BackgroundPrevious studies of DDT and breast cancer assessed exposure later in life when the breast may not have been vulnerable, after most DDT had been eliminated, and after DDT had been banned.ObjectivesWe investigated whether DDT exposure in young women during the period of peak DDT use predicts breast cancer.MethodsWe conducted a prospective, nested case–control study with a median time to diagnosis of 17 years using blood samples obtained from young women during 1959–1967. Subjects were members of the Child Health and Development Studies, Oakland, California, who provided blood samples 1–3 days after giving birth (mean age, 26 years). Cases (n = 129) developed breast cancer before the age of 50 years. Controls (n = 129) were matched to cases on birth year. Serum was assayed for p,p′-DDT, the active ingredient of DDT; o,p′-DDT, a low concentration contaminant; and p,p′-DDE, the most abundant p,p′-DDT metabolite.ResultsHigh levels of serum p,p′-DDT predicted a statistically significant 5-fold increased risk of breast cancer among women who were born after 1931. These women were under 14 years of age in 1945, when DDT came into widespread use, and mostly under 20 years as DDT use peaked. Women who were not exposed to p,p′-DDT before 14 years of age showed no association between p,p′-DDT and breast cancer (p = 0.02 for difference by age).ConclusionsExposure to p,p′-DDT early in life may increase breast cancer risk. Many U.S. women heavily exposed to DDT in childhood have not yet reached 50 years of age. The public health significance of DDT exposure in early life may be large.

We report severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccine effectiveness against infection (VE-I) and death (VE-D) by vaccine type in 780,225 veterans in the Veterans Health Administration, covering 2.7% of the US population. From February to October 2021, VE-I declined for all vaccine types, and the decline was greatest for the Janssen vaccine, resulting in a VE-I of 13.1%. Although breakthrough infection increased risk of death, vaccination remained protective against death in persons who became infected during the Delta variant surge. From July to October 2021, VE-D for age <65 years was 73.0% for Janssen, 81.5% for Moderna, and 84.3% for Pfizer-BioNTech; VE-D for age ≥65 years was 52.2% for Janssen, 75.5% for Moderna, and 70.1% for Pfizer-BioNTech. Findings support continued efforts to increase vaccination, booster campaigns, and multiple additional layers of protection against infection.

ObjectivesDichlorodiphenyltrichloroethane (DDT) was used worldwide until the 1970s, when concerns about its toxic effects, its environmental persistence, and its concentration in the food supply led to use restrictions and prohibitions. In 2001, more than 100 countries signed the Stockholm Convention on Persistent Organic Pollutants (POPs), committing to eliminate the use of 12 POPs of greatest concern. However, DDT use was allowed for disease vector control. In 2006, the World Health Organization and the U.S. Agency for International Development endorsed indoor DDT spraying to control malaria. To better inform current policy, we reviewed epidemiologic studies published from 2003 to 2008 that investigated the human health consequences of DDT and/or DDE (dichlorodiphenyldichloroethylene) exposure.Data sources and extractionWe conducted a PubMed search in October 2008 and retrieved 494 studies.Data synthesisUse restrictions have been successful in lowering human exposure to DDT, but blood concentrations of DDT and DDE are high in countries where DDT is currently being used or was more recently restricted. The recent literature shows a growing body of evidence that exposure to DDT and its breakdown product DDE may be associated with adverse health outcomes such as breast cancer, diabetes, decreased semen quality, spontaneous abortion, and impaired neurodevelopment in children.ConclusionsAlthough we provide evidence to suggest that DDT and DDE may pose a risk to human health, we also highlight the lack of knowledge about human exposure and health effects in communities where DDT is currently being sprayed for malaria control. We recommend research to address this gap and to develop safe and effective alternatives to DDT.

