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Biomedical subjects

A Ahlbom

Publications and source records attributed to A Ahlbom.

At least 37 records · Page 2Linked to original sources
PubMed2001

Family history of coronary heart disease, a strong risk factor for myocardial infarction interacting with other cardiovascular risk factors: results from the Stockholm Heart Epidemiology Program (SHEEP).

We explored the relation between family history of coronary heart disease and the risk of myocardial infarction in a case-control study of subjects, 45 to 70 years of age, living in Stockholm, Sweden. Our cases comprised 1091 male and 531 female first-time acute myocardial infarction patients who had survived at least 28 days after their infarction. Referents were randomly selected from the population from which the cases were derived. The adjusted odds ratio (OR) of myocardial infarction was 2.0 (95% confidence interval [CI] = 1.6-2.6) for men reporting > or = 1 affected parent or sibling, compared with men with no family history of coronary heart disease, and 3.4 (95% CI = 2.1-5.9) for those reporting > or = 2 affected parents or siblings. The corresponding OR for women were 2.1 (95% CI = 1.5-3.0) and 4.4 (95% CI = 2.4-8.1). We found evidence for synergistic interactions in women exposed to family history of coronary heart disease in combination with current smoking and with a high quotient between low-density lipoprotein and high-density lipoprotein cholesterol (>4.0), respectively, which yielded adjusted synergy index scores of 2.9 (95% CI = 1.2-7.2) and 3.8 (95% CI = 1.5-9.7), respectively. Similarly, in men we found evidence for interaction for the co-exposure of family history of coronary heart disease and diabetes mellitus. Our study shows that family history of coronary heart disease is not only a strong risk factor for myocardial infarction in both sexes, but that its effect is synergistic with other cardiovascular risk factors as well.

Aged↗
PubMed2001

Sexual activity as a trigger of myocardial infarction. A case-crossover analysis in the Stockholm Heart Epidemiology Programme (SHEEP).

OBJECTIVE: To investigate sexual activity as a trigger of myocardial infarction and the potential effect modification of physical fitness. DESIGN: A case-crossover study nested in the Stockholm Heart Epidemiology Programme (SHEEP). SETTING: Stockholm County from April 1993 to December 1994. PATIENTS: All patients with a first episode of non-fatal acute myocardial infarction admitted to coronary care units were eligible, and 699 patients participated in an interview. MAIN OUTCOME MEASURES: Relative risks with 95% confidence intervals. RESULTS: Only 1.3% of the patients without premonitory symptoms had sexual activity during two hours before the onset of myocardial infarction. The relative risk of myocardial infarction was 2.1 (95% confidence interval (CI) 0.7 to 6.5) during one hour after sexual activity, and the risk among patients with a sedentary life was 4.4 (95% CI 1.5 to 12.9). CONCLUSIONS: The increased risk of myocardial infarction after sexual activity and the further increase in risk among the less physically fit support the hypothesis of causal triggering by sexual activity. However, the absolute risk per hour is very low, and exposure is relatively infrequent. Thus having sex once a week only increases the annual risk of myocardial infarction slightly. Counselling should focus on encouraging patients to live a physically active life and not on abstaining from sexual activity.

Coitus↗
PubMed2001

Paternal occupational exposures and childhood cancer.

The objective of the study described here was to test the hypothesis that paternal occupational exposure near conception increases the risk of cancer in the offspring. We conducted a cohort study based on a population of 235,635 children born shortly after two different censuses in Sweden. The children were followed from birth to 14 years, and cases of cancer were identified in the Swedish Cancer Registry. Occupational hygienists assessed the probability of exposure to different agents in each combination of the father's industry and occupation as reported in the censuses. We also analyzed individual job titles. We compared the cancer incidence among children of exposed fathers to that among children of unexposed fathers using Cox proportional hazards modeling. The main findings were an increased risk of nervous system tumors related to paternal occupational exposure to pesticides [relative risk (RR) = 2.36; 95% confidence interval (CI), 1.27-4.39] and work as a painter (RR = 3.65; 95% CI, 1.71-7.80), and an increased risk of leukemia related to wood work by fathers (RR = 2.18; 95% CI, 1.26-3.78). We found no associations between childhood leukemia and paternal exposure to pesticides or paint. Our results support previous findings of an increased risk of childhood brain tumors and leukemia associated with certain paternal occupational exposures. Some findings in previous studies were not confirmed in this study.

Adult↗
PubMed2000

Does heavy physical exertion trigger myocardial infarction? A case-crossover analysis nested in a population-based case-referent study.

