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PubMed2005

Developmental antecedents of cardiovascular disease: a historical perspective.

Knowledge of the fetal antecedents of cardiovascular disease has increased rapidly since the association between low birth weight and the disease was demonstrated 20 yr ago. It now is known that individuals who had low birth weight or who were thin or short at birth are at increased risk for both cardiovascular disease and type 2 diabetes. This has been shown in studies in different countries and cannot be explained by confounding variables. Through clinical and animal studies, the biologic processes that underlie the epidemiologic associations and how their effects are modified by postnatal growth and by living conditions in childhood and adult life are beginning to be understood. One such process is altered renal development, with reduced nephron numbers, which may initiate hypertension.

Adult↗
PubMed2006

Exposures to airborne particulate matter and adverse perinatal outcomes: a biologically plausible mechanistic framework for exploring potential effect modification by nutrition.

OBJECTIVES: The specific objectives are threefold: to describe the biologically plausible mechanistic pathways by which exposure to particulate matter (PM) may lead to the adverse perinatal outcomes of low birth weight (LBW), intrauterine growth retardation (IUGR), and preterm delivery (PTD); review the evidence showing that nutrition affects the biologic pathways; and explain the mechanisms by which nutrition may modify the impact of PM exposure on perinatal outcomes. METHODS: We propose an interdisciplinary conceptual framework that brings together maternal and infant nutrition, air pollution exposure assessment, and cardiopulmonary and perinatal epidemiology. Five possible albeit not exclusive biologic mechanisms have been put forth in the emerging environmental sciences literature and provide corollaries for the proposed framework. CONCLUSIONS: Protecting the environmental health of mothers and infants remains a top global priority. The existing literature indicates that the effects of PM on LBW, PTD, and IUGR may manifest through the cardiovascular mechanisms of oxidative stress, inflammation, coagulation, endothelial function, and hemodynamic responses. PM exposure studies relating mechanistic pathways to perinatal outcomes should consider the likelihood that biologic responses and adverse birth outcomes may be derived from both PM and non-PM sources (e.g., nutrition). In the concluding section, we present strategies for empirically testing the proposed model and developing future research efforts.

Air Pollutants↗
PubMed2000

Relationships of active smoking to asthma and asthma severity in the EGEA study. Epidemiological study on the Genetics and Environment of Asthma.

The role of smoking as potential risk factor, selection factor ("healthy smoker" effect) and modifying factor (severity) of asthma was studied in the Epidemiological study on the Genetics and Environment of Asthma, bronchial hyperresponsiveness and atopy (EGEA). The analysis involved 200 adult asthmatic cases recruited in chest clinics, 265 nonasthmatic controls and 586 relatives of asthmatics (147 with asthma). Asthma in childhood was not associated with a reduced take-up of smoking (odds ratio (OR)=1.06 in males and 0.98 in females), but smoker asthmatic cases quit more often than controls (OR = 2.20 (95% confidence interval (95% CI) 1.11-4.34) in males and 2.76 (1.19-6.42) in females). Adult onset asthma was unrelated to ever smoking (OR 1.07 in males and 1.02 in females). In asthmatic cases, active smoking was associated with asthma severity. Current smokers, compared to never and exsmokers, had more asthma symptoms, more frequent (> or =1 attack x day(-1)) asthma attacks (OR 2.39 (95% CI 1.06-5.36)) and higher asthma severity scores. No clear pattern regarding the relationships of smoking habits with asthma was observed in first degree relatives. It is concluded that active smoking is not a risk factor for asthma in adulthood, but that smoking increases asthma severity.

Adolescent↗
PubMed2001

Gene-environment Interactions and Polymorphism Studies of Cancer Risk in the Hospital-based Epidemiologic Research Program at Aichi Cancer Center II (HERPACC-II).

Genetic polymorphisms may modify the effects of environmental risk factors on cancer occurrence. We have recently launched a comprehensive epidemiologic project, HERPACC II (Hospital-based Epidemiologic Research Program at Aichi Cancer Center II), including both lifestyle and polymorphism data, following HERPACC-I which solely concentrated on lifestyle data. As of April 2001, about 3000 samples of DNA are being stored to conduct case-control studies. Genotyping of 46 polymorphisms has been conducted at the laboratory of the Division of Epidemiology and Prevention. Twelve case-control studies and two papers on a new PCR method, PCR-CTPP (polymerase chain reaction with confronting two-pair primers), have been accepted for publication. Significant findings in Japanese were found for 1) gene-environment interaction for esophageal cancer between heavy drinking and aldehyde dehydrogenase 2 (ALDH2), 2) malignant lymphoma risk with methylenetetrahydrofalate reductase (MTHFR) and methionine synthase (MS), 3) interactions between smoking and two polymorphisms, interleukin 1B (IL-1B) and myeloperoxidase (MPO) for Helicobacter pylori infection, and 4) smoking habits with dopamine receptor D2 (DRD2) and IL-1B. Further studies on interactions with polymorphisms will continue to be conducted for Japanese, using larger sizes of samples.

