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PubMed1981

Epidemiologic problems associated with exposure to several agents.

Simultaneous exposure to many potentially hazardous agents in the environment is the rule, yet there have been few studies that have addressed the issue of interactions of these agents in modifying disease outcomes, even though such interactions may potentially be important in terms of policy-making. Epidemiological methods may be an important way to identify interaction effects, especially for chronic disease outcomes. Some examples of epidemiologic investigations of this problem are given, and a matrix method used to evaluate the contribution of nineteen chemicals to the risk of liver angiosarcoma in vinyl chloride workers is discussed.

Air Pollutants, Occupational↗

PubMed1983

A FORTRAN program for stratified analysis of data from case-control studies.

Stratification of study subjects by one or more covariates is a commonly accepted method for dealing with confounding and effect modification in epidemiologic case-control studies. A flexible FORTRAN program is described which facilitates simultaneous stratification by several covariates and which produces summary odds ratio estimates and chi-square statistics by the Mantel-Haenszel method. It also facilitates detection of effect modification by each covariate considered individually. Straightforward means are provided for the user to modify input data before analysis or to exclude certain subjects from analysis, simulating such capabilities in larger statistical packages.

Computers↗

PubMed1997

Estimating health risks from natural hazards using risk assessment and epidemiology.

Risk assessment is the process of estimating the likelihood that an adverse effect may result from exposure to a specific health hazard. The process traditionally involves hazard identification, dose-response assessment, exposure assessment, and risk characterization to answer "How many excess cases of disease A will occur in a population of size B due to exposure to agent C at dose level D?" For natural hazards, however, we modify the risk assessment paradigm to answer "How many excess cases of outcome Y will occur in a population of size B due to natural hazard event E of severity D?" Using a modified version involving hazard identification, risk factor characterization, exposure characterization, and risk characterization, we demonstrate that epidemiologic modeling and measures of risk can quantify the risks from natural hazard events. We further extend the paradigm to address mitigation, the equivalent of risk management, to answer "What is the risk for outcome Y in the presence of prevention intervention X relative to the risk for Y in the absence of X?" We use the preventable fraction to estimate the efficacy of mitigation, or reduction in adverse health outcomes as a result of a prevention strategy under ideal circumstances, and further estimate the effectiveness of mitigation, or reduction in adverse health outcomes under typical community-based settings. By relating socioeconomic costs of mitigation to measures of risk, we we illustrate that prevention effectiveness is useful for developing cost-effective risk management options.

Disaster Planning↗

PubMed2005

HIV/hepatitis C virus co-infection in drug users: risk behavior and prevention.

Studies of HIV-positive patients have consistently shown that drug users, in particular injection drug users (IDU), are far more likely to have hepatitis C virus (HCV) infection than other patient groups. HIV incidence and prevalence in IDU has declined in recent years, but HCV remains endemic in this population. HCV antibody prevalence among non-injection users of drugs such as heroin and cocaine is between 5 and 30%, although there are scant data on specific transmission risk behavior. The control of HIV/HCV co-infection must address HCV prevention. Epidemiological studies have suggested that HCV prevalence in IDU is subject to various influences, some of which may be modifiable by interventions. However, studies have not shown consistent effects of various prevention strategies on HCV transmission, including studies of HCV screening and education, drug treatment or needle exchange. Although some large cross-sectional studies in regions where needle exchange is available to a large number of drug injectors have reported declining HCV prevalence, the scale of services needed is a matter of considerable debate and has not been systematically quantified. Priorities for research related to the prevention of HIV/HCV co-infection should include estimating the effect on disease occurrence of eliminating specific risk factors, and specifying the level of resources needed to alter HCV incidence.

HIV Infections↗

PubMed1999

Environmental tobacco smoke and low birth weight: a hazard in the workplace?

