Intake of red meat and heterocyclic amines, metabolic pathway genes and bladder cancer risk

We analyzed the association between meat intake, heterocyclic amines (HCAs) and bladder cancer (BC) risk in a large case-control study comprised of 884 BC cases and 878 healthy controls, recruited from 1999 to 2009. Epidemiologic and dietary data were collected via an in-person interview. Compared to the lowest quartile of red meat intake, the odds ratios (ORs) for the second, third and fourth quartiles were 1.17 (95% CI: 0.87-1.58), 1.47 (95% CI: 1.09-1.99) and 1.95 (95% CI: 1.41-2.68), respectively, (p-for trend <0.001). In a subset of participants with intakes of HCAs available, compared with those with the lowest quartile of intake, the ORs for the second, third and fourth quartiles were 1.47 (95% CI: 0.60-3.64), 2.58 (95% CI: 1.09-6.11) and 3.32 (95% CI: 1.37-8.01), respectively, (p for trend <0.001). In cumulative analysis of SNPs in the pathway, compared with subjects carrying 0-4 unfavorable genotypes, subjects carrying 5 and 6 or more unfavorable genotypes were at 1.60-fold (95% CI: 1.20-2.12) and 2.37-fold (95% CI: 1.82-3.10) increased risk, respectively. Moreover, subjects carrying six or more unfavorable genotypes and whose red meat intake was in the highest quartile were at 5.09-fold increased risk (95% CI: 2.89-8.96; p < 0.001). These results strongly support that high red meat intake, high intake of HCAs and carrying high number of unfavorable genotypes in the HCA metabolic pathways are associated with increased risk of BC in the study population.     

Comparison of heterocyclic amine levels in home-cooked meats with exposure indicators (United States)

Objective: To compare indicators of heterocyclic amine (HCA) exposure with HCA concentrations in home-cooked meat samples. Methods: Pan-fried hamburger and steak samples were obtained from individuals stating a preference for medium, well done and very well done meat. Concentrations of DiMeIQx, IFP, MeIQx and PhIP were determined by HPLC. Results: HCA concentrations at the three doneness levels were not significantly different using the participants' self-reported doneness preference to categorize samples. Using doneness levels determined at the time the meat was cooked and photograph analysis to categorize samples, HCA concentrations increased with doneness level and significant differences were observed between the very well done and lower doneness levels. When assigned to doneness levels by photograph analysis, mean concentrations (ng/g cooked meat) of DiMeIQx, IFP, MeIQx, and PhIP were 0.18, 0.16, 0.65 and 0.47 in well done hamburger and 0.61, 0.74, 1.88 and 2.04 in very well done hamburger. In steak, mean concentrations were 0.24, 0.10, 0.79 and 0.59 in well done steak and 0.45, 0.14, 1.87 and 0.62 in very well done steak. Conclusions: HCA levels in home-cooked meat samples were significantly different when samples were visually classified for doneness, but not when self-reported doneness preference was used to classify doneness.     

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 January1994 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 60.6percent 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 per cent 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. This revised version was published online in July 2006 with corrections to the Cover Date.     

No effect of meat,meat cooking preferences,meat mutagens or heme iron on lung cancer risk in the prostate,lung, colorectal and ovarian cancer screening trial

