The prevention of suicidal behavior is one of the most important tasks for mental health clinicians. Although a few studies have indicated an increased risk of suicidal behavior among individuals with attention-deficit/hyperactivity disorder, the development of more effective ways of identifying and modifying the risk is hampered by our limited understanding of the underlying mechanisms for this association.
To explore whether attention-deficit/hyperactivity disorder and suicidal behavior share genetic and environmental risk factors.
Matched cohort design across different levels of family relatedness recorded from January 1, 1987, to December 31, 2009. We identified 51?707 patients with attention-deficit/hyperactivity disorder (through patient and prescribed drug registers) in Sweden and their relatives by linking longitudinal population-based registers. Control participants were matched 1:5 on sex and birth year.
Any record of suicide attempt or completed suicide defined by discharge diagnoses of the International Classification of Diseases.
Individuals with attention-deficit/hyperactivity disorder (probands) had increased risks of attempted and completed suicide, even after adjusting for comorbid psychiatric disorders (odds ratio [OR]?=?3.62 [95% CI, 3.29-3.98] and 5.91 [95% CI, 2.45-14.27], respectively). The highest familial risk was observed among first-degree relatives (attempted suicide: OR?=?2.42 [95% CI, 2.36-2.49] among parents of probands with ADHD and OR?=?2.28 [95% CI, 2.17-2.40] among full siblings of probands with ADHD; completed suicide: OR?=?2.24 [95% CI, 2.06-2.43] and OR?=?2.23 [1.83-2.73], respectively), whereas the risk was considerably lower among more genetically distant relatives (attempted suicide: OR?=?1.59 [95% CI, 1.47-1.73] among maternal half siblings, OR?=?1.57 [95% CI, 1.45-1.70] among paternal half siblings, and OR?=?1.39 [95% CI, 1.35-1.43] among cousins; completed suicide: OR?=?1.51 [95% CI, 1.08-2.10], OR?=?2.02 [95% CI, 1.47-2.79], and OR?=?1.51 [95% CI, 1.36-1.67], respectively). These familial aggregation patterns remained similar across sex, after excluding relatives with attention-deficit/hyperactivity disorder and probands with suicidal behavior, and after excluding probands and relatives with severe comorbid disorders.
Attention-deficit/hyperactivity disorder is associated with an increased risk of both attempted and completed suicide. The pattern of familial risks across different levels of relatedness suggests that shared genetic factors are important for this association. This is an important first step toward identifying the underlying mechanisms for the risk of suicidal behavior in patients with attention-deficit/hyperactivity disorder and suggests that individuals with attention-deficit/hyperactivity disorder and their family members are important targets for suicide prevention and treatment.
Celiac disease (CD) is a major public health problem with estimated 1-3% prevalence in the general population. In recent years an increase in CD prevalence has been reported both in Sweden and worldwide. This study aimed at examining the annual incidence rate of biopsy-proven celiac disease among children in Sweden over a 36-year period, to assess variations by age, sex and birth cohort, and to assess the clinical impact of these changes.
The National Swedish Childhood CD Register was used to identify 9107 children aged 0-14.9 years who were diagnosed with CD during the period 1973 to 2009. From 1973 to 1990 the register covered 15% of the nation, this increased to 40% during 1991-1997; a full national coverage was obtained from 1998 onwards. Estimations for the annual incidence rate, cumulative incidence and clinical impact by age groups, calendar month and birth cohorts were made.
CD incidence is continuing to increase in the child population aged 2-14.9 years. A continued variation in CD incidence was observed in children aged 0-1.9 years, characterized by a marked decrease in most recent years. The median age at diagnosis has increased from 1.0 year in the 1970s to 6.8 years in 2009. The average number of new cases has risen from ~200 during 1973-1983 to ~600 during 2004-2009. In the birth cohorts of 2000-2002 the cumulative incidence even exceeded that of the epidemic cohorts at comparable ages. The highest cumulative incidence was observed in the birth cohorts of 1985-1995 and 2000-2002.
CD risk varies between birth cohorts, suggesting cyclic environmental and/or lifestyle risk factors in CD etiology. More research on underlying risk factors is required in order to move forward with preventive strategies.