Low birth weight (LBW) increases infant morbidity and mortality worldwide. One well-established risk factor is maternal smoking. Environmental tobacco smoke (ETS) exposure has recently been focused on as another potential risk factor. In this article, we review epidemiologic literature on the effects of ETS on LBW and intrauterine growth retardation (IUGR), the cause of LBW related to maternal smoking. As we consider the feasibility of modifying women's exposure, we focus our discussion on workplace exposure to ETS. The workplace is particularly important to consider because women of child-bearing age are present in the workplace in greater numbers now than ever before. In addition, certain subgroups of working women may be particularly at risk from the effects of ETS on pregnancy because they work in environments with higher exposure or they are more susceptible to its effects. We conclude that there is consistent evidence to relate maternal ETS exposure to an increased risk of adverse pregnancy outcomes and that this association may be generalized to the work environment. In studies with positive findings, infants exposed to ETS antenatally were 1.5-4 times more likely to be born with LBW, but few studies examined LBW. Most studies looked at measures of IUGR. ETS was associated with reductions in birth weight (adjusted for gestational age) ranging from 25 to 90 g. Infants born to women exposed to ETS were generally 2-4 times more likely to be born small-for-gestational age. ETS exposure in the workplace can and should be minimized to protect pregnant women from its adverse effects.

Adult↗

PubMed2001

Electromagnetic fields and health outcomes.

Over the past two decades, there has been increasing interest in the biological effects and possible health outcomes of weak, low-frequency electric and magnetic fields. Epidemiological studies on magnetic fields and cancer, reproduction and neurobehavioural reactions have been presented. More recently, neurological, degenerative and heart diseases have also been reported to be related to such electromagnetic fields. Furthermore, the increased use of mobile phones worldwide has focussed interest on the possible effects of radiofrequency fields of higher frequencies. In this paper, a summary is given on electromagnetic fields and health outcomes and what policy is appropriate--"no restriction to exposure", "prudent avoidance" or "expensive interventions"? The results of research studies have not been unambiguous; studies indicating these fields as being a health hazard have been published and so were studies indicating no risk at all. In "positive" studies, different types of effects have been reported despite the use of the same study design, e.g., in epidemiological cancer studies. There are uncertainties as to exposure characteristics, e.g., magnetic field frequency and exposure intermittence, and not much is known about possible confounding or effect-modifying factors. The few animal cancer studies reported have not given much help in risk assessment; and in spite of a large number of experimental cell studies, no plausible and understandable mechanisms have been presented by which a carcinogenic effect could be explained. Exposure to electromagnetic fields occurs everywhere: in the home, at work, in school, etc. Wherever there are electric wires, electric motors and electronic equipment, electromagnetic fields are created. This is one of the reasons why exposure assessment is difficult. For epidemiologists, the problems is not on the effect side as registers of diseases exist in many countries today. The problem is that epidemiologists do not know the relevant exposure characteristics to be used in their studies. In international guidelines, limits for restrictions of field exposure are several orders of magnitude above what can be measured from overhead power lines and found in "electrical" occupations. These guidelines emphasize that the state of scientific knowledge today does not warrant limiting exposure levels for the public and the work force, and that further data are required to confirm whether health hazards are present. In some countries, however, the "principle of caution" or "prudent avoidance" has been adopted; meaning the low-cost avoidance of unnecessary exposure as long as there is scientific uncertainty about its health effects.

Cardiovascular Diseases↗

PubMed1984

Relationship between dose and health effects.

The health effects produced by chemicals depend on the inherent toxicity of the chemical and the dose received by the exposed individual. Health effects are modified by genetic make-up, life style, nutrition, and interaction with other chemicals. In some situations it may be difficult to impossible to determine through epidemiologic studies whether exposure to chemicals (naturally occurring or synthetic) has caused harm. For all practical purposes, the risk associated with minuscule doses of most chemicals is negligible.

Adipose Tissue↗

PubMed1998

Differential effects of BMI on diabetes risk among black and white Americans.