To study possible triggering of first events of acute myocardial infarction by heavy physical exertion, the authors conducted a case-crossover analysis (1993-1994) within a population-based case-referent study in Stockholm County, Sweden (the Stockholm Heart Epidemiology Program). Interviews were carried out with 699 myocardial infarction patients after onset of the disease. These cases represented 47 percent of all cases in the study base, and 70 percent of all nonfatal cases. The relative risk from vigorous exertion was 6.1 (95% confidence interval: 4.2, 9.0). The rate difference was 1.5 per million person-hours, and the attributable proportion was 5.7 percent. The risk was modified by physical fitness, with an increased risk being seen among sedentary subjects as in earlier studies, but the data also suggested a U-shaped association. In addition, the trigger effect was modified by socioeconomic status. Premonitory symptoms were common, and this implies risks of reverse causation bias and misclassification of case exposure information that require methodological consideration. Different techniques (the use of the usual-frequency type of control information, a pair-matched analysis, and a standard case-referent analysis) were applied to overcome the threat of misclassification of control exposure information. A case-crossover analysis in a random sample of healthy subjects resulted in a relative risk close to unity, as expected.

Aged↗
PubMed2000

Parental occupational exposure to magnetic fields and childhood cancer (Sweden).

OBJECTIVES: To test the hypothesis that parental occupational exposure to magnetic fields before conception and during pregnancy increases the risk of cancer in the offspring. METHODS: The study is designed as a cohort study based on a population of 235,635 children born shortly after two different censuses in Sweden. The children were followed from birth to 14 years and cases of cancer were identified in the Swedish cancer registry. The parents' occupational titles in the censuses were linked to a job-exposure matrix with information about magnetic field levels in different occupations. The cancer incidence among the exposed was compared to that among the unexposed using Cox proportional hazards modeling. RESULTS: There was no association between childhood cancer and maternal occupational magnetic field exposure. Paternal exposure was associated with an increased risk of childhood leukemia, with a relative risk of 2.0 (95% CI 1.1-3.5) for exposures > or = 0.30 microT. A decreased risk was found for brain tumors (RR = 0.5; 95% CI 0.3-1.0). CONCLUSIONS: The results do not support previous findings of an increased risk of childhood brain tumors associated with paternal occupational exposure to magnetic fields. The finding for childhood leukemia has to be interpreted with caution.

Adolescent↗
PubMed2000

A pooled analysis of magnetic fields and childhood leukaemia.

Previous studies have suggested an association between exposure to 50-60 Hz magnetic fields (EMF) and childhood leukaemia. We conducted a pooled analysis based on individual records from nine studies, including the most recent ones. Studies with 24/48-hour magnetic field measurements or calculated magnetic fields were included. We specified which data analyses we planned to do and how to do them before we commenced the work. The use of individual records allowed us to use the same exposure definitions, and the large numbers of subjects enabled more precise estimation of risks at high exposure levels. For the 3203 children with leukaemia and 10 338 control children with estimated residential magnetic field exposures levels < 0.4 microT, we observed risk estimates near the no effect level, while for the 44 children with leukaemia and 62 control children with estimated residential magnetic field exposures >/= 0.4 microT the estimated summary relative risk was 2.00 (1.27-3.13), P value = 0.002). Adjustment for potential confounding variables did not appreciably change the results. For North American subjects whose residences were in the highest wire code category, the estimated summary relative risk was 1.24 (0.82-1.87). Thus, we found no evidence in the combined data for the existence of the so-called wire-code paradox. In summary, the 99.2% of children residing in homes with exposure levels < 0.4 microT had estimates compatible with no increased risk, while the 0.8% of children with exposures >/= 0.4 microT had a relative risk estimate of approximately 2, which is unlikely to be due to random variability. The explanation for the elevated risk is unknown, but selection bias may have accounted for some of the increase.

Adolescent↗
PubMed2000

Occupational and residential magnetic field exposure and breast cancer in females.

The purpose of this study was to evaluate the effect of occupational magnetic field exposure on breast cancer in females and to combine residential and occupational magnetic field exposure to reduce misclassification. The study was conducted as a case-control study within a population living within 300 meters of transmission lines in Sweden. We identified cases of breast cancer in females from the national cancer registry, and we selected one matched control per case at random. Residential exposure was estimated through calculations of the magnetic fields generated by power lines. We obtained information about occupation from censuses, and the occupations were linked to a job-exposure matrix that was based on magnetic field measurements. For occupational exposure to magnetic fields over 0.25 microT closest in time before diagnosis, the estimated relative risk was 1.0 [96% confidence interval (CI) = 0.6-1.7]. Women below age 50 years at diagnosis had a relative risk of 1.5 (95% CI = 0.6-3.5). For women below 50 years of age who had estrogen receptor-positive breast cancer, there was a relative risk of 3.2 (95% CI = 0.5-18.9). The results for residential and occupational exposures combined showed similar results.

