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PubMed2000

Maternal height, pregnancy weight gain, and birthweight.

The Institute of Medicine recommends that short women gain less weight during pregnancy than taller women in order to reduce the risk of high birthweight, which can lead to feto-pelvic disproportion. This recommendation, however, is based on clinical judgment rather than on epidemiologic evidence, as few studies have examined the relationships between maternal height, pregnancy weight gain, and infant birthweight. Our objective was to determine whether maternal height is an independent risk factor for infant birthweight and to assess whether maternal height modifies the effect of pregnancy weight gain on infant birthweight. We examined the relationship between maternal height and infant birthweight in a multi-ethnic cohort of 8,870 women with uncomplicated pregnancies who delivered singleton infants at the University of California, San Francisco, 1980-1990. Using multiple linear regression, we modeled the contribution of height and weight gain to birthweight in four different ethnic groups. Increasing maternal height was significantly and positively associated with infant birthweight in White, Black, and Asian women, but not Hispanic women. The relationship between pregnancy weight gain and infant birthweight was not modified by maternal height. Am. J. Hum. Biol. 12:682-687, 2000. Copyright 2000 Wiley-Liss, Inc.

Journal Article↗
PubMed2001

Immunotoxicological investigations on rats treated subacutely with dimethoate, As3+ and Hg2+ in combination.

Effects of combined exposure with dimethoate (DM), HgCl2 (Hg), and NaAsO2 (As) were investigated following a 28 - day oral exposure in male Wistar rats. In preliminary experiments, the LOEL (Lowest Observed Effect Level) and NOEL (Non Observed Effect Level) doses of the substances were determined using the same experimental system [determination of body weight gain, organ weights of brain, thymus, heart, lung, kidneys, adrenals, spleen, testicles, popliteal lymph node, white blood cell (WBC) and red blood cell (RBC) count, haematocrit (Ht), mean cell volume (MCV) of RBCs, cell content of the femoral bone marrow, IgM-plaque forming cell (PFC) content of the spleen, delayed type hypersensitivity (DTH) reaction] and animal strain. In the combination studies, LOEL dose of DM (28.2 mg/kg) was combined with NOEL doses of the heavy metals ( HgCl2 = 0.40 mg/kg, NaAsO2 = 3.33 mg/kg), and vice versa (DM = 7.04 mg/kg, HgCl2 = 3.20 mg/kg, NaAsO2 = 13.3 mg/kg). In the DM-Hg combinations, significant alterations were found versus the corresponding high- dose internal control in the body weight gain, relative liver and kidney weights, and in the PFC response. When DM was combined with As, interactions were indicated by changes of relative liver weight, MCV value, and the PFC content of the spleen. These results support the theory that the interactions between pesticides and heavy metals may modify the toxic effects of the single substances, and may also change the functional detection limits of the exposure. The changes in the functional detection limits, if they occur, can lead to false-positive and false-negative results in human epidemiological studies.

Animals↗
PubMed2006

Parasitic infections and allergy--a review.

Parasitic infections have been one of the major health problems in Thailand for decades. However the prevalence of parasitic infections has decreased considerably in recent years due to an increase in personal hygiene and public sanitation. In contrast, allergic diseases, their morbidity, and mortality appear to be on the rise. An immunological explanation and epidemiologic relationship between parasitic infections and allergies has been espoused since the late 1980s. The hygiene hypothesis has been the internationally recognized theory to explain the findings. IgE blocking hypothesis and the modified Th2 responses have also been purposed to describe the effect of preventing allergic diseases by parasitic infections and by IgG4 inducing tolerance, respectively. Several lines of evidence have suggested an inverse association between parasitic infections and the presence of allergic symptoms. Moreover, data have demonstrated interleukin-10 presenting the suppressive effect of parasitic infection to allergic responses. Nevertheless, a causal relationship between parasitic infections and allergies remains to be proven. Future prospective and intervention studies are required to determine the role of parasitic infection with allergic responses to host exposures.

Animals↗
PubMed1994

Antioxidant vitamins in the diet: relationships with other personal characteristics in Finland.

