OBJECTIVES: Self-rated health has been shown to be a predictor for future health status and mortality. The purpose of this study was to investigate age-group and sex differences in genetic and environmental sources of variation for self-rated health. METHODS: A sample of twins from the Swedish Twin Registry participated in a computer-assisted telephone interview with assessment of self-rated health. Structural equation model analyses on 1,243 complete twin pairs provided estimates of genetic and environmental components of variance. RESULTS: Individual differences primarily reflected individual specific environmental influences at all ages. The increase in total variance across age groups was primarily due to genetic influences in the age groups 45--74 years and greater environmental influences in the oldest age group (>74). No significant sex differences were found in variance components. DISCUSSION: Genetic variance in the two middle age groups (45--74) could reflect genetic susceptibility to age-dependent illnesses not yet expressed in the youngest group. The findings suggest that it might be more fruitful to explore the origins of individual differences for self-rated health in the context of an individual's age and birth cohort rather than in the context of sex.
Ambient air pollution has been suggested as a risk factor for chronic obstructive pulmonary disease (COPD). However, there is a lack of longitudinal studies to support this assertion.
To investigate the associations of long-term exposure to elevated traffic-related air pollution and woodsmoke pollution with the risk of COPD hospitalization and mortality.
This population-based cohort study included a 5-year exposure period and a 4-year follow-up period. All residents aged 45-85 years who resided in Metropolitan Vancouver, Canada, during the exposure period and did not have known COPD at baseline were included in this study (n = 467,994). Residential exposures to traffic-related air pollutants (black carbon, particulate matter
Concentrations of cadmium and lead in blood (BCd and BPb, respectively) are traditionally used as biomarkers of environmental exposure. We estimated the influence of genetic factors on these markers in a cohort of 61 monozygotic and 103 dizygotic twin pairs (mean age = 68 years, range = 49-86). BCd and BPb were determined by graphite furnace atomic absorption spectrophotometry. Variations in both BCd and BPb were influenced by not only environmental but also genetic factors. Interestingly, the genetic influence was considerably greater for nonsmoking women (h(2) = 65% for BCd and 58% for BPb) than for nonsmoking men (13 and 0%, respectively). The shared familial environmental (c(2)) influence for BPb was 37% for men but only 3% for women. The association between BCd and BPb could be attributed entirely to environmental factors of mutual importance for levels of the two metals. Thus, blood metal concentrations in women reflect not only exposure, as previously believed, but to a considerable extent hereditary factors possibly related to uptake and storage. Further steps should focus on identification of these genetic factors and evaluation of whether women are more susceptible to exposure to toxic metals than men.
Cites: Occup Environ Med. 1995 Nov;52(11):764-98535497
Previous research in the Swedish Adoption/Twin Study of Aging (SATSA) has found genetic influences on life events (R. Plomin, P. Lichtenstein, N.L. Pedersen, G.E. McClearn, & J.R. Nesselroade, 1990). The present study extends this finding by examining sex differences in genetic and environmental contributions to life events and by examining personality as a mediator of genetic influences on life events in SATSA. Analyses were based on 320 twin pairs, including identical and fraternal twins reared together and apart (mean age = 58.6 years). Controllable, desirable, and undesirable life events were revealed significant genetic variance for women. There was no significant genetic variance for either sex for uncontrollable events. Multivariate analyses of personality (as indexed by Neuroticism, Extraversion, and Openness to Experience) and life events suggest that all of the genetic variance on controllable, desirable, and undesirable life events for women is common to personality. Thus, in this sample of older adult women, genetic influences on life events appear to be entirely mediated by personality.
Residential proximity to road traffic is associated with increased coronary heart disease (CHD) morbidity and mortality. It is unknown, however, whether changes in residential proximity to traffic could alter the risk of CHD mortality.
We used a population-based cohort study with a 5-year exposure period and a 4-year follow-up period to explore the association between changes in residential proximity to road traffic and the risk of CHD mortality. The cohort comprised all residents aged 45-85 years who resided in metropolitan Vancouver during the exposure period and without known CHD at baseline (n = 450,283). Residential proximity to traffic was estimated using a geographic information system. CHD deaths during the follow-up period were identified using provincial death registration database. The data were analyzed using logistic regression.