Journal Article↗
PubMed2002

Isolation of diallyl trisulfide inducible differentially expressed genes in human gastric cancer cells by modified cDNA representational difference analysis.

Extensive epidemiologic studies indicated protective effects of consumption of garlic on reducing human gastric cancer (HGC) incidence. Diallyl trisulfide (DATS), a critical organic allyl sulfur component of garlic, was reported to have chemopreventive effects in inhibiting tumor process. We used DATS to treat HGC cell line BGC823 cells, and showed that DATS induces G1/S arrest and apoptosis in BGC823 cells demonstrated by a flow cytometric analysis. To further isolate DATS inducible differentially expressed genes in BGC823 cells, we combined a highly specific subtractive hybridization of cDNA representational difference analysis (cDNA RDA) with a sensitive bidirectional radioactive detection of mRNA differential display (mRNA DD) to develop a subtractive hybridization differential display (SHDD) method. This modified method adopted a first round of bidirectional subtractive hybridization between two sample cDNAs and a second round of bidirectional subtractive hybridization between the two resultant first-round difference products. Bidirectional subtractive hybridizations magnified the differences between the two sample cDNAs and favored isolating mRNA species with very small expression differences. We employed the SHDD method to detect DATS inducible differentially expressed genes in BGC823 cells. A total of 14 cDNA fragments (11 upregulated and 3 downregulated by DATS treatment) were isolated and confirmed by reverse Northern blot analysis. Our data show that SHDD is a powerful technique for identifying differentially expressed mRNA species between two sample cDNAs and provide useful cellular and molecular information for understanding the effects of garlic against human gastric cancer.

Allyl Compounds↗
PubMed1989

Family-oriented prevention of cardiovascular disease: a social epidemiological approach.

A social epidemiological approach has been used to study social factors associated with chronic disease, as well as to promote community-oriented intervention programs to modify risk for cardiovascular disease. The present review suggests using a social epidemiological approach in a third way; to promote efforts directed toward family-oriented primary prevention of cardiovascular disease. Evidence is presented which shows an association between three family social factors (marital status, family socioeconomic status, family size) and risk for cardiovascular disease. The real determinants of risk, however, may be the underlying health-related behaviors indicated by each of these factors. Evidence is also presented which shows the importance of a fourth family social factor (family age) in promoting effective health education efforts to modify risk. Thus, a social epidemiological approach is more valuable than a single discipline-based approach in identifying, understanding, and modifying family social influences on cardiovascular risk.

Adult↗
PubMed1999

Interactions of infectious symptoms and modifiable risk factors in sudden infant death syndrome. The Nordic Epidemiological SIDS study.

The aim of the study was to investigate the effect of infection on sudden infant death syndrome (SIDS) and to analyse whether modifiable risk factors of SIDS, prone sleeping, covered head and smoking act as effect modifiers. In a consecutive multicentre case-control study of SIDS in Denmark, Norway and Sweden, questionnaires on potential risk factors for SIDS were completed by parents of SIDS victims, and for at least two controls matched for gender, age and place of birth. All SIDS cases were verified by an autopsy. The study comprised 244 SIDS cases and 869 controls, analysed by conditional logistic regression. Significantly more cases than controls presenting symptoms of infectious diseases during the last week and/or last day were treated with antibiotics and had been seen by a physician. The finding is consistent with the hypothesis of an infectious mechanism in SIDS induced by local microorganism growth and toxin or cytokine production, and also adds further support to a possible association between infection and SIDS by loss of protective mechanisms, such as arousal. The risk of SIDS among infants with the combined presence of infectious symptoms and either of the other modifiable risk factors, prone sleeping, head covered or parental smoking, was far greater than the sum of each individual factor. These risk factors thus modify the dangerousness of infection in infancy.

Case-Control Studies↗
PubMed2006

Interpretation of small effect sizes in occupational and environmental neurotoxicology: individual versus population risk.

