AbstractÐBoth carcinogenic and anticarcinogenic properties have been reported for the synthetic antioxidants butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT). The association between dietary intake of BHA and BHT and stomach cancer risk was investigated in the Netherlands Cohort Study (NLCS) that started in 1986 among 120,852 men and women aged 55 to 69 years. A semi-quantitative food frequency questionnaire was used to assess food consumption. Information on BHA or BHT content of cooking fats, oils, mayonnaise and other creamy salad dressings and dried soups was obtained by chemical analysis, a Dutch database of food additives (ALBA) and the Dutch Compendium of Foods and Diet Products. After 6.3 years of follow-up, complete data on BHA and BHT intake of 192 incident stomach cancer cases and 2035 subcohort members were available for case-cohort analysis. Mean intake of BHA or BHT among subcohort members was 105 and 351 "g/day, respectively. For consumption of mayonnaise and other creamy salad dressings with BHA or BHT no association with stomach cancer risk was observed. A statistically non-signi®cant decrease in stomach cancer risk was observed with increasing BHA and BHT intake [rate ratio (RR) highest/lowest intake of BHA=0.57 (95% con®dence interval (CI): 0.25±1.30] and BHT=0.74 (95% CI: 0.38±1.43). In this study, no signi®cant association with stomach cancer risk was found for usual intake of low levels of BHA and BHT. #

Objectives: Associations between cardiovascular mortality and air pollution and noise together were investigated. Methods: Data from the ongoing Netherlands Cohort Study on Diet and Cancer (120 852 subjects; follow-up 1987-1996 were used. Cox proportional hazard analyses were conducted for the association between cardiovascular mortality and exposure to black smoke, traffic intensity on the nearest road and road traffic noise at the home address. Results: The correlations between traffic noise and background black smoke, and traffic intensity on the nearest road were moderate at 0.24 and 0.30, respectively. Traffic intensity was associated with cardiovascular mortality, with highest relative risk (95% confidence interval) for ischaemic heart disease (IHD) mortality being 1.11 (1.03 to 1.20) (increment 10 000 motor vehicles/24 h). Relative risks for black smoke concentrations were elevated for cerebrovascular (1.39 (0.99 to 1.94)) and heart failure mortality (1.75 (1.00 to 3.05)) (increment 10 mg/m 3 ). These associations were insensitive to adjustment for traffic noise. There was an excess of cardiovascular mortality in the highest noise category (.65 dB(A)), with elevated risks for IHD (1.15 (0.86 to 1.53)) and heart failure mortality (1.99 (1.05 to 3.79)). After adjustment for black smoke and traffic intensity, noise risk reduced to unity for IHD mortality and was slightly reduced for heart failure mortality. Conclusions: Associations between black smoke concentrations and traffic intensity on the nearest road with specific cardiovascular causes of death were not explained by traffic noise in this study.Cohort studies have shown associations between long-term exposure to particulate matter air pollution and cardiovascular mortality. [1][2][3][4] Cohort studies which were mostly conducted in Europe have reported associations between traffic-related air pollution and cardiovascular mortality. [5][6][7] Exposure to traffic-related air pollution has been assessed using dispersion modelling, 7 measured or modelled air pollution data and traffic variables assessed with geographical information systems. Motorised traffic is an important source not only of air pollution but also of noise.10 11 Exposure to traffic noise is associated with ischaemic heart disease (IHD) 10 and is usually modelled using traffic intensity, traffic composition, speed, distance to roads, noise barriers and other factors as input variables.The joint association of long-term exposure to air pollution and noise with cardiovascular mortality has not been described before, although we previously reported an association between trafficrelated air pollution, traffic intensity and mortality in a Dutch cohort. 12 In this paper, we study the joint association of long-term exposure to air pollution, traffic intensity and noise with cardiovascular mortality. Because air pollution and noise may be associated with different cardiovascular endpoints, 7 9-11 13 14 we studied overall cardiovascular mortality as well as subcategories of cardiovascul...