STUDY OBJECTIVE: The study aimed to reveal associations between dietary antioxidant vitamins and other personal characteristics. DESIGN: Population based, cross sectional survey. SETTING: Twenty seven rural, industrial, and semiurban communities in six different regions of Finland. PARTICIPANTS: Subjects included 5304 men and 4750 women aged 15 years or older, who were interviewed about their dietary habits at the baseline study of the Finnish Mobile Clinic Health Examination Survey, 1967-72. MAIN RESULTS: Intakes of carotenoids and vitamins A, E, and C were estimated from dietary history interviews covering the subjects' food consumption in the preceding year. In older age groups intakes of all the vitamins studied were low. Occupation had a profound effect on dietary antioxidant vitamins: intakes were highest in white collar workers and lowest in farmers; those classified as service workers, industrial workers, or housewives came in between. Current smoking was inversely associated with dietary carotenoids and vitamin C, especially in men. The vitamin intakes of ex-smokers were equal to or even slightly higher than those of never smokers. Married men had higher intakes of carotenoids and vitamin C than men living alone. Body mass index was not an important determinant of the intake of antioxidant vitamins. CONCLUSIONS: The associations of dietary antioxidant vitamins with sociodemographic characteristics and smoking were strong enough to exert a confounding or modifying effect in studies on diet and diseases.

Adolescent↗
PubMed2002

[Epidemiological data and radiation risk estimates].

The results of several major epidemiology studies on populations with particular exposure to ionizing radiation should become available during the first years of the 21(st) century. These studies are expected to provide answers to a number of questions concerning public health and radiation protection. Most of the populations concerned were accidentally exposed to radiation in ex-USSR or elsewhere or in a nuclear industrial context. The results will complete and test information on risk coming from studies among survivors of the Hiroshima and Nagasaki atomic bombs, particularly studies on the effects of low dose exposure and prolonged low-dose exposure, of different types of radiation, and environmental and host-related factors which could modify the risk of radiation-induced effects. These studies are thus important to assess the currently accepted scientific evidence on radiation protection for workers and the general population. In addition, supplementary information on radiation protection could be provided by formal comparisons and analyses combining data from populations with different types of exposure. Finally, in order to provide pertinent information for public health and radiation protection, future epidemiology studies should be targeted and designed to answer specific questions, concerning, for example, the risk for specific populations (children, patients, people with genetic predisposition). An integrated approach, combining epidemiology and studies on the mechanisms of radiation induction should provide particularly pertinent information.

Adult↗
PubMed2007

Gene-environmental interaction in asthma.

PURPOSE OF REVIEW: Asthma is likely to result from the effects of environmental stimuli in genetically susceptible individuals. This review summarizes recent studies of gene-environmental interaction in the pathogenesis of asthma, focusing on study designs. RECENT FINDINGS: Studies using genetic epidemiology, in-vitro and ex-vivo models and in-vivo model organisms demonstrate that gene-environmental interaction in involved in the development of asthma. Genetic association studies show a reduced risk of asthma and atopy with early life exposure to farming environments and house dust endotoxin, and increased risk with environmental tobacco smoke. These associations are modified by CD14 genotype. In people with a specific genotype, high environmental exposure may have the opposite effect of low exposure, possibly explaining some of the inconsistencies in previous studies. In-vitro and ex-vivo cell culture experiments show gene-environmental interactions with Toll-like receptor agonists, viruses and tobacco smoke. Interactions between innate immunity genes and exposure to endotoxin and air pollution have been observed in in-vivo mouse models. SUMMARY: The expanding evidence for gene-environmental interaction in asthma indicates the importance of measuring environmental factors in genetic studies of asthma. Understanding gene-environmental interaction would facilitate risk prognostication, improve preventive strategies and develop targeted interventions in people with asthma.

Animals↗
PubMed1997

Cohort study of effect of being overweight and change in weight on risk of coronary heart disease in old age.