Some have questioned the importance of the small effect sizes generally reported in epidemiological studies of neurotoxicity. To some extent, this reflects a failure to appreciate the critical distinction between individual and population risk. In the first part of the paper, arguments are marshaled to support the contention that small shifts in the mean value of a health index within a study sample can, under some circumstances, carry substantial implications for the health status of the population from which the study sample was drawn. Under such circumstances, a population-based approach to prevention might be as effective as a patient-based approach. The second part clarifies conditions under which this will be true (e.g., a monotonic relationship between a health index and risk of disease) and conditions under which it might not (e.g., a J-shaped relationship). In the third part, the relative levels of uncertainty in characterizing individual versus population risk are explored. In neurotoxicological studies, uncertainty in characterizing individual risk could be reduced by adjusting, in addition to bone fide confounders, for covariates that are strong predictors of outcome and by more assiduous efforts to characterize major effect modifiers.

Confounding Factors, Epidemiologic↗
PubMed1999

Suicide, religion, and socioeconomic conditions. An ecological study in 26 countries, 1990.

STUDY OBJECTIVE: Relative risks are frequently assumed to be stable across populations but this may not apply in psychiatric epidemiology where sociocultural context may modify them. Such ecological effect modification will give curved associations between aggregated risk factor and outcome. This was examined in connection with the ecological association between suicide rates and an aggregate index of religiosity. DESIGN: Ecological study of associations between suicide rates and an index of religiosity, adjusted for socioeconomic variation. The effect of stratification of the study sample according to levels of religiosity, was examined. SETTING: 26 European and American countries. SUBJECTS: Interview data from 37,688 people aggregated by country. OUTCOME MEASURES: Age and sex specific (1986-1990) suicide rates. MAIN RESULT: Adjusted for socioeconomic variation, negative associations of male suicide rates with religiosity were apparent in the 13 least religious countries only (test for interaction F (1, 25) = 5.6; p = 0.026). Associations between religiosity and female suicide rates did not vary across countries. CONCLUSION: The bent ecological association was apparent only after adjustment for socioeconomic variation suggesting that, rather than confounding, ecological modification of individual level links between religion and male (but not female) suicide risk is the responsible mechanism. This concurs with micro-level findings suggesting that suicide acceptance depends not only on personal but also on contextual levels of religious belief, and that men are more sensitive to this phenomenon than women. In psychiatric epidemiology, relative risks vary with the exposure's prevalence. This has important implications for research and prevention.

Adolescent↗
PubMed1999

Gender differences in the relation between fibrinogen, tissue-type plasminogen activator antigen and markers of insulin resistance: effects of smoking. D.E.S.I.R. Study Group. Data from an Epidemiological Study on Insulin Resistance Syndrome.

A stronger positive association between fibrinogen or tissue-type plasminogen activator antigen (tPA-ag) and fasting insulin is observed in women than in men. We investigated whether this effect could be explained by a difference in smoking habits. The relations between markers for insulin resistance [fasting insulin and insulin resistance as estimated by the homeostasis model assessment (HOMA-IR)] and fibrinogen and tPA-ag were examined cross-sectionally in 4976 (582 for tPA-ag) subjects from the D.E.S.I.R. (Data from an Epidemiological Study on the Insulin Resistance syndrome) study. The modifying effect of smoking habits were evaluated. Seventeen percent of women and 27% of men were smokers. Fibrinogen concentrations were higher in smokers than in non-smokers, in men only. Female smokers had lower concentrations of tPA-ag than non-smokers. In both women and men, fibrinogen was positively associated with fasting insulin [women: beta = 0.33 mg/U (95% confidence interval: 0.29, 0.37); men: beta = 0.15 mg/U (0.11, 0.19)] and with HOMA-IR [women: beta = 0.17 microg/microU mol/l (0.15, 0.19): men: beta = 0.06 (0.04, 0.08)]. For tPA-ag these associations were for insulin beta = 0.76 mg/U (0.54, 0.98) and beta = 0.89 mg/U (0.67, 1.11), and for HOMA-IR beta = 0.47 microg/microU mol/l (0.33, 0.61) and beta = 0.45 microg/microU mol/l (0.33, 0.57), women and men respectively. The associations of fibrinogen and tPA-ag with insulin and HOMA-IR were sharply reduced in male smokers compared to male non-smokers, however the strength of the associations in male non-smokers did not reach that in women. Fibrinogen and tPA-ag are independently related with markers of insulin resistance, with the relation with fibrinogen being stronger in women than in men. The strong modifying effect of smoking habits does not completely explain this gender difference.

Adult↗
PubMed2004

Limb deficiency defects, MSX1, and exposure to tobacco smoke.