Recent epidemiological studies have suggested that red and processed meat may increase the risk of lung cancer. Possible underlying mechanisms include mutagens produced during high‐temperature cooking or preservation, or formed endogenously from heme iron in meat. We used data from 99,579 participants of both screened and nonscreened arms of the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial, aged 55–74 years, to investigate whether meat type, cooking method, doneness level, intake of specific meat mutagens 2‐amino‐3,8‐dimethylimidazo[4,5‐f]quinoxaline (MeIQx), 2‐amino‐3,4,8‐trimethylimidazo[4,5‐f]quinoxaline] (DiMeIQx), 2‐amino‐1‐methyl‐6‐phenylimidazo[4,5‐b]pyridine (PhIP) and benzo(a)pyrene (B(a)P)] and heme iron are associated with lung cancer. Participants' diet was assessed prospectively using a 124‐item food frequency questionnaire and an additional meat‐cooking module. Dietary data were used in conjunction with a database to estimate intake of MeIQx, DiMeIQx, PhIP, B(a)P and heme iron. After up to 8 years of follow‐up, 782 incident lung cancer cases were ascertained. Lung cancer risk was not associated with the consumption of either red (men: HR_{Q5 vs. Q1} = 1.11, 95% CI = 0.79–1.56, P_trend = 0.42; women: HR_{Q5 vs. Q1} = 1.30, 95% CI = 0.87–1.95, P_trend = 0.65) or processed meat (men: HR_{Q5 vs. Q1} = 1.12, 95% CI = 0.83–1.53, P_trend = 0.22; women: HR_{Q5 vs. Q1} = 0.98, 95% CI = 0.68–1.41, P_trend = 0.32) in multivariable models. High‐temperature cooking methods, level of meat doneness, meat mutagens and heme iron had no effect on lung cancer risk. In this population, we found no association between meat type, cooking method, doneness level or intake of specific meat mutagens or heme iron and lung cancer risk.     

Previous lung disease and lung cancer risk among women (United States)

Objective:The association between previous lung diseases (PLD) and lung cancer risk has not been studied extensively. We conducted a registry-based case–control study to examine the relation between previous lung diseases and lung cancer among women in Missouri. Methods:Incident cases (n = 676) were identified through the Missouri Cancer Registry for the period 1 January 1993 to 31 January 1994. Controls (n = 700) were selected through drivers' license files and Medicare files. Results:Whether analyzing all respondents or in-person interviews only, elevated effect estimates were noted for several types of PLD. Elevated relative risk estimates were shown for chronic bronchitis (odds ratio [OR] = 1.7; 95% confidence interval [CI] = 1.2–2.3), emphysema (OR = 2.7; 95% CI = 1.8–4.2), pneumonia (OR = 1.6; 95% CI = 1.2–2.0), and for all PLDs combined (OR = 1.5; 95% CI = 1.2–1.9). Analysis of only direct interviews did not show a substantial or consistent pattern of change in relative risk estimates. Because PLDs identified close to the time of cancer diagnosis could conceivably be misdiagnosed, resulting from early lung cancer symptoms, we evaluated the effects on risk estimates of a latency exclusion of up to threeyears. When these exclusions were taken into account, ORs remained statistically significantly elevated only for emphysema. Conclusion:When earlier epidemiologic findings and underlying biological and genetic factors are taken into account, an association between PLD and lung cancer is plausible.     

Dietary carotenoids,vegetables, and lung cancer risk in women: the Missouri women's health study (United States)

Objective: To examine the effect of specific dietary carotenoids and their primary plant food sources on lung cancer risk in a population-based case–control study of women. Methods: Data were available for 587 incident primary lung cancer cases and 624 controls frequency matched to cases based on age. A modified version of the 100-item NCI-Block food-frequency questionnaire was used to obtain information concerning usual diet 2–3 years prior to interview. Results: In models adjusted for age, total calorie intake, pack-years of smoking, and education, -carotene, -cryptoxanthin, lutein + zeaxanthin, and total carotenoid intake were each associated with a significantly lower risk of lung cancer. Several vegetable groups were predictive of lower lung cancer risk, particularly the frequency of total vegetable intake. Individual and total carotenoids were no longer significantly associated with lower lung cancer risk in models adjusted for total vegetable intake. However, total vegetable intake remained significantly inversely associated with risk in models adjusted for total carotenoids. Conclusions: These results indicate that consumption of a wide variety of vegetables has a greater bearing on lung cancer risk in a population of smoking and nonsmoking women than intake of any specific carotenoid or total carotenoids.     