Compared with the subjects consistently living away from road traffic (>150 m from a highway or >50 m from a major road) during the 9-year study period, those consistently living close to traffic (
Clinicians and researchers have characterized early life experiences as permanent and stable influences on the personality and subsequent life experiences of an individual. Recent conceptualizations have suggested that personal and environmental factors influencing development are not deterministic. Multiple pathways into adulthood are possible. Adoption is one potential early life stressor that may illustrate the usefulness of such conceptualizations for assessing long-term effects in adulthood. Previous studies of adoption have characterized the effects of adoption into adolescence and young adulthood. The purpose of this study was to provide an initial assessment of the long-term impact of adoption. The participants were taken from the Swedish Adoption/Twin Study of Aging. From the original sample, we identified a subsample of 60 pairs of twins who were separated and reared apart, with one member being raised by a biological parent or parents and the other by an adoptive parent or parents with no biological relationship. A series of univariate and multivariate analyses were undertaken to assess the elements associated with being reared in either an adoptive home or the home of biological parent(s). The results suggest few significant effects of adoption on the adult adjustment of adoptees. In particular, the results reflect the important mediating role of childhood socioeconomic status, suggesting that the stress of adoption itself is mediated by the type of rearing environment provided by the adoption process.
Recent evidence suggests that chronic exposure to high levels of ambient particulate matter (PM) is associated with decreased pulmonary function and the development of chronic airflow obstruction. To investigate the possible role of PM-induced abnormalities in the small airways in these functional changes, we examined histologic sections from the lungs of 20 women from Mexico City, a high PM locale. All subjects were lifelong residents of Mexico City, were never-smokers, never had occupational dust exposure, and never used biomass fuel for cooking. Twenty never-smoking, non-dust-exposed subjects from Vancouver, British Columbia, Canada, a low PM region, were used as a control. By light microscopy, abnormal small airways with fibrotic walls and excess muscle, many containing visible dust, were present in the Mexico City lungs. Formal grading analysis confirmed the presence of significantly greater amounts of fibrous tissue and muscle in the walls of the airways in the Mexico City compared with the Vancouver lungs. Electron microscopic particle burden measurements on four cases from Mexico City showed that carbonaceous aggregates of ultrafine particles, aggregates likely to be combustion products, were present in the airway mucosa. We conclude that PM penetrates into and is retained in the walls of small airways, and that, even in nonsmokers, long-term exposure to high levels of ambient particulate pollutants is associated with small airway remodeling. This process may produce chronic airflow obstruction.
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Evidence suggests that air pollution exposure adversely affects pregnancy outcomes. Few studies have examined individual-level intraurban exposure contrasts.
We evaluated the impacts of air pollution on small for gestational age (SGA) birth weight, low full-term birth weight (LBW), and preterm birth using spatiotemporal exposure metrics.
With linked administrative data, we identified 70,249 singleton births (1999-2002) with complete covariate data (sex, ethnicity, parity, birth month and year, income, education) and maternal residential history in Vancouver, British Columbia, Canada. We estimated residential exposures by month of pregnancy using nearest and inverse-distance weighting (IDW) of study area monitors [carbon monoxide, nitrogen dioxide, nitric oxide, ozone, sulfur dioxide, and particulate matter
Cites: Occup Environ Med. 2008 Sep;65(9):579-8618070798
Cites: J Expo Anal Environ Epidemiol. 2005 Mar;15(2):185-20415292906
Here we compare PM(2.5) (particles with aerodynamic diameter less than 2.5 microm) mass and filter absorbance measurements with elemental carbon (EC) concentrations measured in parallel at the same site as well as collocated PM(2.5) and PM(10) (particles with aerodynamic diameter less than 10 microm) mass and absorbance measurements. The data were collected within the Traffic-Related Air Pollution on Childhood Asthma (TRAPCA) study in Germany, The Netherlands and Sweden. The study was designed to assess the health impact of spatial contrasts in long-term average concentrations. The measurement sites were distributed between background and traffic locations. Annual EC and PM(2.5) absorbance measurements were at traffic sites on average 43-84% and 26-76% higher, respectively, compared to urban background sites. The contrast for PM(2.5) mass measurements was lower (8-35%). The smaller contrast observed for PM(2.5) mass in comparison with PM(2.5) absorbance and EC documents that PM(2.5) mass underestimates exposure contrasts related to motorized traffic emissions. The correlation between PM(10) and PM(2.5) was high, documenting that most of the spatial variation of PM(10) was because of PM(2.5). The measurement of PM(2.5) absorbance was highly correlated with EC measurements and suggests that absorbance can be used as a simple, inexpensive and non-destructive method to estimate motorized traffic-related particulate air pollution. The EC/absorbance relation differed between countries and site type (background/traffic), supporting the need for site-specific calibrations of the simple absorbance method. While the ratio between PM(2.5) and PM(10) mass ranged from 0.54 to 0.68, the ratio of PM(2.5) absorbance and PM(10) absorbance was 0.96-0.97, indicating that PM(2.5) absorbance captures nearly all of the particle absorbance.
