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

Charcoal Cigarette Filters and Lung Cancer Risk in Aichi Prefecture, Japan

The lung cancer mortality rate has been lower in Japan than in the United States for several decades. We hypothesized that this difference is due to the Japanese preference for cigarettes with charcoal-containing filters, which efficiently absorb selected gas phase components of mainstream smoke including the carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone. We analyzed a subset of smokers (396 cases and 545 controls) from a case-control study of lung cancer conducted in Aichi Prefecture, Japan. The risk associated with charcoal filters (73% of all subjects) was evaluated after adjusting for age, sex, education and smoking dose. The odds ratio (OR) associated with charcoal compared with 'plain' cigarette filters was 1.2 (95% confidence intervals [CI] 0.9, 1.6). The histologic-specific risks were similar (e.g. OR = 1.3, 95% CI 0.9, 2.1 for adenocarcinoma). The OR was 1.7 (95% CI 1.1, 2.9) in smokers who switched from 'plain' to charcoal brands. The mean daily number of cigarettes smoked in subjects who switched from 'plain' to charcoal brands was 22.5 and 23.0, respectively. The findings from this study did not indicate that charcoal filters were associated with an attenuated risk of lung cancer. As the detection of a modest benefit or risk (e.g. 10-20%) that can have significant public health impact requires large samples, the findings should be confirmed or refuted in larger studie

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

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

Time to First Cigarette after Waking Predicts Cotinine Levels

There is wide variability in cotinine levels per cigarette smoked. We hypothesized that in addition to smoking frequency, other behavioral measures of nicotine dependence, such as the time to first cigarette after waking, are associated with cotinine levels. To test this hypothesis, we measured plasma and urinary cotinine in a community-based study of 252 black and white daily cigarette smokers. Among one pack per day smokers, plasma cotinine levels varied from 16 to 1,180 ng/mL, a 74-fold difference. Two nicotine dependence phenotypes were discerned by time after waking. Subjects in the “low” dependent phenotype smoked > 30 minutes after waking and nearly all smoked ≤20 cigarettes per day. Cotinine levels increased linearly with cigarette consumption in this group. Subjects in the “high” dependent phenotype smoked ≤30 minutes after waking but had a wide range in the frequency of daily cigarettes (6-70). Compared with the low dependent phenotype, there were relatively small differences in cotinine by cigarette frequency with evidence of a plateau effect in heavy smokers (∼30). After adjusting for cigarette frequency, the levels of cotinine by time to first cigarette were as follows: ≤5 minutes, 437 [95% confidence limits (CL), 380-494]; 6 to 30 minutes, 352 (95% CL, 291-413), 31 to 60 minutes, 229 (95% CL, 140-317), and > 60 minutes, 215 (95% CL, 110-321). Similar findings were observed for urinary cotinine. These findings suggest that the time to first cigarette is a strong predictor of nicotine uptake and should be considered in the design of smoking interventions. (Cancer Epidemiol Biomarkers Prev 2009;18(12):3415–20

Risk of squamous cell carcinoma and adenocarcinoma of the lung in relation to lifetime filter cigarette smoking

Over the past few decades, the incidence of adenocarcinoma (AC) of the lung increased much more rapidly than that of squamous cell carcinoma (SCC) in men and women. During this time period, filter cigarettes with substantially reduced ‘‘tar’’ and nicotine yields in the smoke came to dominate the market. METHODS. The risk of SCC and AC in lifelong smokers of filter cigarettes relative to lifelong nonfilter cigarette smokers was assessed in a case-control study performed between 1977 and 1995 with 2292 lung carcinoma patients and 1343 hospital controls who were current smokers. RESULTS. Odds ratios (OR) for SCC in male and female subjects who had smoked filter cigarettes exclusively during their lives were slightly reduced relative to lifetime nonfilter cigarette smokers in men (OR . 0.8; 95% confidence interval [CI], 0.5–1.2), and significantly reduced in women (OR = 0.4; 95% CI, 0.2–0.8). No reduction in risk was observed for AC of the lung in men or women. CONCLUSIONS. Evidence that the increasing predominance of AC over SCC may be due in part to the reduced risk of SCC (but not AC) associated with lifelong filter cigarette smoking is strongest in women; for men, further studies that include larger numbers of lifetime filter smokers are needed to confirm this finding. A lack of protection against AC from low yield filter cigarettes may result from smokers’ ‘‘compensating’’ with deeper and more frequent inhalation, thereby increasing delivery of carcinogens to the peripheral lung. The smoke of modern cigarettes also contains higher concentrations of nitrosamines that primarily produce AC

