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Nutritional status is known to alter immune function, a suspected risk factor for non-Hodgkin lymphoma (NHL). To investigate whether long-term over, or under, nutrition is associated with NHL, self-reported anthropometric data on weight and height from over 10,000 cases of NHL and 16,000 controls were pooled across 18 case-control studies identified through the International Lymphoma Epidemiology Consortium. Study-specific odds ratios (OR) were estimated using logistic regression and combined using a random-effects model. Severe obesity, defined as BMI of 40 kg m(-2) or more, was not associated with NHL overall (pooled OR = 1.00, 95% confidence interval (CI) 0.70-1.41) or the majority of NHL subtypes. An excess was however observed for diffuse large B-cell lymphoma (pooled OR = 1.80, 95% CI 1.24-2.62), although not all study-specific ORs were raised. Among the overweight (BMI 25-29.9 kg m(-2)) and obese (BMI 30-39.9 kg m(-2)), associations were elevated in some studies and decreased in others, while no association was observed among the underweight (BMI < 18.5 kg m(-2)). There was little suggestion of increasing ORs for NHL or its subtypes with every 5 kg m(-2) rise in BMI above 18.5 kg m(-2). BMI components height and weight were also examined, and the tallest men, but not women, were at marginally increased risk (pooled OR = 1.19, 95% CI 1.06-1.34). In summary, whilst we conclude that there is no evidence to support the hypothesis that obesity is a determinant of all types of NHL combined, the association between severe obesity and diffuse large B-cell lymphoma may warrant further investigation.

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In 2004-2007 4 independent case-control studies reported evidence that sun exposure might protect against NHL; a fifth, in women only, found increased risks of NHL associated with a range of sun exposure measurements. These 5 studies are the first to examine the association between personal sun exposure and NHL. We report here on the relationship between sun exposure and NHL in a pooled analysis of 10 studies participating in the International Lymphoma Epidemiology Consortium (InterLymph), including the 5 published studies. Ten case-control studies covering 8,243 cases and 9,697 controls in the USA, Europe and Australia contributed original data for participants of European origin to the pooled analysis. Four kinds of measures of self-reported personal sun exposure were assessed at interview. A two-stage estimation method was used in which study-specific odds ratios (ORs) and 95% confidence intervals (CIs), adjusted for potential confounders including smoking and alcohol use, were obtained from unconditional logistic regression models and combined in random-effects models to obtain the pooled estimates. Risk of NHL fell significantly with the composite measure of increasing recreational sun exposure, pooled OR = 0.76 (95% CI 0.63-0.91) for the highest exposure category (p for trend 0.01). A downtrend in risk with increasing total sun exposure was not statistically significant. The protective effect of recreational sun exposure was statistically significant at 18-40 years of age and in the 10 years before diagnosis, and for B cell, but not T cell, lymphomas. Increased recreational sun exposure may protect against NHL.

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BACKGROUND: The aim was to investigate whether 2 subgroups of Hodgkin lymphoma (Epstein-Barr virus-positive and Epstein-Barr virus-negative) are associated with smoking or alcohol. METHODS: Patients with lymphoma diagnosed between age 16 and 69 years in geographically defined areas of England were recruited between 1998 and 2003. One control, matched to each lymphoma case on sex, date of birth, and area of residence, was randomly selected from population registers. Self-reported histories of tobacco and alcohol use were collected during face-to-face interviews with cases and controls. RESULTS: Compared with lifelong nonsmokers, ever-smokers were at increased risk of Hodgkin lymphoma (odds ratio =1.4; 95% confidence interval = 1.1-1.9). This excess was among current smokers, defined as smoking 2 years before diagnosis (1.7; 1.2-2.3). An increasing trend was observed with rising numbers of years smoked. Risks fell as the number of years stopped smoking increased, becoming equivalent to that of a nonsmoker 10 or more years after quitting. Associations were suggested for Epstein-Barr virus-positive Hodgkin lymphoma, but less so for Epstein-Barr negative Hodgkin lymphoma. No associations between Hodgkin lymphoma and alcohol consumption were observed. CONCLUSIONS: The association between smoking and Hodgkin lymphoma in general, and Epstein-Barr-positive Hodgkin lymphoma in particular, is consistent with previous studies. Further exploration of the relationship between Hodgkin lymphoma and smoking and of the potential mechanisms by which smoking could interact with Epstein-Barr virus status to increase Hodgkin lymphoma risk are required.