OBJECTIVE: To evaluate risk of late life coronary heart disease associated with being overweight in late middle or old age and to assess whether weight change modifies this risk. DESIGN: Longitudinal study of subjects in the epidemiological follow up study of the national health and nutrition examination survey I. SETTING: United States. SUBJECTS: 621 men and 960 women free of coronary heart disease in 1982-84 (mean age 77 years). MAIN OUTCOME MEASURE: Incidence of coronary heart disease. RESULTS: Body mass index of 27 or more in late middle age was associated with increased risk of coronary heart disease in late life (relative risk = 1.7 (95% confidence interval 1.3 to 2.1)) while body mass index of 27 or more in old age was not (1.1 (0.8 to 1.5)). This difference in risk was due largely to weight loss between middle and old age. Exclusion of those with weight loss of 10% or more increased risk associated with heavier weight in old age (1.4 (1.0 to 1.9)). Thinner older people who lost weight and heavier people who had gained weight showed increased risk of coronary heart disease compared with thinner people with stable weight. CONCLUSIONS: Heavier weight in late middle age was a risk factor for coronary heart disease in late life. Heavier weight in old age was associated with an increased risk once those with substantial weight loss were excluded. The contribution of weight to risk of coronary heart disease in older people may be underestimated if weight history is neglected.

Adult↗
PubMed2001

Some considerations concerning multimedia-multipollutant risk assessment methodology: use of epidemiologic data for non-cancer risk assessment in Russia.

The highly industrialized small town of Verkhnyaya Pyshma (in the Urals region of Russia) was chosen as the site of a multimedia-multipollutant risk assessment using the U.S. Environmental Protection Agency methodology. The assessment was based on routine environmental pollution monitoring data for ambient air, soils, drinking water, and food, and the international environmental epidemiology literature. Using an a priori set of the preliminary health-based criteria, we selected nine pollutants for risk assessment: total suspended particles (TSP), sulfur dioxide, nitrogen dioxide, benzo(a)pyrene (BaP), ammonia arsenic, copper, cadmium, and lead. We used dose-response functions derived from epidemiologic studies to assess individual and population risks for TSP, SO2, NO2, As, Cd, and Pb. We assessed both cancer (for BaP, As, and Cd) and non-cancer (for all the chosen pollutants but BaP) responses, but in this paper we discuss only the assessments of noncarcinogenic risks due to TSP, SO2, NO2, Pb, and Cd as examples of how the quantitative estimates of health effects can be produced by using a risk function approach. We also schematically present a modified conceptual model of multimedia-multipollutant risk assessment taking into account the experience gained with this study.

Adolescent↗
PubMed2001

A rotavirus vaccine for prevention of severe diarrhoea of infants and young children: development, utilization and withdrawal.

The importance of rotaviruses (RVs) as the single most important cause of severe diarrhoea of infants and young children is well recognized. At NIH, we developed a quadrivalent (tetravalent [TV]) vaccine to protect against the four epidemiologically important RV serotypes. It is comprised of live attenuated rhesus RV (RRV), a VP7 serotype G3 strain (the 'Jennerian' approach), and three reassortant RVs, each containing 10 RRV genes and one human RV gene that codes for the major outer protein, VP7, that determines serotype G1, G2 or G4 specificity (the 'modified Jennerian' approach). The vaccine was safe and effective against severe diarrhoea in a major prelicensure collaborative effort of phase III trials. In February 1998 and again in June 1998, the Advisory Committee on Immunization Practices (ACIP) recommended routine immunization with three oral doses at 2, 4 and 6 months of age. The tetravalent vaccine (RotaShield) was licensed in the USA by the FDA in August 1998. In July 1999, after about 1.5 million doses had been given, the CDC recommended suspending administration of the vaccine because post-licensure surveillance of adverse events had suggested an association with intussusception. After further investigation by CDC, in October 1999, the ACIP withdrew its recommendation concluding that '...intussusception occurs with significantly increased frequency in the first 1-2 weeks after vaccination with RRV-TV, particularly following the first dose'. The implications of these developments from a practical, epidemiological, analytical and ethical perspective are discussed.

Child↗
PubMed2006

PROVE-IT proves that lower is better: a contrary view.

Epidemiological studies have demonstrated that low density lipoprotein (LDL) cholesterol and C-reactive protein (CRP) are both independent risk factors for future cardiovascular events. Statin therapy, initially developed to modify blood lipid concentrations, has also been shown to have potentially important pleiotropic effects, including a reduction in CRP concentrations. Recent clinical trials have demonstrated conflicting results regarding the benefits associated with intensively lowering LDL cholesterol. An analysis of these results suggests that the different effects of specific statins on CRP concentrations may be an important determinant of the observed overall benefit associated with therapy. These studies together prove that while lowering LDL is beneficial, lowering LDL and CRP is better.