Carcinogen metabolism genes, red meat and poultry intake, and colorectal cancer risk

Diets high in red meat are established risk factors for colorectal cancer (CRC). Carcinogenic compounds generated during meat cooking have been implicated as causal agents. We conducted a family-based case-control study to investigate the association between polymorphisms in carcinogen metabolism genes (CYP1A2 -154A>C, CYP1B1 Leu432Val, CYP2E1 -1054C>T, GSTP1 Ile105Val, PTGS2 5UTR -765, EPHX1 Tyr113His, NAT2 Ile114Thr, NAT2 Arg197Gln and NAT2 Gly286Glu) and CRC risk. We tested for gene-environment interactions using case-only analyses (N = 577) and compared statistically significant results to those obtained using case-unaffected sibling comparisons (N = 307 sibships). Our results suggested that CYP1A2 -154A>C might modify the association between intake of red meat cooked using high temperature methods and well done on the inside and CRC risk (case-only interaction OR = 1.53; 95% CI = 1.19-1.97; p = 0.0008) and the association between intake of red meat heavily browned on the outside and rectal cancer risk (case-only interaction OR = 0.65; 95% CI = 0.48-0.86; p = 0.003). We also found that GSTP1 Ile105Val might modify the association between intake of poultry cooked with high temperature methods and CRC risk (p = 0.0035), a finding that was stronger among rectal cancer cases. Our results support a role for heterocyclic amines that form in red meat as a potential explanation for the observed association between diets high in red meat and CRC. Our findings also suggest a possible role for diets high in poultry cooked at high temperatures in CRC risk.     

Dietary cholesterol,fat, and lung cancer incidence among older women: The Iowa Women's Health Study (United States)

To test the hypothesis that a high intake of dietary cholesterol and fat is associated with elevated risks of lung cancer, we analyzed data from a population-based, prospective, cohort study conducted among 41,837 postmenopausal Iowa (United States) women who completed, in 1986, a comprehensive mailed questionnaire including information on usual intake of 127 food items. All cohort members were followed for cancer incidence through the statewide cancer registry. By 1991, after six years of follow-up, 272 incident lung-cancer cases were identified. After controlling for total energy intake and other confounding factors, dietary cholesterol, total fat, and animal fat were unrelated to lung cancer risk. Intake in the upper three quartiles of plantderived fat, however, was related to a 30 to 40 percent lower incidence of lung cancer, compared with those in the lowest quartile, with more pronoucned reduction in risk observed among smokers (relative risk=0.6, 95 percent confidence interval=0.4–0.9). This prospective cohort study suggests that high intake of fat of plant origin may be associated with reduced risk of lung cancer, while dietary cholesterol and animal fat intake is unrelated to the etiology of this malignancy in postmenopausal women.This study was supported by grant R01 CA 39742 of the US National Cancer Institute.     

Fried foods, olive oil and colorectal cancer.

BACKGROUND: The epidemiologic evidence for an etiologic role of fried foods and heterocyclic amines in colorectal carcinogenesis is inconsistent. PATIENTS AND METHODS: We have investigated the relation between fried foods and colorectal cancer risk using data from a large, multicentric case-control study conducted in Italy and Switzerland between 1992 and 2000, with 1394 cases of colon cancer, 886 cases of rectal cancer and 4765 controls. RESULTS: After allowing for major relevant covariates, the multivariate odds ratios (ORs) for an increment of one portion per week of fried foods were 0.97 [95% confidence interval (CI)=0.93-1.01] for colon cancer and 1.04 (95% CI=1.00-1.09) for rectal cancer. When we analyzed the type of fats mainly used for frying, we found that olive oil, but not other types of oils, appeared to protect from colon cancer risk (OR=0.89, 95% CI=0.82-0.98). CONCLUSIONS: Our results do not indicate a relevant role of fried foods on colorectal cancer risk. We found a possible favorable effect of (fried) olive oil on colon cancer risk but not on rectal cancer risk.     