Cites: Gut. 2013 Jan;62(1):43-5222345659
Cites: N Engl J Med. 2002 Sep 19;347(12):911-2012239261
The authors conducted an analysis of all 677 cases of Kaposi's sarcoma among the 3,047 cases of acquired immunodeficiency syndrome diagnosed in homosexual/bisexual men in Canada between 1980 and 1989. The proportion with Kaposi's sarcoma declined from 32.2% during 1980-1985 to 15.0% in 1989. The proportion with Kaposi's sarcoma was significantly higher in primary epidemic centers (Vancouver, Toronto, and Montreal) and in men in the 1945-1954 birth cohort independent of year of diagnosis. These data are consistent with an environmental cofactor for Kaposi's sarcoma which is likely to be a sexually transmitted agent.
Although unemployment may be a stressful life event, its association with coronary heart disease (CHD) remains unclear. This study examines the association between unemployment and later hospitalisation due to CHD.
The study was based on a Swedish military conscription cohort of 18 to 20-year-old men from 1969/1970 (n=49 321) with information provided on health status and health behaviours. Information on unemployment in middle age was obtained from national registers. CHD information was obtained from hospital registers and the cause of death register. Cox proportional hazard analyses were run on the 39 243 individuals who were in paid employment in 1996 and 1997.
It was found that =90 days of unemployment was associated with subsequent CHD during 8 years follow-up (crude HR=1.47, 95% CI 1.23 to 1.75). Controlling for known risk factors for CHD reduced the association but a significant association remained (HR=1.24, 95% CI 1.04 to 1.48); =90 days of unemployment was significantly associated with CHD during the first 4 years (HR adjusted for known risk factors=1.31, 95% CI 1.01 to 1.71).
Unemployment was associated with increased risk of CHD after adjustment for confounders. We interpret the increased risk of CHD associated with unemployment as potentially the somatic result of a process started by stress.
Beginning in 1948, the Soviet Union initiated a program for production of nuclear materials for a weapons program. The first facility for production of plutonium was constructed in the central portion of the country east of the southern Ural Mountains, about halfway between the major industrial cities of Ekaterinburg and Chelyabinsk. The facility, now known as the Mayak Production Association, and its associated town, now known as Ozersk, were built to irradiate uranium in reactors, separate the resulting plutonium in reprocessing plants, and prepare plutonium metal in the metallurgical plant. The rush to production, coupled with inexperience in handling radioactive materials, led to large radiation exposures, not only to the workers in the facilities, but also to the surrounding public. Fuel processing started with no controls on releases, and fuel dissolution and accidents in reactors resulted in release of ~37 PBq of I between 1948 and 1967. Designed disposals of low- and intermediate-level liquid radioactive wastes, and accidental releases via cooling water from tank farms of high-level liquid radioactive wastes into the small Techa River, caused significant contamination and exposures to residents of numerous small riverside villages downstream of the site. Discovery of the magnitude of the aquatic contamination in late 1951 caused revisions to the waste handling regimes, but not before over 200 PBq of radionuclides (with large contributions of Sr and Cs) were released. Liquid wastes were diverted to tiny Lake Karachay (which today holds over 4 EBq); cooling water was stopped in the tank farms. In 1957, one of the tanks in the tank farm overheated and exploded; over 70 PBq, disproportionately Sr, was blown over a large area to the northeast of the site. A large area was contaminated and many villages evacuated. This area today is known as the East Urals Radioactive Trace (EURT). Each of these releases was significant; together they have created a unique group of cohorts with their chronic, low dose-rate radiation exposure. The 26,000 workers at Mayak were highly exposed to external gamma and inhaled plutonium. A cohort of individuals raised as children in Ozersk is under evaluation for their exposures to radioiodine. The Techa River Cohort consists of over 30,000 people who were born before the start of exposure in 1949 and lived along the Techa River. The Techa River Offspring Cohort consists of ~21,000 persons born to one or more exposed parents of this group, many who also lived along the contaminated river. The EURT Cohort consists of ~18,000 people who were evacuated from the EURT soon after the 1957 explosion and another 8,000 who remained. These groups together are the focus of dose reconstruction and epidemiological studies funded by the United States, Russia, and the European Union to address the question, "Are doses delivered at low dose rates as effective in producing health effects as the same doses delivered at high dose rates?"Introduction of Joint U.S. and Russian Studies of Population Exposures (Video 2:13, http://links.lww.com/HP/A28).