Summary The association between the intake of nitrate or nitrite and gastric cancer risk was investigated in a prospective cohort study started in 1986 in the Netherlands, of 120 852 men and women aged 55-69 years. At baseline, data on dietary intake, smoking habits and other covariates were collected by means of a setf-administered questionnaire. For data anatysis, a case-cohort approach was used, in which the person-years at risk were estimated from a randomly selected subcohort (1688 men and 1812 women). After 6.3 years of follow-up, 282 microscopicalty confirmed incident cases of stomach cancer were detected: 219 men and 63 women. We did not find a higher risk of gastric cancer among people with a higher nitrate intake from food [rate ratio (RR) highest/lowest quintile = 0.80, 95% Cl 0.47-1.37, trend-P = 0.18], a higher nitrate intake from drinking water (RR highestAowest quintile = 0.88, 95% Cl 0.59-1.32, trend-P = 0.39) or a higher intake of nitrite (RR highestAowest quintile = 1.44, 95% Cl 0.95-2.18, trend-P = 0.24). Rate ratios for gastric cancer were also computed for each tertile of nitrate intake from foods within tertiles of vitamin C intake and intake of beta-carotene, but no consistent pattem was found. Therefore, our study does not support a positive association between the intake of nitrate or nitrite and gastric cancer risk. Both ascorbic acid and beta-carotene may act as scavengers for free radicals. thus preventing oxidative damage in gastric mucosa and mutations in DNA (Kyrtopoulos. 1987). Furthermore, the conversion of nitrate to nitrite may be inhibited by storage of foods in the refrigerator or freezer (Boeing. 1991 ). Other factors such as smoking habits, socioeconomic status. family history of stomach cancer and prevalence of stomach disorders may confound the association between nitrate or nitrite intake and gastric cancer risk (Boeing et al. 1991: Palli et al, 1994: Kono and Hirohata. 1996: van Loon et al. 1998. Numerous epidemiological studies which have been undertaken on the association between nitrate intake and gastric cancer risk show a lack of consistency (Jensen. 1982: Clough. 1983: Gilli et al. 1984: Beresford. 1985: Risch et al. 1985: Buiatti et al. 1990: Boein, et al. 1991: Leclerc et al. 1991: Palli et al. 1992: Rademacher et al. 1992: Xu et al. 1992: Gonzalez et al. 1994: Hansson et al. 1994: La Vecchia et al. 1994: Pobel et al. 1995 However. in most of these studies high nitrate consumption via ingested food showed no association with gastric cancer risk or even an inverse association. This finding might result from the fact that vegetables -the main source of nitrate -also contain vitamin C and beta-carotene. which appear to be protective factors for gastric cancer. Therefore, intake of nitrate from foods must be studied separately from intake of nitrate from drinking water. which does not contain protective substances.So far. epidemiological studies on nitrate intake and gastric cancer risk have been ecological or case-control in design. in which problems arise with co...

Objectives: To assess the association of whole-grain and (cereal) fibre intake with body mass index (BMI) and with the risk of being overweight (BMIX25) or obese (BMIX30 kg m À2 ). Subjects: A total of 2078 men and 2159 women, aged 55-69 years, were included in the analysis, after exclusion of subjects with diagnosed cancer or deceased within 1 year after baseline or with missing dietary information. Results: We found an inverse association between whole-grain consumption and BMI and risk of overweight and obesity in men as well as women. The association in men was stronger than in women; the risk of being obese as compared to normal weight was 10% (95% CI: 2-16%) and 4% (95% CI: 1-7%) lower for each additional gram of (dry) grain consumption in men and women, respectively. Fibre and cereal fibre intake were inversely associated with BMI in men only. Associations were similar after exclusion of likely under-and overreporters of energy. A retrospective analysis of baseline fibre intake and weight gain after the age of 20 years also showed a slight inverse association. Conclusions: Whole-grain consumption may protect against becoming overweight or obese; however, the cross-sectional design of the study does not allow conclusions about the causality of the association.

Individuals exposed to the Dutch Famine of 1944-45 during gestation have increased adiposity, which might be due to changes in energy intake, physical activity, or metabolic efficiency. We studied 357 persons born between January 1945 and March 1946 whose mothers experienced famine during or immediately preceding pregnancy, 298 persons born in the same 3 institutions during 1943 or 1947 (time controls), and 311 same-sex sibling controls. We obtained food frequency and physical activity data by questionnaire between 2003 and 2005 (mean age 58 y). We defined gestational exposure as exposure to a ration of <3762 kJ/d (<900 kcal/d) for at least 10 wk. For the whole study population, energy intake was 9225 +/- 2650 kJ/d and physical activity was 7380 +/- 4331 metabolic equivalents (MET).min/wk. Compared with time controls, gestational famine exposure was associated with 113 kJ/d (95% CI, -272, 502) higher energy intake, 0.01 percentage point (95% CI, -0.88, 0.89) higher fat density, 688 MET.min/wk (95% CI, -1398, 23) lower physical activity, and 63 kJ/d (95% CI, -130, 259) higher predicted energy expenditure (pEE). Compared with sibling controls, gestational famine exposure was associated with 4 kJ/d (95% CI, -702, 711) higher energy intake, 2.01 percentage points (95% CI, 0.38, 3.63) higher fat density, 97 MET.min/wk) (95% CI, -1243, 1050) lower physical activity score, and 188 kJ/d (95% CI, -163, 539) higher pEE. Gender-specific associations (P < 0.05 for heterogeneity) emerged for protein density and pEE using time controls and for energy intake using sibling controls. Associations were weak, differed by choice of control, and may reflect sampling variability or methodological differences. Persistent small energy imbalances could explain the increased weight of famine-exposed individuals.