Attributable risk of lung cancer in lifetime nonsmokers and long-term ex-smokers (Missouri,United States)

A population-based, case-control study of incident lung cancer among women in Missouri (United States) who were lifetime nonsmokers and long-term ex-smokers was conducted between 1986 and 1992. The study included 618 lung cancer cases and 1,402 population-based, age matched controls. Information on lung-cancer risk factors was obtained by interviewing cases, next-of-kin of cases (36 percent and 64 percent of the cases, respectively) and controls. Year-long radon measurements also were sought in every dwelling occupied for the previous five to 30 years. Population attributable risks (PAR) for specific risk factors were computed for all subjects, for lifetime nonsmokers, for long-term ex-smokers, by histologic cell type (i.e., adenocarcinoma cf nonadenocarcinoma) and for direct interviews with case (for living cases) and for next-of-kin interviews (for dead cases or cases too ill to complete an interview). The mean age at lung cancer diagnosis was 71 years, and nearly 50 percent of the lung cancers were histologically confirmed adenocarcinomas. Almost 40 percent of all lung cancers among lifetime nonsmokers and almost 50 percent of lung cancers among all subjects could be explained by the risk factors under study. Dietary intake of saturated fat and nonmalignant lung disease were the two leading identified risk factors for lung cancer among the lifetime nonsmokers, followed by environmental tobacco smoke, and occupational exposures to known carcinogens. A small nonsignificant risk was found for study subjects exposed to median domestic radon concentration of 4 pCi/l (25-year time-weight average). Since only a small fraction of the population is exposed at this level, it is estimated that the PAR for domestic radon was less than two percent in Missouri. The risk for saturated fat intake was similar for lifetime nonsmokers, ex-somkers, adenocarcinoma cases, and nonadenocarcinoma cases; however, the increased risk was much more pronounced for next-of-kin interviews (PAR=31 percent) than for interviews with the study subjects (PAR = nine percent). A similar pattern of PAR was identified among ex-smokers but, in this group, the lingering effect of a history of smoking was also very important. Along with saturated fat intake (PAR=20 percent), the combined effect of previous active and passive smoking even after 15 years of cessation of active smoking was responsible for more lung cancer than any other risk factor under study (PAR=59 percent).Drs Alavanja, Benicbou, Swanson, and Boice are with the Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, MD, USA. Dr Brownson is with the Department of Community Health, Saint Louis University School of Public Health, St Louis, MO, USA. Address correspondence to Dr Alavanja, Epidemiology and Biostatistics Program, National Cancer Institute, EPN/543, 6130 Executive Blvd, Bethesda, MD 20892, USA.     

Sugar,meat, and fat intake,and non-dietary risk factors for colon cancer incidence in Iowa women (United States)

To investigate the relation of dietary intakes of sucrose, meat, and fat, and anthropometric, lifestyle, hormonal, and reproductive factors to colon cancer incidence, data were analyzed from a prospective cohort study of 35,215 Iowa (United States) women, aged 55–69 years and without a history of cancer, who completed mailed dietary and other questionnaires in 1986. Through 1990, 212 incident cases of colon cancer were documented. Proportional hazards regression was used to adjust for age and other risk factors. Risk factors found to be associated significantly with colon cancer included: (i) sucrose-containing foods and beverages other than ice cream/milk; relative risks (RR) across the quintiles=1.00, 1.73, 1.56, 1.54, and 2.00 (95% confidence intervals [CI] for quintiles two and five exclude 1.0); (ii) sucrose; RR across the quintiles=1.00, 1.70, 1.81, 1.82, and 1.45 (CI for quintiles two through four exclude 1.0); (iii) height; RR=1.23 for highest to lowest quintile (P for trend-0.02); (iv) body mass index; RR=1.41 for highest to lowest quintile (P for trend=0.03); and (v) number of livebirths, RR=1.59 for having had one to two livebirths and 1.80 for having had three or more livebirths compared with having had none (P for trend=0.04). These data support hypotheses that sucrose intake or being tall or obese increases colon cancer risk; run contrary to the hypothesis that increased parity decreases risk; support previous findings of no association with demographic factors other than age, cigarette smoking, or use of oral contraceptives or estrogen replacement therapy; and raise questions regarding previous associations with meat, fat, protein, and physical activity.Cancer Causes and Control 1994, 5, 38–52.This project was supported by research grant CA 39742 from the US National Cancer Institute.     