Abstract-This study prospectively investigates the contribution of pregnancy complications and other reproductive age risk factors on the risk of subsequent cardiovascular disease death. Participants were 14 403 women in the Child Health and Development Studies pregnancy cohort drawn from the Kaiser Permanente Health Plan in California. Only women with nonmissing parity and no previously diagnosed heart conditions were included. A total of 481 had observed preeclampsia, and 266 died from cardiovascular disease. The median age at enrollment was 26 years, and the median follow-up time was 37 years. 3,4 and that PE is one indicator of this health burden. 5 Following from the idea of pregnancy as a stress test, there is continuing debate around whether PE is only an indication of pre-existing risk factors or is itself an independent factor on the causal pathway to CVD. 4 -7 Complicating this debate, PE is a complex syndrome that has yet to be homogeneously diagnosed or defined. 8 Many researchers consider early or severe PE to be a different diagnosis than late PE that occurs near or at delivery and is usually milder. 9 -12 This is borne out by observations that early PE is linked with decreased gestational age and birth weight, as well as intrauterine growth restriction (IUGR) more generally, whereas late PE is characterized by a disproportionate number of high birth weight infants. 13,14 The problem of overlapping risk factors (exemplified by the strong association between PE and IUGR) is ubiquitous in investigations of the association between PE and CVD. Traditional risk factors for CVD, such as increased body mass index and pre-existing hypertension, are also known to be associated with increased risk of PE. Such overlapping risk factors continue to provoke a multitude of questions about independence and confounding.This study investigates the predictors of PE to establish the sequence of maternal markers. Then the separate and combined effects of PE and other CVD risk factors are examined in an attempt to unravel their relationship with the causes of CVD death. This study further investigates the varying effects of PE on CVD death by gestational timing to clarify the spectrum of PE and its impact on subsequent CVD. Methods Study PopulationThe subjects in this study were women enrolled in the original Child Health and Development Studies (CHDS) cohort. 15 They were members of the Kaiser Permanente Health Plan in the East Bay Area

This prospective human study links measured DDT exposure in utero to risk of breast cancer. Experimental studies are essential to confirm results and discover causal mechanisms. Findings support classification of DDT as an endocrine disruptor, a predictor of breast cancer, and a marker of high risk.

A multidisciplinary group of experts gathered in Parma Italy for a workshop hosted by the University of Parma, May 16–18, 2014 to address concerns about the potential relationship between environmental metabolic disrupting chemicals, obesity and related metabolic disorders. The objectives of the workshop were to: 1. Review findings related to the role of environmental chemicals, referred to as “metabolic disruptors”, in obesity and metabolic syndrome with special attention to recent discoveries from animal model and epidemiology studies; 2. Identify conclusions that could be drawn with confidence from existing animal and human data; 3. Develop predictions based on current data; and 4. Identify critical knowledge gaps and areas of uncertainty. The consensus statements are intended to aid in expanding understanding of the role of metabolic disruptors in the obesity and metabolic disease epidemics, to move the field forward by assessing the current state of the science and to identify research needs on the role of environmental chemical exposures in these diseases. We propose broadening the definition of obesogens to that of metabolic disruptors, to encompass chemicals that play a role in altered susceptibility to obesity, diabetes and related metabolic disorders including metabolic syndrome.

The hypothesis that meal frequency is associated with plasma cholesterol was tested in a population-based sample of 2034 white men and women aged 50-89 y. Total, low-density-lipoprotein (LDL) and high-density-lipoprotein (HDL) cholesterol and triglycerides were measured after a 12-h fast in a Lipid Research Clinic laboratory and meal frequency was obtained by questionnaire. The age-adjusted total cholesterol concentrations for men and women reporting greater than or equal to 4 meals/d averaged 0.23 mmol/L lower than for those who reported 1-2 meals/d (P = 0.01). Similarly, LDL concentrations were lower in those reporting higher meal frequency (0.16 mmol/L, P = 0.06). These associations persisted after adjustment for smoking, alcohol, waist-to-hip ratio, systolic blood pressure, body mass index, and dietary nutrients. These results suggest that cholesterol reductions might be achieved by modest increases in meal frequency without an increase in caloric intake.

This paper presents results of a study designed to: 1) test for a sex difference in the relative lengths of the finger bones, including the second-to-fourth digit ratio (2D:4D), using left-hand radiographs taken in young children, 2) test whether sex differences can be explained by sex differences in fetal growth, and 3) test the serial stability of sex differences in relative digit lengths, including 2D:4D. Results are presented from 1,060 subjects of the California Child Health and Development Studies. One serial replication at about 9 years old is available from 271 subjects. Results indicate that relative digit lengths are sex-dimorphic in children (Manning et al. [1998] Hum. Reprod. 13:3000-3004, [2004] Early Hum. Dev. 80:161-168). Sex differences in digit length ratios are more pronounced within sibships, where shared family factors are controlled, and are not strongly associated with gross measures of fetal growth, like birth length or weight. Thus, sex differences in the fetal growth of the body are not implicated in sex differences in digital formulae, leaving open the possibility of more direct hormonal and/or genetic causation. However, 2D:4D declined between ages 6-8 in a longitudinal sample, and was a less consistent sex-dimorphic marker than 3D:4D across ethnic groups, suggesting that 3D:4D may be a better marker of perinatal sex differentiation. Prior conflicting findings about 2D:4D may be partly explained by variations in age and ethnicity of populations studied.