OBJECTIVE: To determine whether the associations of BMI and fat distribution with diabetes risk are modified by race. RESEARCH DESIGN AND METHODS: Data from the National Health and Nutrition Examination Survey, Epidemiologic Follow-up Study (1971-1992), were used to investigate potential interactions of BMI and fat distribution with race. Incident diabetes was defined by self-report of physician-diagnosed diabetes, hospital and nursing home discharge records, and death certificates. RESULTS: Among the 1,531 black and 9,852 white subjects who were nondiabetic at baseline, 1,139 (10.0%) developed diabetes during 20 years of follow-up. Although the cumulative risk of diabetes increased with baseline BMI in all four race-sex groups, the sex-specific odds ratios (ORs) for black:white subjects decreased with increasing BMI. In particular, for BMI of 22 kg/m2, the OR of diabetes for black:white individuals was 1.87 and 1.76 (P < 0.01) for men and women, respectively; for BMI of 32 kg/m2, the OR decreased to 0.99 and 1.20 (NS) for men and women, respectively. Skinfold ratio was also associated with increased diabetes risk in all race-sex groups, but did not modify the association between race and diabetes. CONCLUSIONS: These findings suggest that the effect of BMI on diabetes risk is different for black and white Americans, with a larger risk for blacks than whites at low BMI and an equivalent risk for both groups at high BMI. A lower degree of visceral adiposity among blacks at higher BMI or a greater impact of visceral adiposity among blacks at low BMI may help explain the interaction of race and BMI on diabetes risk.

Adult↗

PubMed1995

Evaluation of the allergic/irritant potential of air pollutants: detection of proteins modified by volatile organic compounds from oilseed rape (Brassica napus ssp. oleifera) using electrospray ionization-mass spectrometry.

BACKGROUND: Upward trends in allergy and asthma rates have been reported in most western societies, including the UK, where around 15-20% of the population now suffer from allergy or asthma. Scientific proof of the causes of these increases relies on accurate assessment of exposure and standardized diagnostic tests, such as for specific IgE in blood serum and skin testing. For many air pollutants it has proven difficult to assess an individual's exposure outside an occupational environment and reliable test development is hampered by not knowing whether an allergic or irritant mechanism is involved. These problems are particularly evident in the controversial issue of whether airborne releases from oilseed rape can cause health effects. OBJECTIVE: To develop a method for evaluating the allergic/irritant potential of air pollutants and to assess whether the volatile organic compounds emitted by oilseed rape have this potential. METHODS: Proteins were exposed in vitro to volatile organic compounds emitted by oilseed rape. Electrospray ionization-mass spectrometry was used to detect any resultant protein modifications. RESULTS: Dimethyl disulphide, thiocyanic acid methyl ester and 2-methyl-propanenitrile were able to modify human proteins. In addition, two isothiocyanates which can be emitted by damaged oilseed rape also have this ability. The major products emitted by undamaged oilseed rape, terpenes, a sesquiterpene and a terpene alcohol did not have this property, but the possible role of their oxidized products is discussed. CONCLUSION: Some of the volatile organic compounds emitted by oilseed rape have the potential to be allergens/irritants. Standardized modified proteins produced by this method should prove useful for biomonitoring human exposure in molecular epidemiological studies as well as in diagnostic tests. This method should find further application in investigations into the possible health effects of other environmental pollutants.

Air Pollutants↗

PubMed2004

Lung cancer risk after exposure to polycyclic aromatic hydrocarbons: a review and meta-analysis.

Typical polycyclic aromatic hydrocarbon mixtures are established lung carcinogens, but the quantitative exposure-response relationship is less clear. To clarify this relationship we conducted a review and meta-analysis of published reports of occupational epidemiologic studies. Thirty-nine cohorts were included. The average estimated unit relative risk (URR) at 100 Mu g/m (superscript)3(/superscript) years benzo[a]pyrene was 1.20 [95% confidence interval (CI), 1.11-1.29] and was not sensitive to particular studies or analytic methods. However, the URR varied by industry. The estimated means in coke ovens, gasworks, and aluminum production works were similar (1.15-1.17). Average URRs in other industries were higher but imprecisely estimated, with those for asphalt (17.5; CI, 4.21-72.78) and chimney sweeps (16.2; CI, 1.64-160.7) significantly higher than the three above. There was no statistically significant variation of URRs within industry or in relation to study design (including whether adjusted for smoking), or source of exposure information. Limited information on total dust exposure did not suggest that dust exposure was an important confounder or modified the effect. These results provide a more secure basis for risk assessment than was previously available.

Environmental Pollutants↗

PubMedDate not supplied

Does an interaction between smoking and drinking influence the risk of Alzheimer's disease? Results from three Canadian data sets.