There is increasing evidence from epidemiologic studies that genetic susceptibilities may modify the teratogenic effects of smoking. A previous study suggested that maternal smoking in the presence of a dinucleotide repeat polymorphism for MSX1 produced an almost fivefold increased risk for limb anomalies, providing evidence for a gene-environment interaction. The current study examined this potential interaction, using case-control data with several methodologic improvements, including a larger sample size and more detailed information on cigarette smoke exposures. Cases (n = 92) were ascertained from pregnancies ending in 1987-1989, and controls (n = 180) were randomly selected from eligible liveborn infants. In telephone interviews, women reported smoking behaviors during the month before pregnancy through the end of the first trimester. Odds ratios (OR) for maternal and paternal smoking ranged from 1.0 to 1.4, risk estimates were imprecise; for example, the OR for maternal smoking >or=20 cigarettes per day, versus none, was 1.3 (95% confidence interval (CI) 0.5-3.4). Relative to the homozygous wildtype, the OR was 1.5 (95% CI 0.7-3.5) for the homozygous variant genotype and 0.8 (95% CI 0.5-1.4) for the heterozygous variant genotype. There was no evidence that maternal smoking or both parents smoking, in combination with a susceptible MSX1 genotype, conferred an additional increase in risk of limb defects. This study did not find a gene-environment interaction between maternal smoking, infant MSX1 CA repeat polymorphism, and risk of limb deficiency defects. This finding contrasts with results of a previous study, which provided initial evidence for such an interaction. Several important methodological differences may have contributed to the differences in findings between the two studies.

Adult↗
PubMed2004

Predicting the impact of a nonsterilizing vaccine against human immunodeficiency virus.

Studies of human immunodeficiency virus (HIV) vaccines in animal models suggest that it is difficult to induce complete protection from infection (sterilizing immunity) but that it is possible to reduce the viral load and to slow or prevent disease progression following infection. We have developed an age-structured epidemiological model of the effects of a disease-modifying HIV vaccine that incorporates the intrahost dynamics of infection, a transmission rate and host mortality that depend on the viral load, the possible evolution and transmission of vaccine escape mutant viruses, a finite duration of vaccine protection, and possible changes in sexual behavior. Using this model, we investigated the long-term outcome of a disease-modifying vaccine and utilized uncertainty analysis to quantify the effects of our lack of precise knowledge of various parameters. Our results suggest that the extent of viral load reduction in vaccinated infected individuals (compared to unvaccinated individuals) is the key predictor of vaccine efficacy. Reductions in viral load of about 1 log(10) copies ml(-1) would be sufficient to significantly reduce HIV-associated mortality in the first 20 years after the introduction of vaccination. Changes in sexual risk behavior also had a strong impact on the epidemic outcome. The impact of vaccination is dependent on the population in which it is used, with disease-modifying vaccines predicted to have the most impact in areas of low prevalence and rapid epidemic growth. Surprisingly, the extent to which vaccination alters disease progression, the rate of generation of escape mutants, and the transmission of escape mutants are predicted to have only a weak impact on the epidemic outcome over the first 25 years after the introduction of a vaccine.

AIDS Vaccines↗
PubMedDate not supplied

Recent developments in the epidemiology of lung cancer.

Lung cancer is currently the leading cause of cancer death in the United States and also the most common tumor worldwide. Changes in the distribution of histologic types over the past two decades in the United States, as well as high rates of lung cancer in certain subpopulations, require explanation. While cigarette smoking and specific occupational exposures are firmly established as important risk factors for lung cancer, recent work provides evidence that other factors may play a role either as independent risk factors or as modifiers of the effect of smoking. This paper reviews the epidemiology of lung cancer, with an emphasis on developments in the past decade.

Air Pollution↗
PubMed1983

[Epidemiologic cancer research--new aspects for health education and early detection?].

Effective prevention has in the first place to be based on the knowledge of causal factors. In preventive oncology difficulties arise from the fact that our knowledge of causal mechanisms is--with some exceptions--not sufficient to provide clear guidelines for preventive action. Furthermore, it seems beyond doubt that development of cancer is a multifactorial process in which individual disposition, age and exposure to carcinogens participate. Only exposure can be modified by preventive measures. Epidemiological analysis of available data suggests that the effect of environmental carcinogens such as air pollution, contamination of food or occupational hazards on the general population is usually overestimated, although their effect cannot be ignored altogether. On the other hand, the real impact of tobacco products on carcinogenesis seems not yet to be fully realized. Not enough details are known about the probably major importance of dietary habits. In secondary prevention screening programs for the general population are only to be recommended at present for early detection of carcinoma of the cervix uteri. On the other hand, selective case finding in general practice, on the basis of knowledge of risk factors which are at least partially known, could be substantially improved.

