensive black men were 10 milligrams per deciliter greater than for black men with normal blood pressure (P<.10).