Atherosclerosis↗
PubMed1999

Evolution of infant nutrition.

Homo sapiens has developed during the course of over two million years. The social and physical conditions of life, the availability of milk and infant foods as well as the presence of diseases have all undergone radical transformations from the Stone Age, at first without and then with fire, to the hunter-gatherer, farmer-herder, agricultural and, now, developed societies. These changes in the human environment may have induced modifications in the length of pregnancy, the development of the neonate at birth, the duration of lactation, the composition of breast milk and use of weaning foods and milk substitutes. Darwinian selection for the nutrient, anti-infective and other components of breast milk may have been determined by the effects of nutrition, through genetic variations in milk composition, on the survival of infants and perhaps also on fecundity and disease resistance in later adult life. Today Darwinian selection may no longer be effective in maintaining or modifying human mammary function, because modern hygienic environments, together with the availability of nutritionally adequate breast-milk substitutes, permit infant survival even under conditions of total lactational failure. National and international promulgations strictly control the composition of infant formulas offered as breast-milk substitutes or as weaning foods. These recommendations are modified as beliefs suggest, and research indicates, the effects of nutrients and other factors on the health and well-being of the child. Preliminary observations on child health have often proved valuable in furthering research. Unquestioning acceptance of apparently desirable, but untested, epidemiological associations have led to unexpected but dangerous iatrogenic problems. Recommendations for change cannot safely be made without proper comparisons with present products and procedures under practical conditions. Such tests are time consuming and require protocols of appropriate statistical design and power while still meeting the required sociological and ethical constraints, but are essential to identify possible harmful effects of any proposed change. It is suggested that no novel ingredients should be added, or major changes permitted in any component, until appropriate trials have established the value and safety of the proposed modifications. Breast-feeding is vital to maximize infant survival in developing countries. There are major difficulties in assessing any differences in morbidity and mortality of breast-fed v. artificially reared infants in the developed world. Carefully controlled studies with comparisons of health and well-being, not only in infancy but throughout life, are desirable if the effects of infant nutrition on adult well-being, suggested by epidemiological studies, are to be validated and ultimately applied. There are considerable variations in the composition of breast milk. This variance suggests that it may ultimately be possible to design formulas better able to meet the needs of individual infants than the milk available from the mother's breast.

Adult↗
PubMed2001

Oxidants in cigarette smoke extract modify low-density lipoprotein in the plasma and facilitate atherogenesis in the aorta of Watanabe heritable hyperlipidemic rabbits.

Epidemiological studies have shown that cigarette smoking is a major cause of atherosclerosis. Oxidants as well as nicotine in cigarette smoke have been implicated in atherogenesis. To clarify the mechanism involved, we examined the chronic effects of nicotine and nicotine-free cigarette smoke extracts (CSE) on oxidative modification of low-density lipoprotein (LDL) in the plasma of Watanabe heritable hyperlipidemic rabbits and atherogenesis in the aorta. CSE was prepared by bubbling the gas phase of smoke (1 ml/three cigarettes) into phosphate buffer saline, and 3 ml of this CSE was injected daily into the ear vein of the rabbit for five months. The rabbits treated with CSE showed an increase in lipid peroxide levels, estimated as thiobarbituric acid reactive substances (TBARS), with a corresponding decrease in vitamin E levels in the plasma. They also showed enhanced oxidative modification of LDL, assessed by anion-exchange HPLC, incorporation into macrophages and measurement of TBARS. These events could be efficiently prevented by administering vitamin E (150 mg/kg/day, p.o.). Nicotine alone (0.5 mg/kg/day, s.c.) led to a temporary increase in the plasma triglyceride level. At the end of the experiment, CSE but not nicotine had caused progression of atherosclerotic lesions together with accumulation of cholesteryl ester in the thoracic aorta, while vitamin E had significantly prevented such atheromatous formation. These results indicate that oxidants in CSE can promote the development of atherosclerosis through oxidative modification of plasma LDL, particularly in hypercholesterolemia, and offer evidence for increased vitamin E utilization in smokers.

Animals↗
PubMed1980

Parity and breast cancer: evidence of a dual effect.