Investigation of the relationship of smoking and drinking to Alzheimer's disease (AD) may advance research on the cause of AD and provide a basis for treatment. Pharmacological mechanisms for an involvement of smoking and drinking are plausible but epidemiologic reports are inconsistent. Evidence of behavioural and physiological interactions suggests that tobacco and alcohol use may not only individually affect AD, but may also modify each other's effects. A modelling strategy was developed to examine the interaction between smoking and drinking on the risk of AD. Three Canadian data sets were analysed: the University of Western Ontario Dementia Study (UWODS) (n=363); the Canadian Study of Health and Aging (CSHA) (n=516), and the database from the Clinic for Alzheimer Disease and Related Disorders at the Vancouver Hospital and Health Sciences Centre, University of British Columbia site (UBC) (n=843). Multiple logistic regression models were adjusted for the potential confounders age, age squared, sex, education, family history of dementia, head injury and hypertension. Analysis of the CSHA provided evidence consistent with the hypothesis that smoking and drinking influence each other's effects on AD, with smoking reducing the risk of AD among drinkers. A similar interaction was marginally significant (p=0.052) in the UWODS data set, but not significant in the UBC data. Extension of these analyses, particularly in longitudinal studies and within genetic risk groups, is needed to determine whether this interaction can be replicated. If so, research on the biological interactions of nicotine and alcohol may provide a basis for the development of therapeutic interventions as well as providing clues to the cause of this disorder.

Aged↗

PubMed2001

Shifting paradigms in gene-mapping methodology for complex traits.

The analysis of genetic linkage has been highly successful in the mapping of the genes responsible for Mendelian diseases. In the past decade, attempts have been made to extend this approach to multifactorial disorders and other health-related traits. It has proved difficult, however, to obtain strong and replicable linkage findings for the common forms of heritable diseases. This, together with the rapid pace of development of molecular technology and expansion of genome sequence information, has resulted in significant shifts in research paradigm. There is an increasing recognition of the need to understand the population genetics and biometrical properties of clinically relevant traits so that phenotypes can be defined in such a way that maximises the chances of successful gene mapping. There is a trend towards systematic association analysis with increasing sophistication in the analysis of pooled DNA samples and multi-locus haplotypes, and in the use of unlinked background markers to protect against spurious associations. We can expect increasing integration between genetics, epidemiology and clinical trials leading to genetically informative designs that will not only identify susceptibility genes but also clarify how the environment influences their effects and how they may modify the response to therapeutic interventions.

Animals↗

PubMed2004

A reanalysis of thyroid neoplasms in the Israeli tinea capitis study accounting for dose uncertainties.

In the 1940s and 1950s, children in Israel were treated for tinea capitis by irradiation to the scalp to induce epilation. Follow-up studies of these patients and of other radiation- exposed populations show an increased risk of malignant and benign thyroid tumors. Those analyses, however, assume that thyroid dose for individuals is estimated precisely without error. Failure to account for uncertainties in dosimetry may affect standard errors and bias dose-response estimates. For the Israeli tinea capitis study, we discuss sources of uncertainties and adjust dosimetry for uncertainties in the prediction of true dose from X-ray treatment parameters. We also account for missing ages at exposure for patients with multiple X-ray treatments, since only ages at first treatment are known, and for missing data on treatment center, which investigators use to define exposure. Our reanalysis of the dose response for thyroid cancer and benign thyroid tumors indicates that uncertainties in dosimetry have minimal effects on dose-response estimation and for inference on the modifying effects of age at first exposure, time since exposure, and other factors. Since the components of the dose uncertainties we describe are likely to be present in other epidemiological studies of patients treated with radiation, our analysis may provide a model for considering the potential role of these uncertainties.

Adolescent↗

PubMedDate not supplied

Relationships between laboratory and human studies.

The problems encountered in trans-species extrapolation of the results of chemical carcinogenesis experiments to man are considered from the viewpoints of experimental techniques for establishing chemicals as carcinogens and the effect of modifying factors therein. Extrapolations from the effects of high doses of carcinogens in experimental animals to low doses in man present problems which are beyond the reach of present epidemiological and experimental methodology. The author prefers a pragmatic approach to the latter problems rather than the use of largely unsupported mathematical methodology.

Animals↗

PubMed1995

[Basedow's disease and pregnancy in a black African population. Epidemiology and interrelations in 51 pregnancies].