One of the largest reported campylobacteriosis outbreaks in Canada occurred in June 2007 in British Columbia, associated with a mountain bike race that took place in muddy conditions. A retrospective cohort study was conducted and environmental samples were collected and tested. There were 537 racers included in the study and 225 racers (42%) reported diarrhoeal illness after the race. C. jejuni clinical isolates (n=14) were found to be identical by multi-locus sequence typing. Although univariate analysis suggested water consumption and mud exposure as significant risk factors, multivariate analysis revealed that on direct ingestion mud was significantly associated with illness (OR 4·08, 95% CI 2·03-8·21). Contaminated mud was thus the most likely source of Campylobacter infection. We identified other unpublished reports of outbreaks associated with bike races in rainy or muddy conditions; these underscore the importance of educating racers and raising public awareness of the risks of mud ingestion.
Osteoporosis is a major health problem affecting more than 75 million people throughout Europe, the United States, and Japan. Epidemiologic studies have determined that both genetic and environmental factors contribute to the pathogenesis of osteoporosis. We have investigated the association between polymorphisms at the osteocalcin locus and variables linked to bone health. Osteocalcin provides a link between bone and energy metabolism, hence its potential importance as an osteoporosis candidate gene. In this study, we included a total of 996 women (all aged 75 years) from the Osteoporosis Prospective Risk Assessment (OPRA) cohort. We sequenced the osteocalcin gene along with flanking regions to search for novel coding polymorphisms. We also analyzed four polymorphisms selected from within and flanking regions of the osteocalcin gene to study their association with serum total osteocalcin levels (S-TotalOC), total-body (TB) bone mineral density (BMD), fracture, TB fat mass, and body mass index (BMI). The promoter polymorphism rs1800247 was significantly associated with S-TotalOC (p = .012) after controlling for BMI and TB BMD. The polymorphism rs1543297 was significantly associated with prospectively occurring fractures (p = .008). In a model taking into account rs1543297 and rs1800247, along with TB BMD, BMI, smoking, and S-TotalOC, the polymorphisms together were able to identify an additional 6% of women who sustained a fracture (p = .02). We found no association between the polymorphisms and TB BMD, BMI, or TB fat mass. In conclusion, polymorphisms in and around the osteocalcin locus are significantly associated with S-TotalOC and fracture. Genotyping at the osteocalcin locus could add valuable information in the identification of women at risk of osteoporosis.
The objective of this study was to assess respiratory outcomes and environmental exposure levels of workers in cage-housed and floor-housed poultry operations.
Poultry operations were evaluated for total dust, endotoxin, and ammonia, and respiratory symptoms and lung function tests of workers were conducted.
Workers in floor-housed poultry operations had significantly greater exposures to total dust and ammonia, whereas workers from cage-housed poultry operations reported greater frequency of current and chronic symptoms overall and significantly greater current and chronic phlegm (39% vs 18% and 40% vs 11%, respectively). Endotoxin concentration (EU/mg) was a significant predictor (P = 0.05) of chronic phlegm for all poultry workers.
Greater endotoxin concentration in the presence of significantly lower total dust, in conjunction with greater respiratory symptoms in workers from cage-housed poultry operations, as compared with workers from floor-housed poultry operations, appears to indicate that differences in environmental exposures may impact respiratory outcomes of workers.