OBJECTIVES: The purpose of the present report was to assess whether occupational magnetic field exposure is a risk factor for dementia, in particular for Alzheimer's disease. METHODS: Case-control analyses were applied to 77 dementia cases, 55 of whom had Alzheimer's disease, ascertained from the population-based Swedish twin register. Two reference groups were derived, with 228 and 238 persons, respectively. Occupations were linked to a job-exposure matrix based on magnetic field measurements. Primary occupation, last occupation before reference date, and the occupation with the highest magnetic field exposure during the subject's lifetime were evaluated. RESULTS: For primary occupation, all relative risk estimates were close to unity. For last occupation, at the exposure level > or = 0.2 microT, a relative risk was found for dementia estimated at 3.3 [95% confidence interval (95% CI) 1.3-8.6] and 3.8 (95% CI 1.4-10.2) for reference groups 1 and 2, respectively. The relative risk for Alzheimer's disease was estimated at 2.4 (95% CI 0.8-6.9) and 2.7 (95% CI 0.9-7.8), respectively. For the occupation with the highest magnetic field exposure, the relative risk estimates were close to unity for reference group 1 and slightly elevated for reference group 2. The relative risk estimates were greater for the subjects who were younger at onset (
The goal was to investigate the epidemiological features of incident bronchiolitis by using a population-based infant cohort.
Outpatient and inpatient health records were used to identify incident bronchiolitis cases among 93,058 singleton infants born in the Georgia Air Basin between 1999 and 2002. Additional health-related databases were linked to provide data on sociodemographic variables, maternal characteristics, and birth outcome measures.
From 1999 to 2002, bronchiolitis accounted for 12,474 incident health care encounters (inpatient or outpatient contacts) during the first year of life (134.2 cases per 1000 person-years). A total of 1588 hospitalized bronchiolitis cases were identified (17.1 cases per 1000 person-years). Adjusted Cox proportional-hazard analyses for both case definitions indicated an increased risk of incident bronchiolitis in the first year of life (follow-up period: 2-12 months) for boys, infants of First Nations status, infants with older siblings, and infants living in neighborhoods with smaller proportions of maternal postsecondary education. The risk also was elevated for infants born to young mothers (
There is increasing recognition of the importance of early environmental exposures in the development of childhood asthma. Outdoor air pollution is a recognized asthma trigger, but it is unclear whether exposure influences incident disease. We investigated the effect of exposure to ambient air pollution in utero and during the first year of life on risk of subsequent asthma diagnosis in a population-based nested case-control study.
We assessed all children born in southwestern British Columbia in 1999 and 2000 (n = 37,401) for incidence of asthma diagnosis up to 34 years of age using outpatient and hospitalization records. Asthma cases were age- and sex-matched to five randomly chosen controls from the eligible cohort. We estimated each individual's exposure to ambient air pollution for the gestational period and first year of life using high-resolution pollution surfaces derived from regulatory monitoring data as well as land use regression models adjusted for temporal variation. We used logistic regression analyses to estimate effects of carbon monoxide, nitric oxide, nitrogen dioxide, particulate matter
BACKGROUND: The relative importance of genetic influences on longevity was studied on data from the population-based Swedish Twin Registry. METHODS: A sample of 3,656 identical and 6,849 like-sexed fraternal twin pairs was studied regarding mortality rates and within-pair similarity for age at death. Genetic and environmental contributions to variation in longevity, expressed by integrated mortality rates, were estimated from a subsample of 1,734 twin pairs reared together and 130 twin pairs reared apart from the cohorts born 1886 to 1900. RESULTS: The intraclass correlation coefficients suggested that the genetic effect was small, and, for males, perhaps absent. Among pairs in which both twins died relatively young and among pairs in which both twins lived until very old age, the variance in age at death seemed to have no genetic component. Model fitting procedures based on twins reared apart and twins reared together indicated that most of the variance in longevity was explained by environmental factors. CONCLUSIONS: Over the total age range examined, a maximum of around one third of the variance in longevity is attributable to genetic factors, and almost all of the remaining variance is due to nonshared, individual specific environmental factors. The evidence that genetic factors play a minor role depending upon age at death merits further examination.