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OBJECTIVE: The aim of the study was to investigate the relationship between Hodgkin lymphoma (HL) and obesity. METHODS: A population-based case-control study recruited incident cases of lymphoma in England during 1998-2003. Information on height and weight was collected from 216 cases with a histologically confirmed incident diagnosis of HL and their age- and sex-matched controls. RESULTS: Obesity, defined as a body mass index of 30 kg m(-2) or above at 5 years prior to diagnosis, increased the risk of HL more than 2-fold compared to those in the normal range of 18.5-<25 kg m(-2) (odds ratio (OR) = 2.2, 95% confidence interval (CI): 1.1, 4.3). The association was more prominent among men (OR = 2.8, 95% CI: 1.2, 6.5) than women (OR = 1.1, 95% CI: 0.3, 3.8). Elevated risks tended to be among older (aged 36-50 and 51-69) rather than younger persons (aged < or =35 years), and for EBV-ve, rather than EBV+ve, HL. CONCLUSIONS: This study suggests that obesity may increase the risk of HL, particularly among men. Further investigations are needed to confirm these findings.

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Genetic variation in innate immunity may alter host-pathogen defence mechanisms and promote aberrant immune responses and non-Hodgkin lymphoma (NHL). To test this hypothesis, we investigated polymorphisms in innate immune genes in a pooled analysis of two population-based case-control studies of NHL from the San Francisco Bay Area (308 cases, 684 controls) and UK (596 cases, 758 controls). The caspase recruitment domain-containing protein 1007fs homozygote variant was positively associated with NHL risk (odds ratios (OR) = 3.1, 95% confidence intervals (CI) 1.1-8.8), whereas the toll-like receptor 4 1063A>G variant allele was inversely associated with diffuse large cell lymphoma (OR = 0.67, 95% CI 0.45-0.99). These results suggest that variation in innate immune genes may alter NHL susceptibility.

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Genetic instability, including chromosomal imbalance, is important in the pathogenesis of lymphoproliferative disorders such as non-Hodgkin lymphoma (NHL). DNA synthesis and methylation, which are closely linked to folate metabolism and transport, may be affected by polymorphisms in genes involved in these pathways. Folate metabolism polymorphisms have been linked to acute lymphoblastic leukemia and colorectal cancer. To evaluate whether genetic variation in folate metabolism and transport may have a role in determining the risk of developing NHL, we analyzed several polymorphisms using DNA obtained as part of a large U.K. population-based case-control study of lymphoma. Polymorphisms studied include methylenetetrahydrofolate reductase (MTHFR) 677 C >T and 1298 A >C, methionine synthase (MTR) 2756 A>G, serine hydroxymethyltransferase (SHMT1) 1420 C >T, thymidylate synthase (TYMS) 1494del6 and 28-bp repeat, and reduced folate carrier (RFC) 80 G >A. Increased risks for NHL [odds ratio (OR), 1.48; 95% confidence intervals (CI), 1.12-1.97], and marginal zone lymphoma (OR, 3.38; 95% CI, 1.30-8.82) were associated with the TYMS 2R/3R variant. Marginal increased risks were also observed for diffuse large B cell lymphoma with the TYMS homozygous 6 bp deletion (OR, 1.61; 95% CI, 0.99-2.60) and for follicular lymphoma with RFC 80AA (OR, 1.44; 95% CI, 0.94-2.22) and TYMS 28-bp repeat 2R/3R (OR, 1.45; 95% CI, 0.96-2.2). We observed no association between NHL and haplotypes for MTHFR or TYMS. These findings are somewhat inconsistent with those of others, but may reflect differences in circulating folate levels between study populations. Thus, further investigations are warranted in larger series with dietary information to determine the roles that genetics and folic acid status play in the etiology of lymphoma.

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BACKGROUND: Previous epidemiological studies of the relation between alcohol consumption and risk of non-Hodgkin lymphoma (NHL) have been inconsistent, probably because of small sample sizes of individual studies that result from stratification by NHL subtype and type of alcoholic beverage. We aimed to assess the role of alcohol consumption in NHL with sufficient sample size to analyse by both type of alcoholic beverage and disease subtype. METHODS: We obtained original data from nine case-control studies from the USA, UK, Sweden, and Italy in the International Lymphoma Epidemiology Consortium (InterLymph), yielding a pooled study population of 15 175 individuals (6492 cases and 8683 controls). We derived odds ratios (OR) and 95% CI from unconditional logistic regression models, controlling for study centre and other confounding factors. Heterogeneity between studies was assessed by comparison of results from joint fixed-effects logistic regression and two-stage random-effects logistic regression, and by calculation of Wald chi(2) statistics. FINDINGS: People who drank alcohol had a lower risk of NHL than did non-drinkers (OR 0.83 [95% CI 0.76-0.89]). Compared with non-drinkers, risk estimates were lower for current drinkers than for former drinkers (0.73 [0.64-0.84] vs 0.95 [0.80-1.14]), but risk did not decrease with increasing alcohol consumption. The protective effect of alcohol did not vary by beverage type, but did change with NHL subtype. The lowest risk estimates were recorded for Burkitt's lymphoma (0.51 [0.33-0.77]). INTERPRETATION: People who drink alcoholic beverages might have a lower risk of NHL than those who do not, and this risk might vary by NHL subtype. Further study designs are needed to determine whether confounding lifestyle factors or immunomodulatory effects of alcohol explain this association.