Epidemiological studies have shown that early first pregnancy reduces the risk of developing breast cancer, which indicates that initiation of the disease occurs at an early age. Thus the subclinical lesion of breast cancer might already be present in the breast before childbearing begins and the growth of any such focus might be modified by the endocrine changes of pregnancy. To test this hypothesis the relation between parity and age at presentation was studied in 341 unselected patients with breast cancer presenting to a single clinic. The mean age at presentation was 5.2 years lower in parous than nulliparous women (p < 0.001) and fell with increasing parity. It is concluded that reproductive history influences not only the risk of breast cancer but also the latent interval of a proportion of breast carcinomas.

Adolescent↗
PubMed1996

Carcinogen-DNA and protein adducts: biomarkers for cohort selection and modifiable endpoints in chemoprevention trials.

Chemical-specific markers have been developed for a number of environmental carcinogens for use as molecular dosimeters of individual exposure. In addition to contributing substantially to the specificity and sensitivity of epidemiological studies aimed at determining the role of environmental agents in the etiology of human cancers, some of these biomarkers may prove to be useful endpoints for assessing the efficacy of preventive interventions including exposure avoidance or remediation and chemoprevention. Biomarkers of the biologically effective dose may be particularly useful in this context in that they provide a mechanistic linkage between exposure and disease outcome. The biologically effective dose reflects the amount of toxicant that has interacted with its critical molecular target and can be measured through a variety of analytical techniques as either carcinogen-DNA or -protein adducts. Approaches for the development and validation of aflatoxin adduct biomarkers are presented as a paradigm for the application of carcinogen-specific markers for cohort selection and as modifiable endpoints for assessing efficacy in chemoprevention trials.

Aflatoxin B1↗
PubMed2025

Causal relationships between modifiable risk factors and heart failure: A comprehensive Mendelian randomization study.

Heart failure threatens human health across the globe. Comprehensively identifying its risk factors has public health importance. This work utilized the Mendelian randomization (MR) method to evaluate the effects of over 200 modifiable factors on heart failure. The data from genome-wide association studies (GWAS) was used, with the sample size ranging from 711 to 1232,091. Two distinct GWAS datasets for heart failure were employed for results validation. The inverse variance weighted (IVW) method was used and other supplementary models were employed for comparison. Sensitivity analysis was conducted to verify the results. After integrating the MR estimates derived from heart failure GWAS datasets from integrative epidemiology unit (IEU) and Finngen, we found that body measurement indices like body mass index, whole body fat mass, trunk fat mass, basal metabolic rate, body fat percentage, waist circumference, and waist-hip ratio, were associated with a higher risk of heart failure. Similarly, smoking behavior, sedentary behavior, overall health rating, and type 2 diabetes were determined to increase the risk of heart failure. In contrast, college or university degree showed a protective effect on heart failure. Among these significant findings, body mass index, whole body fat mass, trunk fat mass, basal metabolic rate, body fat percentage, overall health rating, smoking initiation, waist circumference, lifetime smoking index, college or university degree, sedentary behavior, waist-hip ratio, and type 2 diabetes were replicated validated. This MR work figured out that obesity, socioeconomic factors, lifestyle factors, and metabolic features showed broad relations with heart failure. The findings would provide evidence for future policy development for the management of heart failure.

Humans↗
PubMed2004

The effect of particulate matter on resistance and conductance vessels in the rat.

Epidemiological and clinical studies suggest that air pollution, in particular ambient particulate matter (PM), increases mortality in patients with cardiovascular disease (CVD). Several in vivo studies have shown an increase of blood pressure by PM, but so far the mechanism or responsible particle-component has not been elucidated. We exposed small mesenteric rat artery (SMRA) and rat aorta to ambient particles (EHC-93) to test the ability of ambient particles to modify the vascular tone of different vessel types. PM suspensions (10-100 microg/ml) and filtrates containing only the water-soluble components failed to modify the resting tension of either the aorta or SMRA. However, PM did elicit a dose-dependent vasorelaxation in phenylephrine precontracted SMRA and aorta. The effect of the PM suspensions was higher than that of PM filtrate (without particles). The relaxation was already visible at 10 microg/ml, and the difference with filtrate became significant at 100 microg/ml for aorta (maximal relaxation E(max) = 18% vs. 12% PM filtrate) and as low as 30 microg/ml for SMRA (E(max) = 13% vs. 5% PM filtrate). Although the effect of PM was biggest in aorta, the concentration to cause half of the maximal effect (EC(50)) of suspension and filtrate was the same in both capacity (aorta) and resistance vessels (SMRA). The main difference seen between SMRA and aorta was that PM did not modify the phenylephrine-induced dose-response vasoconstriction in SMRA, while it did do so in the aorta. In conclusion, the in vitro exposure of precontracted blood vessels to ambient PM results in an acute vasorelaxation, which is in contrast to the observation that PM can cause increased blood pressure. Dose calculations show that the elevation of blood pressure observed in vivo is not likely due to direct effects of particles or constituents. We therefore suggest that the in vivo effect of PM on vasoconstriction acts through other pathways, such as the central nervous system.