A population-based twin study is a useful design for quantification of the effects of genes and environmental factors in disease etiology. We used data from 10,000 Swedish twin pairs to quantify genetic and environmental contributions to tooth loss and periodontal health. Oral health information was obtained from telephone interviews. Structural equation models measured the relative importance of genetic and environmental factors. Genetic factors contributed to 14% of variation in tooth loss among women, and 39% among men. Non-shared environmental factors accounted for one-quarter of risk; environmental factors shared by twins comprised the remainder. Heritability estimates of periodontal disease were 39% and 33% for women and men, respectively, while non-shared environmental factors accounted for the remaining variation. Heritability for both conditions varied as a function of age and smoking status. Analysis of data from this large, population-based study demonstrates a moderate role of genetic factors in oral diseases, and suggests potential gene-environment interactions.
BACKGROUND: As part of a multicenter study relating traffic-related air pollution with incidence of asthma in three birth cohort studies (TRAPCA), we used a measurement and modelling procedure to estimate long-term average exposure to traffic-related particulate air pollution in communities throughout the Netherlands; in Munich, Germany; and in Stockholm County, Sweden. METHODS: In each of the three locations, 40-42 measurement sites were selected to represent rural, urban background and urban traffic locations. At each site and fine particles and filter absorbance (a marker for diesel exhaust particles) were measured for four 2-week periods distributed over approximately 1-year periods between February 1999 and July 2000. We used these measurements to calculate annual average concentrations after adjustment for temporal variation. Traffic-related variables (eg, population density and traffic intensity) were collected using Geographic Information Systems and used in regression models predicting annual average concentrations. From these models we estimated ambient air concentrations at the home addresses of the cohort members. RESULTS: Regression models using traffic-related variables explained 73%, 56% and 50% of the variability in annual average fine particle concentrations for the Netherlands, Munich and Stockholm County, respectively. For filter absorbance, the regression models explained 81%, 67% and 66% of the variability in the annual average concentrations. Cross-validation to estimate the model prediction errors indicated root mean squared errors of 1.1-1.6 microg/m for PM(2.5) and 0.22-0.31 *10(-5) m for absorbance.CONCLUSIONS: A substantial fraction of the variability in annual average concentrations for all locations was explained by traffic-related variables. This approach can be used to estimate individual exposures for epidemiologic studies and offers advantages over alternative techniques relying on surrogate variables or traditional approaches that utilize ambient monitoring data alone.
Radiographers process X-ray films using developer and fixer solutions that contain chemicals known to cause or exacerbate asthma. In a study in British Columbia, Canada, radiographers' personal exposures to glutaraldehyde (a constituent of the developer chemistry), acetic acid (a constituent of the fixer chemistry), and sulfur dioxide (a byproduct of sulfites, present in both developer and fixer solutions) were measured. Average full-shift exposures to glutaraldehyde, acetic acid, and sulfur dioxide were 0.0009 mg/m3, 0.09 mg/m3, and 0.08 mg/m3, respectively, all more than one order of magnitude lower than current occupational exposure limits. Local exhaust ventilation of the processing machines and use of silver recovery units lowered exposures, whereas the number of films processed per machine and the time spent near the machines increased exposures. Personnel in clinic facilities had higher exposures than those in hospitals. Private clinics were less likely to have local exhaust ventilation and silver recovery units. Their radiographers spent more time in the processor areas and processed more films per machine. Although exposures were low compared with exposure standards, there are good reasons to continue practices to minimize or eliminate exposures: glutaraldehyde and hydroquinone (present in the developer) are sensitizers; the levels at which health effects occur are not yet clearly established, but appear to be lower than current standards; and health effects resulting from the mixture of chemicals are not understood. Developments in digital imaging technology are making available options that do not involve wet-processing of photographic film and therefore could eliminate the use of developer and fixer chemicals altogether.
Numerous epidemiologic studies report associations between outdoor concentrations of particles and adverse health effects. Because personal exposure to particles is frequently dominated by exposure to nonambient particles (those originating from indoor sources), we present an approach to evaluate the relative impacts of ambient and nonambient exposures.
We developed separate estimates of exposures to ambient and nonambient particles of different size ranges (PM2.5, PM10-2.5 and PM10) based on time-activity data and the use of particle sulfate measurements as a tracer for indoor infiltration of ambient particles. To illustrate the application of these estimates, associations between cardiopulmonary health outcomes and the estimated exposures were compared with associations computed using measurements of personal exposures and outdoor concentrations for a repeated-measures panel study of 16 patients with chronic obstructive pulmonary disease conducted in the summer of 1998 in Vancouver.