Epidemiologic Methods↗
PubMed1987

N-nitroso compounds as a cause of human cancer.

Simultaneous consideration of epidemiological and experimental findings leads to the conclusion that the tobacco-specific nitrosamines (TSNA) 4-(N-nitrosomethylamino)-1-(3-pyridyl)-1-butanone (NNK) and N'-nitrosonornicotine (NNN) probably cause oral and respiratory cancers in humans. The role of other N-nitroso compounds (NOC) in the etiology of human cancer may best be defined by the study of known human carcinogens, such as certain foods eaten exclusively by populations with exceptionally high incidences and mortality rates for certain cancers. The evidence that NOC may be responsible for these elevated rates is reviewed in relation to two such high-risk populations: (i) residents of Lin-xian county in northern China, who have a striking excess of cancer of the oesophagus, and (ii) Cantonese people who have high rates of nasopharyngeal carcinoma (NPC). More studies are needed to define clearly the relationship between various types of cancers and prenatal or lifetime exposures to passive smoking. If passive smoking is found to increase the risk of developing various childhood and adult cancers, the NOC in tobacco are likely to be among the relevant carcinogens. Carcinogenesis models for studying the effects of prenatal exposure to NNK and NNN and other NOC seem particularly promising for the study of low-dose effects and modifying factors.

Adult↗
PubMed1998

Interaction of apolipoprotein E epsilon 4 with other genetic and non-genetic risk factors in late onset Alzheimer disease: problems facing the investigator.

The Apolipoprotein E4 allele (Apo-epsilon4) is the major susceptibility gene for late onset Alzheimer Disease (AD) but epidemiological data suggest that the effect of this allele is modified in different individuals by genetic or environmental factors. Age and head injury are major non-genetic factors modifying the Apo-epsilon4 risk. There is conflicting data as to whether alleles of other chaperon proteins (such as alpha-1-antichymotrypsin (ACT)) or Apo-epsilon4 receptors (such as the VDRL receptor) modify the Apo-epsilon4 risk for AD. We analyze problems posed by genetic association studies including those of multiple comparisons and selection of controls, the latter problem exacerbated by the wide variations in Apolipoprotein E allele frequencies observed in different groups and localities.

Alzheimer Disease↗
PubMed1998

Estrogen replacement inhibits intimal hyperplasia and the accumulation and effects of transforming growth factor beta1.

BACKGROUND: The role of estrogens in providing atheroprotection has been well documented in both epidemiologic and experimental studies. This phenomenon has traditionally been attributed to the beneficial lipid-modifying effects of estrogens. Previous studies have used models of either diet- or injury-induced atherosclerosis. As such, the interrelationship between estrogens, lipids, and atherosclerosis remains unclear. We hypothesized that estrogens are atheroprotective independent of changes in serum lipids by directly influencing the accumulation and effects of the peptide growth factor transforming growth factor beta1 (TGF-beta1). MATERIAL AND METHODS: Thirteen female sheep (8 years old) were randomized to sham, ovariectomy, or ovariectomy with 17beta-estradiol replacement. Serum lipid levels were serially measured. At 9 months, necropsy was performed with histologic morphometric analysis of the aortoiliac bifurcation. Levels of TGF-beta1 were determined in serum and aortic tissue. Human aortic smooth muscle cells were isolated and cultured. RESULTS: Serum triglyceride, lipoprotein a, and total, low-density lipoprotein, and high-density lipoprotein cholesterol levels were similar and normal between groups. Ovariectomy resulted in aortoiliac intimal hyperplasia compared with sham (P < 0.001) and hormone replacement (P < 0.001) groups. Compared with ovariectomy, estrogen replacement attenuated aortic accumulation of TGF-beta1 (P < 0.02). In vitro, estradiol potentiated TGF-beta1 inhibition of human vascular smooth muscle cell (VSMC) proliferation and increased TGF-beta1 release in stimulated VSMCs (P < 0.001). CONCLUSIONS: Without dietary manipulation, ovarian ablation induces aortic intimal hyperplasia in the ewe. Estradiol abrogates this response independently of its effects on serum lipids. Hormone replacement decreases the accumulation of TGF-beta1, suggesting that estrogens may provide atheroprotection both by modifying local production and by modulating the influence of TGF-beta1 on VSMC growth.

Animals↗