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BACKGROUND: The International Lymphoma Epidemiology Consortium (InterLymph) provides an opportunity to analyze the relationship between cigarette smoking and non-Hodgkin lymphoma with sufficient statistical power to consider non-Hodgkin lymphoma subtype. The results from previous studies of this relationship have been inconsistent, likely due to the small sample sizes that arose from stratification by disease subtype. To clarify the role of cigarette smoking in the etiology of non-Hodgkin lymphoma, we conducted a pooled analysis of original patient data from nine case-control studies of non-Hodgkin lymphoma conducted in the United States, Europe, and Australia. METHODS: Original data were obtained from each study and uniformly coded. Risk estimates from fixed-effects and two-stage random-effects models were compared to determine the impact of interstudy heterogeneity. Odds ratios (OR) and 95% confidence intervals (95% CI) were derived from unconditional logistic regression models, controlling for study center, age, sex, and race. RESULTS: In our pooled study population of 6,594 cases and 8,892 controls, smoking was associated with slightly increased risk estimates (OR, 1.07; 95% CI, 1.00-1.15). Stratification by non-Hodgkin lymphoma subtype revealed that the most consistent association between cigarette smoking and non-Hodgkin lymphoma was observed among follicular lymphomas (n = 1452). Compared with nonsmokers, current smokers had a higher OR for follicular lymphoma (1.31; 95% CI, 1.12-1.52) than former smokers (1.06; 95% CI, 0.93-1.22). Current heavy smoking (> or = 36 pack-years) was associated with a 45% increased OR for follicular lymphoma (1.45; 95% CI, 1.15-1.82) compared with nonsmokers. CONCLUSIONS: Cigarette smoking may increase the risk of developing follicular lymphoma but does not seem to affect risk of the other non-Hodgkin lymphoma subtypes we examined. Future research is needed to determine the biological mechanism responsible for our subtype-specific results.

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OBJECTIVE: The aim was to test whether non-Hodgkin lymphoma (NHL) is associated with smoking or alcohol. METHODS: A case-control study recruited NHL cases aged 18-64 in parts of England between 1998 and 2001. One control was matched to each case on sex, date of birth and area of residence. Self-reported histories of tobacco and alcohol consumption were collected during face-to-face interviews. RESULTS: Among 700 cases and 915 controls, no association of smoking with the risk of NHL was observed [odds ratio (OR) = 1.04, 95% confidence interval (CI): 0.85-1.28]. Risks were not raised with age started smoking, number of years smoked, and number of years stopped smoking. Compared with persons who drank alcohol once or twice a week, neither abstainers (OR = 1.03, 95% CI: 0.64-1.67), nor consumers of alcohol one to five times a year (OR = 1.35, 95% CI: 0.95-1.93), one to two times a month (OR = 1.20, 95% CI: 0.87-1.65), three to four times a week (OR = 0.82, 95% CI: 0.62-1.10), or most days (OR = 0.94, 95% CI: 0.70-1.25) increased their risk of developing NHL. Average daily volume or high occasional alcohol consumption were not associated with NHL. CONCLUSIONS: NHL was not associated with smoking or alcohol, but collaborative studies could further investigate the risks of rarer WHO subtypes following these exposures.

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Acute myeloid leukaemia (AML) cases with different chromosomal abnormalities may reflect different aetiologies. Benzene exposure, from a number of sources including smoking, is one risk factor for AML. Individual susceptibility to benzene may depend on differences in expression of metabolizing enzymes. We tested the hypothesis that smoking as well as genetic polymorphisms in the microsomal epoxide hydrolase gene (HYL1), an enzyme involved in benzene metabolism, could be risk factors for AML with defined chromosomal abnormalities. Twenty-six AML cases with -7/del(7q) and 24 cases with t(8;21), as well as 43 cases with normal karyotype and 155 age-, sex- and residence-matched controls, were drawn from a large case-control study on adult acute leukaemia. Current smoking was significantly associated with the cytogenetic abnormalities t(8;21) or -7/del(7q) (OR = 4.9; 95%CI = 2.1-11.5) but not with a normal karyotype, relative to individuals who were not current smokers. A putative high activity HYL1 phenotype [exon 3, residue 113 (Tyr/Tyr) and exon 4, residue 139 (His/Arg or Arg/Arg)] was associated with a significantly increased AML risk in men with -7/del(7q) or t(8;21) (OR = 4.4; 95%CI 1.1-17.0) but not with a normal karyotype. This suggests that AML cases with defined chromosomal abnormalities could be related to specific carcinogen exposures and, furthermore, suggests that smoking and genetic polymorphisms in HYL1 could be risk factors for AML with -7/del(7q) or t(8;21).

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