Total personal fine particle exposures were dominated by exposures to nonambient particles, which were not correlated with ambient fine particle exposures or ambient concentrations. Although total and nonambient particle exposures were not associated with any of the health outcomes, ambient exposures (and to a lesser extent ambient concentrations) were associated with decreased lung function, decreased systolic blood pressure, increased heart rate, and increased supraventricular ectopic heartbeats. Measures of heart rate variability showed less consistent relationships among the various exposure metrics.
These results demonstrate the usefulness of separating total personal particle exposures into their ambient and nonambient components. The results support previous epidemiologic findings using ambient concentrations by demonstrating an association between health outcomes and ambient (outdoor origin) particle exposures but not with nonambient (indoor origin) particle exposures.
BACKGROUND: Little is known about the role of genetic and environmental factors in irritable bowel syndrome. Various extra-intestinal manifestations are more prevalent in cases than in controls. Genetic effects may be important in the liability to develop functional bowel disorders. AIMS: To evaluate the associations of irritable bowel syndrome with several disorders co-morbid with the condition, using both a case-control design and a co-twin control design. METHODS: A sample of 850 Swedish twin pairs, aged 18-85 years, was contacted for a telephone interview. Through a diagnostic algorithm, 72 unrelated cases of irritable bowel syndrome and 216 age- and gender-matched controls were identified. Fifty-eight twin pairs discordant for irritable bowel syndrome were evaluated in co-twin analyses. RESULTS: Renal problems (odds ratio (OR)=3.3; confidence interval (CI), 1.3-8.2), obesity (OR=2.6; CI, 1.0-6.4), underweight in the past (OR=2.4; CI, 1.1-6.4), gluten intolerance (OR=9.0; CI, 1.4-60.1), rheumatoid arthritis (OR=3.2; CI, 1.1-9.4) and poor self-rated health (OR=1.8; CI, 1.0-3.2) were significantly associated with irritable bowel syndrome. In the co-twin analyses, the only factors maintaining significance were renal and recurrent urinary tract problems. CONCLUSIONS: The association between irritable bowel syndrome and renal and urinary tract problems does not reflect a genetic or familial mediation. Eating disorders in childhood represent a familial-environmental influence on irritable bowel syndrome, whereas the association with rheumatoid arthritis and perhaps gluten intolerance probably reflects genetic mediation.
To assess the role of genetic and environmental factors in female alcoholism using a large population-based twin sample, taking into account possible differences between early and late onset disease subtype.
Twins aged 20-47 years from the Swedish Twin Registry (n=24 119) answered questions to establish lifetime alcohol use disorders. Subjects with alcoholism were classified for subtype. Structural equation modeling was used to quantify the proportion of phenotypic variance due to genetic and environmental factors and test whether heritability in women differed from that in men. The association between childhood trauma and alcoholism was then examined in females, controlling for background familial factors.
Lifetime prevalence of alcohol dependence was 4.9% in women and 8.6% in men. Overall, heritability for alcohol dependence was 55%, and did not differ significantly between men and women, although women had a significantly greater heritability for late onset (type I). Childhood physical trauma and sexual abuse had a stronger association with early onset compared to late onset alcoholism [odds ratio (OR) 2.54, 95% confidence interval (CI) 1.53-3.88 and OR 2.29, 95% CI 1.38-3.79 respectively]. Co-twin analysis indicated that familial factors largely accounted for the influence of physical trauma whereas the association with childhood sexual abuse reflected both familial and specific effects.
Heritability of alcoholism in women is similar to that in men. Early onset alcoholism is strongly association with childhood trauma, which seems to be both a marker of familial background factors and a specific individual risk factor per se.
Self-reported joint pain, a typical manifestation of osteoarthritis, was examined using 335 twin pairs from the Swedish Adoption/Twin Study of Aging to estimate relative genetic and environmental influences on self-reported joint pain and to examine the relationships between joint pain, health behavior, and psychological variables. Findings suggest that family resemblance for self-reported joint pain represents similar environments more than genetic similarity. Data from the early 1970s, including exercise, physical activity at work, obesity, and neuroticism, were used to predict joint pain in 1993. For men, moderate amounts of exercise decreased the likelihood of joint pain, but strenuous amounts of physical activity in the workplace had the opposite effect. For women, exercise and physical activity were not significant predictors, but past obesity and higher levels of neuroticism increased the likelihood of reporting joint pain in 1993.