Biomarkers, Tumor↗
PubMed2000

Occupational exposures and pancreatic cancer: a meta-analysis.

OBJECTIVES: Consolidation of epidemiological data on pancreatic cancer and worksite exposures. METHODS: Publications during 1969-98 were surveyed. Studies without verified exposures were excluded. Meta-analyses were conducted on data from 92 studies covering 161 populations, with results for 23 agents or groups of agents. With a standard format, five epidemiologists extracted risk estimates and variables of the structure and quality of each study. The extracted data were centrally checked. Random meta-models were applied. RESULTS: Based on 20 populations, exposure to chlorinated hydrocarbon (CHC) solvents and related compounds was associated with a meta-risk ratio (MRR) of 1.4 (95% confidence interval (95% CI) 1.0 to 1.8). Nickel and nickel compounds were considered in four populations (1.9; 1.2 to 3.2). Excesses were found also for chromium and chromium compounds (1.4; 0.9 to 2.3), polycyclic aromatic hydrocarbons (PAHs) (1.5; 0.9 to 2.5), organochlorine insecticides (1.5; 0.6 to 3.7), silica dust (1.4; 0.9 to 2.0), and aliphatic and alicyclic hydrocarbon solvents (1.3; 0.8 to 2.8). Evidence on pancreatic carcinogenicity was weak or non-positive for the following agents: acrylonitrile (1.1; 0.0 to 6.2); arsenic (1.0; 0.6 to 1.5); asbestos (1.1; 0.9 to 1.5); diesel engine exhaust (1.0; 0.9 to 1.3); electromagnetic fields (1.1; 0.8 to 1.4); formaldehyde (0. 8; 0.5 to 1.0); flour dust (1.1; 0.3 to 3.2); cadmium and cadmium compounds (0.7; 0.4 to 1.4); gasoline (1.0; 0.8 to 1.2); herbicides (1.0; 0.8 to 1.3); iron and iron compounds (1.3; 0.7 to 2.5); lead and lead compounds (1.1; 0.8 to 1.5); man-made vitreous fibres (1.0; 0.6 to 1.6); oil mist (0.9; 0.8 to 1.0); and wood dust (1.1; 0.9 to 2.5). The occupational aetiological fraction of pancreatic cancer was estimated at 12%. In a subpopulation exposed to CHC solvents and related compounds, it was 29%; to chromium and chromium compounds, 23%; to nickel and nickel compounds, 47%; to insecticides, 33%; and to PAHs, 33%. CONCLUSION: Occupational exposures may increase risk of pancreatic cancer. High quality studies are called for on interactions between occupational, environmental, and lifestyle factors as well as interactions between genes and the environment.

Air Pollutants, Occupational↗
PubMed2000

Plasma levels of tissue plasminogen activator/plasminogen activator inhibitor-1 complex and von Willebrand factor are significant risk markers for recurrent myocardial infarction in the Stockholm Heart Epidemiology Program (SHEEP) study.

An impaired fibrinolytic function due to elevated plasma levels of plasminogen activator inhibitor (PAI)-1 activity or tissue plasminogen activator (tPA) antigen is correlated with the development of myocardial infarction (MI) in patients with manifest coronary heart disease. Recently, methods for determining the specific tPA/inhibitor complexes constituting tPA antigen in plasma have become available. In the Stockholm Heart Epidemiology Program (SHEEP) study, 86 of 1212 MI patients, subjected to blood sampling in a metabolically stable period, suffered reinfarction before the end of 1996. These individuals have been compared with an approximately equal number of matched MI patients without recurrence and a group of matched healthy control subjects regarding the plasma concentrations of some hemostatic factors. The hemostatic compounds studied (fibrinogen, von Willebrand factor, tPA antigen, PAI-1, and the tPA/PAI-1 complex) were typically higher in the groups (men and women) with recurrence of MI compared with those without. The plasma concentrations were also typically higher in the pooled groups of patients compared with the groups of healthy control subjects. The largest between-group differences were found for the plasma tPA/PAI-1 complex. The crude odds ratio for reinfarction associated with higher concentration (>/=75th percentile among the control subjects) of tPA/PAI-1 was 1.8 (95% CI 1.1 to 3.1); the corresponding crude odds ratio for von Willebrand factor was 2.3 (1. 3 to 4.0). The tPA/PAI-1 complex correlated strongly with PAI-1 and tPA antigen in all groups and with serum triglycerides and body mass index in all groups except for women with reinfarction. An increased plasma level of tPA/PAI-1 complex is a novel risk marker for recurrent MI in men and women. Most likely, increased plasma levels of tPA/PAI-1 complex reflect impaired fibrinolysis, because the correlation with PAI-1 is strong. Further support is obtained indicating that the plasma concentration of von Willebrand factor is also an important risk marker for recurrent MI.