Nonsteroidal antiinflammatory drugs and colorectal cancer

Background. The association between the use of nonsteroidal antiinflammatory drugs (NSAID) and large bowel cancer was examined in a hospital-based case-control study of 511 patients with colorectal cancer and 500 age-sex matched control subjects. Methods. Regular NSAID use was defined as at least 3 times per week for 1 or more years before the date of hospital admission. Odds ratios (OR) were calculated by the duration of NSAID use and according to the medical reasons given for taking NSAIDs. Results. The prevalences of regular NSAID use were 15% for male patients, 8% for female patients, and 20% for control subjects. Overall, NSAID use was associated with a statistically significant risk reduction in men (OR = 0.64; 95% confidence interval [CI], 0.42-0.97) and in women (OR = 0.32; 95% CI, 0.18-0.57). The estimate decreased with duration among men but increased with duration among women. The risk reduction among patients who took NSAIDs to prevent heart disease was 0.67 (95% CI, 0.38-1.13) for men and 0.43 (95% CI, 0.12-1.59) for women. For treating headache pain, the OR was 0.5 (95% CI, 0.23-1.09) for men and 0.64 (95% CI, 0.25-1.62) for women. The use of NSAID was not found to be associated with the stage of cancer at diagnosis. The OR for daily acetaminophen use was 1.07 (95% CI, 0.35-3.23) for men and 0.59 (95% CI, 0.27-1.25) for women. Conclusions. The regular use of NSAIDs was associated with an overall significant risk reduction of colorectal cancer in men and in women. Among female patients, the greater protective effect associated with short term NSAID use compared with long term NSAID use may reflect a sampling bias

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

Handheld cellular telephone use and risk of brain cancer

Context. A relative paucity of data exist on the possible health effects of using cellular telephones. Objective. To test the hypothesis that using handheld cellular telephones is related to the risk of primary brain cancer. Design and Setting. Case-control study conducted in 5 US academic medical centers between 1994 and 1998 using a structured questionnaire. Patients. A total of 469 men and women aged 18 to 80 years with primary brain cancer and 422 matched controls without brain cancer. Main Outcome Measure. Risk of brain cancer compared by use of handheld cellular telephones, in hours per month and years of use. Results. The median monthly hours of use were 2.5 for cases and 2.2 for controls. Compared with patients who never used handheld cellular telephones, the multivariate odds ratio (OR) associated with regular past or current use was 0.85 (95% confidence interval [CI], 0.6-1.2). The OR for infrequent users (10.1 h/mo) was 0.7 (95% CI, 0.3-1.4). The mean duration of use was 2.8 years for cases and 2.7 years for controls; no association with brain cancer was observed according to duration of use (P=.54). In cases, cerebral tumors occurred more frequently on the same side of the head where cellular telephones had been used (26 vs 15 cases; P=.06), but in the cases with temporal lobe cancer a greater proportion of tumors occurred in the contralateral than ipsilateral side (9 vs 5 cases; P=.33). The OR was less than 1.0 for all histologic categories of brain cancer except for uncommon neuroepitheliomatous cancers (OR, 2.1; 95% CI, 0.9-4.7). Conclusions. Our data suggest that use of handheld cellular telephones is not associated with risk of brain cancer, but further studies are needed to account for longer induction periods, especially for slow-growing tumors wit

Menthol Smoking in relation to Time to First Cigarette and Cotinine: Results from a Community-based Study

Smokers who have their first cigarette shortly after waking, an indicator of nicotine dependence, have substantially higher cotinine levels. There is controversy regarding the role of menthol in nicotine dependence. We hypothesized that menthol smokers have a shorter time to first cigarette (TTFC), and tested whether any statistical association actually reflects increased dependence by measuring nicotine uptake (e.g. cotinine) in the same group of smokers. A cross-sectional community-based study was conducted that included 495 black and white daily cigarette smokers. Results showed a trend between menthol smoking and a shorter TTFC (P less than 0.04 in blacks). Menthol was not an independent predictor of cotinine or an effect modifier with TTFC on cotinine levels in blacks and whites. These results show that while menthol in tobacco is associated with an indicator of nicotine dependence in blacks, menthol was not associated with biological uptake of nicotine in black and white smokers