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Conjectured associations between dietary acrylamide intake and cancer have been evaluated in more than 15 epidemiologic studies examining almost every major cancer site. We have critically reviewed the epidemiologic studies of estimated dietary acrylamide exposure and cancer. As substantially greater acrylamide exposure occurs through tobacco smoke than dietary exposure, we present the results separately for never smokers or adjusted statistically for smoking status, where possible. After an extensive examination of the published literature, we found no consistent or credible evidence that dietary acrylamide increases the risk of any type of cancer in humans, either overall or among nonsmokers. In particular, the collective evidence suggests that a high level of dietary acrylamide intake is not a risk factor for breast, endometrial, or ovarian cancers, which have generated particular interest because of a conjectured hormonal mechanism of acrylamide. Moreover, the absence of a positive association between smoking and ovarian and endometrial cancers suggests that any association of these cancers with the much lower, more sporadic dietary acrylamide intake is unlikely. In conclusion, epidemiologic studies of dietary acrylamide intake have failed to demonstrate an increased risk of cancer. In fact, the sporadically and slightly increased and decreased risk ratios reported in more than two dozen papers examined in this review strongly suggest the pattern one would expect to find for a true null association over the course of a series of trials. Therefore, continued epidemiologic investigation of acrylamide and cancer risk appears to be a misguided research priority.

To compare temporal trends in the incidence and mortality of renal cell cancer among blacks and whites for clues to etiologic differences. We examined trends in age-adjusted and age-specific Surveillance Epidemiology and End Results incidence and US mortality rates for renal cancer for 1973 through 2007, as well as nephrectomy rates from surgery codes for kidney cancer for 2000 through 2007. For nearly four decades, incidence rates for renal cell cancer have been rising more rapidly among blacks than whites, leading to a shift in excess from among whites to among blacks, almost entirely accounted for by an excess of localized disease. The incidence patterns are puzzling, as localized renal cell cancer is primarily detected incidentally by imaging, to which blacks have historically had less access. In contrast to the incidence patterns, there has been an unexpected convergence of renal cancer mortality rates, which have been virtually identical among blacks and whites since the early 1990 s. Nephrectomy rates, regardless of stage, were lower among blacks than among whites, despite almost identical cause-specific survival rates in both races. The identical mortality patterns, combined with higher and more rapidly increasing incidence and lower rates of nephrectomies among blacks, suggest that renal cell cancer may tend to be a less aggressive tumor in blacks. This hypothesis is supported by the favorable stage distribution among blacks and their higher survival for distant and unstaged cancer. Further research into the enigmatic descriptive epidemiology and the biology and natural history of renal cell cancer may shed light on the etiology of this malignancy and its more frequent occurrence among black Americans.

Occupational exposure to vinyl chloride (VC) is causally related to liver angiosarcoma, whereas there is inconsistent epidemiologic evidence for other neoplasms. Two pooled analyses of worker cohorts from 56 plants in North America and Europe provide the most comprehensive and updated data on cancer risk among workers exposed to VC. These included over 22,000 workers, with a total of 640,000 person-years of observation, followed-up for up to 50 years. Overall, a total of 1,778 cancer deaths were observed versus 1,829.46 expected, corresponding to a standardized mortality ratio (SMR) of 0.97 (95% confidence interval (CI)=0.93-1.02). Excluding 71 confirmed angiosarcomas, there were 60 deaths from liver cancers versus 44.35 expected (SMR=1.35, 95% CI=1.03-1.74). Lung and laryngeal cancer mortality were significantly lower than expected (SMR=0.88 and 0.59, respectively). The SMRs for soft tissue sarcoma, brain, lymphoid and haematopoietic system cancers were not materially different from unity. Thus, the aggregate data from over 20,000 VC workers in North America and Europe exclude any excess mortality from lung, laryngeal, soft tissue sarcoma, brain, lymphoid and haematopoietic neoplasms. There appears to be a slight excess of liver cancer other than angiosarcoma, which is difficult to interpret and is likely due to residual misclassification of angiosarcomas.

The objective of this study is to determine correlates of prolactin and growth hormone levels among pregnant women in the USA and China. We studied 304 pregnant Caucasian and 335 pregnant Chinese women. Levels of prolactin and growth hormone were measured at weeks 16 and 27 of gestation, and correlated with maternal, gestational and perinatal characteristics. Both growth hormone and, to a lesser extent, prolactin were inversely associated with pregnancy weight and body mass index, history of a previous live birth and newborn size, whereas educated women had higher levels of both hormones. Growth hormone levels were lower in women who gained more weight, smoked and had nausea and vomiting during pregnancy, whereas prolactin increased with longer total gestation. We found robust associations between maternal and newborn characteristics on the one hand and prolactin and growth hormone during pregnancy on the other.

The objective of this study is to examine perinatal correlates of oestradiol (E2), oestriol (E3), progesterone and sex hormone-binding globulin (SHBG) among pregnant women in the USA and China. Three hundred and four Caucasian women in Boston and 335 Chinese women in Shanghai were studied. Levels of E2, E3, progesterone and SHBG were measured in maternal blood at weeks 16 and 27 of gestation, and correlated with maternal, gestational and perinatal characteristics. Height, weight and body mass index (BMI) before pregnancy is inversely associated with E2 and SHBG, whereas E3 is inversely associated with height and progesterone is inversely associated with weight and BMI. A previous live birth is associated with lower E2 and SHBG in the index pregnancy. Total gestation duration is inversely associated with E2, E3 and progesterone, whereas weight gain during pregnancy is inversely associated with progesterone and SHBG. In the US, pregnancies with female fetuses are characterized by significantly reduced progesterone. Pregnancy hormones are associated with several maternal, gestational and neonatal characteristics.

The relation of Wolfe's parenchymal patterns and radiographically-assessed breast size with breast cancer risk was evaluated in a population-based nested case-control study in Uppsala, Sweden. All women who attended a mammographic screening programme in Uppsala county starting in 1988 have been followed for the occurrence of breast cancer through 1993. The analysis was based on 295 cases and 589 age-matched controls, whose mammograms were blindly evaluated for parenchymal pattern and breast size. Women with P2 or DY pattern had a significantly elevated risk of breast cancer compared with women with N1 or P1 (OR = 2.09; 95% CI = 1.52-2.86). There was an inverse association of breast size with breast cancer risk, which disappeared after adjusting for parenchymal pattern, because breasts of smaller size tended to have high-risk parenchymal patterns. It is concluded that in Swedish women, and perhaps in Caucasian women in general, small breast size is associated with increasing breast risk through its association with high-risk parenchymal pattern. This is in contrast to the fact that Asian women, who in general have breasts of smaller size, have low prevalence of high-risk parenchymal pattern as well as low rates of breast cancer.