Aged↗
PubMed1999

Role of medical history in brain tumour development. Results from the international adult brain tumour study.

In an international population-based case-control study carried out in 8 centres in 6 countries, we investigated the role of specific medical conditions in the aetiology of brain tumours in adults. Recruited were 1,178 glioma and 331 meningioma cases and 2,493 age- and gender-matched population controls. Only medical conditions occurring at least 2 years before brain tumour diagnosis were considered. Relative risks (RRs) and 95% confidence intervals (CIs) were estimated using a conditional logistic regression model. Heterogeneity between centres was tested. No association between meningioma and previous medical conditions was observed. For glioma, there was an increased risk associated with epilepsy (RR = 6.55, 95% CI 3.40-12.63), but this was considerably weaker for epilepsy of more than 20 years duration. The risk remained elevated after adjustment for use of anti-epileptic drugs. There was a statistically significant inverse association between glioma and all allergic diseases combined (RR = 0.59, 95% CI 0.49-0.71); this was also observed for specific allergic conditions, namely, asthma and eczema. Subjects who reported a history of infectious diseases (e.g., colds, flu) showed a 30% reduction in risk (RR = 0.72, 95% CI 0.61-0.85). The decreased risks for glioma in subjects reporting a history of allergic conditions or infectious diseases may indicate an influence of immunological factors on the development of glioma. The association between glioma and epilepsy has to be interpreted cautiously and needs further investigation.

Adult↗
PubMed1999

DNA copy number losses at 1p32-pter in monozygotic twins concordant for breast cancer.

To find similarities that may possibly indicate novel mutations, we performed comparative genomic hybridization (CGH) analysis following degenerate oligonucleotide primed polymerase chain reaction (PCR) for DNA obtained from unique material of breast cancer that developed in monozygotic twin-pairs. Polymerase chain reaction amplification was successful in 12 samples for 11 patients, including 3 pairs. Six samples exhibited DNA copy number changes. Gains (76%) were more frequent than losses (24%). Gains or high-level amplifications in 8q were present in all but 1 of the abnormal cases. Frequent gains were detected with a minimal common overlapping region at 5p (4 cases), at 1q25-qter (3 cases), and at 20q12-qter (2 cases). The most frequent loss, detected in half of the abnormal cases, was at 1p32-pter. One twin-pair showed similar changes in 4 chromosomal locations involving loss of 1p32-pter and gains in 1q25-qter, 5, and 8q.

Base Sequence↗
PubMed1999

Mortality and cancer incidence in biomedical laboratory personnel in Sweden.

BACKGROUND: The work in biomedical laboratories is associated with exposure to a mixture of known and potential chemical carcinogens, mutagens, and teratogens. Previous studies have suggested an excess of brain tumors and hematopoietic system malignancies as well as breast cancers in women. METHODS: This retrospective cohort study investigated the standardized mortality ratio (SMR) and the standardized incidence ratio (SIR) for cancer in biomedical research laboratory personnel in Swedish universities 1970-1992. The cohort comprised 5,035 laboratory and, as an internal reference group, 2,923 nonlaboratory employees. RESULTS: The overall death rate was lower in both groups than in the general population. The SIR for brain tumors among male laboratory workers was 1.69 (0.62-3.68) and among male laboratory scientists, after more than 10 years of work (4 cases), it was 3.11 (0.85-7.56). There was an elevated SIR for malignant melanoma among female scientists in laboratories (3.51, 0.96-8.98) and for male scientists in nonlaboratory departments (2.86, 1.05-6.22). The SIR for breast cancer among female laboratory scientists was 1.62 (0.78-2.98). CONCLUSIONS: The present findings lend some support to an excess of brain tumors among male scientists and of breast cancer in female scientists in biomedical research laboratories.

Adult↗