Meat intake and meat preparation in relation to risk of postmenopausal breast cancer in the NIH‐AARP diet and health study

A number of studies have reported that intake of red meat or meat cooked at high temperatures is associated with increased risk of breast cancer, but other studies have shown no association. We assessed the association between meat, meat‐cooking methods, and meat‐mutagen intake and postmenopausal breast cancer in the NIH‐AARP Diet and Health Study cohort of 120,755 postmenopausal women who completed a food frequency questionnaire at baseline (1995–1996) as well as a detailed meat‐cooking module within 6 months following baseline. During 8 years of follow‐up, 3,818 cases of invasive breast cancer were identified in this cohort. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (95% CI). After adjusting for covariates, intake of total meat, red meat, meat cooked at high temperatures, and meat mutagens showed no association with breast cancer risk. This large prospective study with detailed information on meat preparation methods provides no support for a role of meat mutagens in the development of postmenopausal breast cancer. © 2008 Wiley‐Liss, Inc.     

Risk factor information found in medical records of lung and prostate cancer cases, New Mexico Tumor Registry (United States)

The conduct of public health surveillance and epidemiologicinvestigations would be enhanced by a cost-effective method for thecollection of population-based cancer risk-factor data. We assessed thefeasibility of ascertaining such data from hospital medical records duringroutine abstraction of information from a cancer registry. We examined themedical records of a representative sample of prostate and lung cancer casesdiagnosed during 1992 and 1993 from the New Mexico (United States) TumorRegistry (NMTR) database. Registry personnel abstracted ancillary informationfrom the medical records of 575 prostate and 273 lung cancer cases. Ofmedical records from 848 cases, 90 percent documented a history of tobaccouse, 77 percent contained any family medical history, and 48 percentdocumented occupational information sufficient to allow coding into standardoccupational groups. Availability of occupation and industry varied bypatient ethnicity, age at diagnosis, marital status , and type of hospital,indicating the potential for bias in studies using occupational informationfrom medical records. Our findings suggest that risk factor informationabstracted from medical records may provide valuable information for publichealth surveillance, but is generally too incomplete to serve as a singlesource of exposure information for etiologic studies. Family histories inmedical records may be sufficient for population-based ascertainment ofaffected relative pairs for genetic epidemiology studies for some cancertypes.     

Interplay between heterocyclic amines in cooked meat and metabolic phenotype in the etiology of colon cancer

Although the etiology of colon cancer remains uncertain, an increasing body of epidemiologic evidence indicates that red meat consumption is an important risk factor. The cooking of red meat produces a class of potent experimental carcinogens, the heterocyclic aromatic amines (HAA). These induce cancers in several different sites, including the colon, in rats and mice. Other epidemiologic studies indicate that an individual's genetically determined metabolic phenotype (polymorphisms for N-acetyltransferase and N-hydroxylase) modulates the risk of colon cancer. Both N-acetyltransferase and N-hydroxylase are involved in the metabolism of HAA. An increased risk of colon cancer has been observed in rapid acetylators in four of five studies; further, in two of these the association was found only in meat eaters. The latter observation supports the hypothesis that HAA are involved in colon carcinogenesis. Considerable progress has been made in the study of the molecular pathogenesis of colon cancer, which typically entails the cumulation of several genetic events (mutations and deletions) in oncogenes and tumor suppressor genes. It would now be a crucial contribution to elucidating the causation of colon cancer to show that such mutations are induced in human colonic mucosa by food-borne heterocyclic aromatic amines.This work has been supported in part by the Associazione Italiana per la Ricerca sul Cancro and by the Italian National Research Council (Progetto Finalizzato ACRO, Grant No. 93.04716.CT04).     