Adrenergic alpha-Agonists↗
PubMed1997

Exercise and its role in the prevention and rehabilitation of cardiovascular disease.

The purpose of this article is to review the beneficial effects of regular exercise in the primary and secondary prevention of coronary artery disease (CAD). Epidemiologic studies indicate that a physically inactive life-style is associated with twice the risk of developing CAD. The magnitude of risk is similar to that of other modifiable risk factors. Meta-analysis of studies of cardiac rehabilitation after myocardial infarction demonstrate that cardiac rehabilitation participants lower their risk of death by 20% to 25% compared to controls. Exercise training results in several beneficial physiological changes including an increase in exercise endurance, higher resting and exercise stroke volumes, lower resting and submaximal exercise heart rates, and increased capillary density and oxidative enzyme capacity in skeletal muscle. In patients with established CAD, exercise training improves symptoms of angina and congestive heart failure and attenuates the severity of exercise-induced ischemia. Regular exercise can favorably modify other risk factors, but the benefits are modest. Reductions in systolic and diastolic blood pressure readings average 6 to 9 mm Hg; decreases in total and low-density lipoprotein (LDL) cholesterol approximate 5 to 10 mg/dL; and increases in high-density lipoprotein (HDL) cholesterol approximate 2 mg/dL. Exercise training as a sole intervention does not appear to enhance smoking cessation. Regular exercise does improve psychosocial well-being. Most studies of physical activity have enrolled predominantly middle-aged men; however, available evidence suggests similar cardiovascular benefits for women, the elderly, and children and youth. Physical activity levels decrease substantially during the school-age-adolescent transition in both males and females. More than half of the adult population is sedentary or inactive. Collectively, accumulated data suggest the need for both individualized/high-risk and population-based approaches to increasing physical activity across the life span.

Adult↗
PubMed2005

Phospholipid mediators in the vessel wall: involvement in atherosclerosis.

PURPOSE OF REVIEW: This review provides a brief update on the involvement of major phospholipid mediators, with the emphasis on platelet-activating factor and its analogues generated upon the oxidation of lipoproteins in vascular pathology, including atherogenesis. RECENT FINDINGS: Phospholipid mediators are produced during inflammation by various enzymes, mostly from pre-existing membrane phospholipids, and trigger cellular signaling via G-coupled receptors. A short description of lysophosphatidic acid, lysophosphocholine and sphingosine-1 phosphate receptors and their actions is given, but attention is focused mainly on platelet-activating factor and its analogues. The majority of these mediators participate in leukocyte adhesiveness to the endothelium, leukocyte transmigration into the vessel wall and the subsequent formation of various chemokines leading to foam cell formation and smooth muscle cell proliferation and dedifferentiation. Platelet-activating factor and platelet-activating factor-like phospholipids are degraded in plasma by the lipoprotein-bound enzyme of myeloid origin, PAF-acetylhydrolase, also known as LDL-PLA2. Although the overexpression of PAF-acetylhydrolase shows marked anti-atherogenic properties in animal models, epidemiological data in the Caucasian population have demonstrated that its level might be a risk factor for cardiovascular disease. Recent genetic studies have shown, however, that the A379V polymorphism of this gene, responsible for slightly higher enzymatic activity, exerts a protective effect, probably by modifying the enzyme function towards a less atherogenic form. SUMMARY: Phospholipid-borne mediators are certainly key players in inflammation and thus in atherosclerosis. The generation of such biologically active molecules is possibly dependent on nutritional habits and the availability of antioxidants, including enzymes protective against oxidative damage, including PAF-acetylhydrolase.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