Forty one patients with 51 pregnancies form the basis of this study of etiological factors and reciprocal effects of pregnancy and thyrotoxicosis. Pregnancy influences the course of thyrotoxicosis and may modify its diagnostic aspects, clinical course, variations in laboratory parameters and treatment. The effect of thyrotoxicosis on pregnancy may lead to abortions, premature labour and/or toxemia. It may sometimes influence the products of conception. The essential point appears to be to seek the minimal dose of antithyroid drug capable of controlling thyroid disease without impairing fetal thyroid function.

Adult↗

PubMed1980

[Effectivity of drugs in the elderly with regard to their pharmacokinetics and pharmacodynamics (author's transl)].

In principle, in all periods of life drugs act with the same mechanisms. Characteristics modifications of drug effects are caused by age dependent special constellations of pathogenesis and course of the illness, as well as of the multimorbidity in relation to physiological ageing. The most important functional process of ageing is the progressively decreasing adaptability towards environmental conditions with interindividually distinct deviations. If elderly patients react quantitatively in an unexpected fashion, the reason can be a different absorption, distribution, renal or metabolic elimination of the drug. But there exists also an age dependent sensitivity towards drugs, which can be explained in a modified reaction-pattern of the receptors.

Aged↗

PubMed2000

Ecological effects in multi-level studies.

Multi-level research that attempts to describe ecological effects in themselves (for example, the effect on individual health from living in deprived communities), while also including individual level effects (for example, the effect of personal socioeconomic disadvantage), is now prominent in research on the socioeconomic determinants of health and disease. Such research often involves the application of advanced statistical multi-level methods. It is hypothesised that such research is at risk of reaching beyond an epidemiological understanding of what constitutes an ecological effect, and what sources of error may be influencing any observed ecological effect. This paper aims to present such an epidemiological understanding. Three basic types of ecological effect are described: a direct cross level effect (for example, living in a deprived community directly affects individual personal health), cross level effect modification (for example, living in a deprived community modifies the effect of individual socioeconomic status on individual health), and an indirect cross level effect (for example, living in a deprived community increases the risk of smoking, which in turn affects individual health). Sources of error and weaknesses in study design that may affect estimates of ecological effects include: a lack of variation in the ecological exposure (and health outcome) in the available data; not allowing for intraclass correlation; selection bias; confounding at both the ecological and individual level; misclassification of variables; misclassification of units of analysis and assignment of individuals to those units; model mis-specification; and multicollinearity. Identification of ecological effects requires the minimisation of these sources of error, and a study design that captures sufficient variation in the ecological exposure of interest.

Bias↗

PubMed2005

Role of lipoprotein-associated phospholipase A2 in atherosclerosis: biology, epidemiology, and possible therapeutic target.

The development of atherosclerotic vascular disease is invariably linked to the formation of bioactive lipid mediators and accompanying vascular inflammation. Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an enzyme that is produced by inflammatory cells, co-travels with circulating low-density lipoprotein (LDL), and hydrolyzes oxidized phospholipids in LDL. Its biological role has been controversial with initial reports purporting atheroprotective effects of Lp-PLA2 thought to be a consequence of degrading platelet-activating factor and removing polar phospholipids in modified LDL. Recent studies, however, focused on pro-inflammatory role of Lp-PLA2 mediated by products of the Lp-PLA2 reaction (lysophosphatidylcholine and oxidized nonesterified fatty acids). These bioactive lipid mediators, which are generated in lesion-prone vasculature and to a lesser extent in the circulation (eg, in electronegative LDL), are known to elicit several inflammatory responses. The proinflammatory action of Lp-PLA2 is also supported by a number of epidemiology studies suggesting that the circulating level of the enzyme is an independent predictor of cardiovascular events, despite some attenuation of the effect by inclusion of LDL, the primary carrier of Lp-PLA2, in the analysis. These observations provide a rationale to explore whether inhibiting Lp-PLA2 activity and consequent interference with the formation of bioactive lipid mediators will abrogate inflammation associated with atherosclerosis, produce favorable changes in intermediate cardiovascular end points (eg, biomarkers, imaging, and endothelial function), and ultimately reduce cardiovascular events in high-risk patients.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