Meat consumption, heterocyclic amines and colorectal cancer risk: the Multiethnic Cohort Study

Greater consumption of red and processed meat has been associated with an increased risk of colorectal cancer in several recent meta-analyses. Heterocyclic amines (HCAs) have been hypothesized to underlie this association. In this prospective analysis conducted within the Multiethnic Cohort Study, we examined whether greater consumption of total, red or processed meat was associated with the risk of colorectal cancer among 165,717 participants who completed a detailed food frequency questionnaire at baseline. In addition, we examined whether greater estimated intake of HCAs was associated with the risk of colorectal cancer among 131,763 participants who completed a follow-up questionnaire that included a meat-cooking module. A total of 3,404 and 1,757 invasive colorectal cancers were identified from baseline to the end of follow-up and from the date of administration of the meat-cooking module to the end of follow-up, respectively. Proportional hazard models were used to estimate basic and multivariable-adjusted relative risks (RRs) and 95% confidence intervals for colorectal cancer associated with dietary exposures. In multivariable models, no association with the risk of colorectal cancer was detected for density-adjusted total meat (RR(Q5 vs. Q1) = 0.93 [0.83-1.05]), red meat (RR = 1.02 [0.91-1.16]) or processed meat intake (RR = 1.06 [0.94-1.19]) or for total (RR = 0.90 [0.76-1.05]) or specific HCA intake whether comparing quintiles of dietary exposure or using continuous variables. Although our results do not support a role for meat or for HCAs from meat in the etiology of colorectal cancer, we cannot rule out the possibility of a modest effect.     

Racial and socioeconomic disparities in lung cancer screening in the United States: A systematic review

Nonsmall cell lung cancer (NSCLC) is the leading cause of cancer deaths. Lung cancer screening (LCS) reduces NSCLC mortality; however, a lack of diversity in LCS studies may limit the generalizability of the results to marginalized groups who face higher risk for and worse outcomes from NSCLC. Identifying sources of inequity in the LCS pipeline is essential to reduce disparities in NSCLC outcomes. The authors searched 3 major databases for studies published from January 1, 2010 to February 27, 2020 that met the following criteria: 1) included screenees between ages 45 and 80 years who were current or former smokers, 2) written in English, 3) conducted in the United States, and 4) discussed socioeconomic and race-based LCS outcomes. Eligible studies were assessed for risk of bias. Of 3721 studies screened, 21 were eligible. Eligible studies were evaluated, and their findings were categorized into 3 themes related to LCS disparities faced by Black and socioeconomically disadvantaged individuals: 1) eligibility; 2) utilization, perception, and utility; and 3) postscreening behavior and care. Disparities in LCS exist along racial and socioeconomic lines. There are several steps along the LCS pipeline in which Black and socioeconomically disadvantaged individuals miss the potential benefits of LCS, resulting in increased mortality. This study identified potential sources of inequity that require further investigation. The authors recommend the implementation of prospective trials that evaluate eligibility criteria for underserved groups and the creation of interventions focused on improving utilization and follow-up care to decrease LCS disparities.     

Estimation and projection of population lung cancer trends (United Kingdom)

Objective: Reduction of overall cancer mortality in the UK will require a marked decrease in lung cancer incidence and mortality. A method was sought to predict future lung cancer trends at regional and subregional levels to improve planning, aid the monitoring of health promotion strategies, and to assess health gains that might be achieved. Methods: Data on 55,000 lung cancer patients were used in an age-cohort model of lung cancer incidence (1981–95) and a parametric model of survival (1981–91). Indicators of deprivation were included in the models. Prevalence was estimated from the product of incidence and survival. Lung cancer trends were predicted to 2015, both at steady state and with an incidence perturbation. Results: Female lung cancer is predicted to increase, until by 2015 the numbers will almost equal those in men. Cohort coefficients reveal an increasing risk of lung cancer in females born after 1941. Changing these female cohort coefficients to equate to a declining risk after 1941 suggests that, by 2015, around 200 cases per year might be prevented. This would necessitate a marked change in smoking behavior. Survival from lung cancer was significantly associated with social deprivation and health authority of residence. Conclusions: A credible model has been derived which can be used for health service and outcome monitoring. The model results have highlighted a priority area for smoking intervention which currently seems to attract little attention.     

A meta-analysis of asthma and risk of lung cancer (United States)

Objective: To review epidemiologic evidence that asthma is a risk factor for lung cancer, with particular attention to the role of smoking on this association. Methods: Through MEDLINE computer searches (January 1966 to April 2002) and a review of references, we identified studies with quantitative data on the relation of asthma to lung cancer. Summary estimates of relative risks (RR) were calculated using the fixed-effects model or the random-effects model as appropriate. Results: The combined results from five case–control studies – that presented data limited to individuals who had never smoked – showed a 1.8-fold increase in lung cancer risk among asthmatics (95% confidence interval (CI) = 1.3–2.3). The results from six case–control and four cohort studies, which controlled for smoking history also were significant (RR = 1.7; 95% CI = 1.3–2.2). Finally, to illustrate the potential confounding by tobacco, we combined data from seven cohort studies that did not control for smoking history and found an overall RR of 1.4 (95% CI = 1.2–1.6). Conclusions: The increased risk of lung cancer among never smoking individuals with asthma supports a direct relation between asthma and lung cancer. There is biological evidence to support this association.     

Prospective study of smoking, antioxidant intake, and lung cancer in middle-aged women (USA)

Background: Although substantial evidence suggests that higher intake of fruits and vegetables can reduce the adverse impact of smoking on lung cancer risk, great uncertainty exists regarding the specific foods and their constituents that are protective. We therefore examine prospectively the relation between cigarette smoking and lung cancer incidence among women, and quantify the associations between dietary antioxidants, other nutrients, and lung cancer risk.Methods: In a 16-year prospective cohort study (the Nurses'2 Health Study), 593 cases of lung cancer were confirmed during 1,793,327 person-years of follow-up. Dietary data, including vitamin supplement use and food intake, were collected in 1980 using a validated semiquantitative food frequency questionnaire.Results: The risk of lung cancer increased with the number of cigarettes smoked and with early onset of cigarette smoking. The risk decreased rapidly with the discontinuation of smoking but took 15 years to fall to about the level of risk for women who had never smoked. Dietary intake of fat was not related to the risk of lung cancer. Although -carotene intake was not related to risk, intake of carrots showed a strong inverse relation: women who reported consuming five or more carrots per week had a relative risk of 0.4 (95% CI = 0.2–0.8) compared with the risk for women who never ate carrots.Conclusions: Smoking is the most important risk factor for lung cancer in women, as it is in men. Higher vegetable consumption, particularly of carrots, may significantly reduce the risk of lung cancer, but dietary modification cannot be considered a substitute for smoking prevention and cessation.     

Association between meat and saturated fatty acid intake and lung cancer risk: The Japan Public Health Center-based prospective study

Red meat or saturated fatty acid (SFA) intake has been reported to increase lung cancer (LC) risk in several western countries. However, in Asia, studies on the relationship between meat and SFA intake with LC incidence are still relatively insufficient, and their conclusions are inconsistent. We investigated the association of meat and SFA intake with LC incidence in a population-based prospective cohort study in Japan. Cox regression was used to estimate the hazard ratio (HR) and 95% confidence interval (CI) for LC risk according to meat intake and SFA intake. A total of 73 187 participants (32 934 men and 40 253 women) aged 45 to 74 years participated in our study. During the follow-up period of 1 151 839 person-years (median, 16.0 year) from 1995 to 2013 for Cohort I and from 1998 to 2013 for Cohort II, 1315 (901 men and 414 women) newly diagnosed cases of LC were identified. In men, we found an adverse association between total red meat intake (HR and 95% CI: 1.25 [1.02-1.53]; P_trend = .008) and LC risk. Additionally, borderline statistically significant elevated risks of LC were seen with high intake of unprocessed red meat and processed red meat. However, no positive association between total red meat intake and LC risk was observed in women. In contrast, poultry and fish intake were not associated with LC risk in either men or women. We concluded that a high total intake of total red meat was associated with moderately elevated LC risk in men.