This study was undertaken to investigate geographic residence in Vancouver's Downtown Eastside (DTES), Canada's poorest urban neighborhood, as an environmental risk factor for HIV infection among a cohort of injection drug users. HIV incidence rates were examined using Kaplan-Meier methods, and Cox proportional hazards regression was used to determine independent risk factors for HIV seroconversion. After intensive multivariate adjustment, DTES residence remained an independent predictor of HIV seroconversion (relative hazard=2.0, 95% CI: 1.4-3.0, p
The Central Drug Registry in Finland ascertained 5,920 incident cases of Type 1 (insulin-dependent) diabetes mellitus diagnosed under the age of 15 years, during 1965-1984. The incidence was higher for males 29.2/100,000 (95% confidence intervals 28.2-30.2/100,000) than for females 26.1/100,000 (25.1-27.1/100,000). A non-linear increase in incidence with age was confirmed, with peaks at ages 2, 9 and 14 years in males and at 3, 5-6 and 11 years in females. A significant temporal variation in incidence was found, adjusting for age and sex. During 1965 to 1984 the incidence rose by about 57% or by 2.4% annually. However, a non-linear curve with two incidence peaks in 1978 and 1983 would better describe the temporal pattern than a linear trend. There was no significant difference in the temporal variation between males and females. The changes in diabetes risk appeared to affect proportionally all age groups under 15 years. Two possible mechanisms were explored: a calendar period effect vs a birth cohort effect. The calendar time period effect was significant alone and also when adjusted for the birth cohort effect. One the contrary, the birth cohort effect was not significant, when adjusted for the calendar period effect. In conclusion, over the past two decades, the incidence of childhood Type 1 diabetes in Finland has increased by about 57%. The pattern of change was a steady rising background incidence superimposed by sudden outbreaks suggesting environmental causative factors.
The problems of differentiation between environmental and genetic influences on the development of multiple sclerosis are well known. Twin studies may provide valuable information on this question. However, most published twin series are selected and no through clinical twin studies based on epidemiologic series have been carried out. In this study, all available same-sex twin pairs with clinically definite multiple sclerosis derived from the Finnish Twin Cohort of 15815 pairs were studied by clinical evaluation, magnetic resonance imaging, and visual and auditory evoked responses. The mean length of follow-up of the pairs after the onset of symptoms of multiple sclerosis was 20 years. Two of the seven monozygotic pairs were concordant; one was definitely so, and in the other, the co-twin of the index case had, in addition to clinical findings, white matter changes suggestive of multiple sclerosis in magnetic resonance imaging and abnormal visual evoked responses. All six dizygotic pairs were discordant. The frequency of the HLA antigen DR2 in probands (69%) was significantly increased, but the distribution among the healthy subjects and patients showed nonsignificant differences. The results indicate a genetic influence on the susceptibility to multiple sclerosis, although still unknown genetic determinants are possible involved.
Childhood lead exposure has been associated with growth delay. However, the association between blood lead levels (BLLs) and insulin-like growth factor 1 (IGF-1) has not been characterized in a large cohort with low-level lead exposure.
We recruited 394 boys 8-9 years of age from an industrial Russian town in 2003-2005 and followed them annually thereafter. We used linear regression models to estimate the association of baseline BLLs with serum IGF-1 concentration at two follow-up visits (ages 10-11 and 12-13 years), adjusting for demographic and socioeconomic covariates.
At study entry, median BLL was 3 µg/dL (range,
Cites: Life Sci. 1984 Oct 22;35(17):1747-546090848
Laboratory studies suggest that fine particulate matter (= 2.5 ?m in diameter; PM(2.5)) can activate pathophysiological responses that may induce insulin resistance and type 2 diabetes. However, epidemiological evidence relating PM2.5 and diabetes is sparse, particularly for incident diabetes.
We conducted a population-based cohort study to determine whether long-term exposure to ambient PM(2.5) is associated with incident diabetes.
We assembled a cohort of 62,012 nondiabetic adults who lived in Ontario, Canada, and completed one of five population-based health surveys between 1996 and 2005. Follow-up extended until 31 December 2010. Incident diabetes diagnosed between 1996 and 2010 was ascertained using the Ontario Diabetes Database, a validated registry of persons diagnosed with diabetes (sensitivity = 86%, specificity = 97%). Six-year average concentrations of PM2.5 at the postal codes of baseline residences were derived from satellite observations. We used Cox proportional hazards models to estimate the associations, adjusting for various individual-level risk factors and contextual covariates such as smoking, body mass index, physical activity, and neighborhood-level household income. We also conducted multiple sensitivity analyses. In addition, we examined effect modification for selected comorbidities and sociodemographic characteristics.
There were 6,310 incident cases of diabetes over 484,644 total person-years of follow-up. The adjusted hazard ratio for a 10-?g/m(3) increase in PM(2.5) was 1.11 (95% CI: 1.02, 1.21). Estimated associations were comparable among all sensitivity analyses. We did not find strong evidence of effect modification by comorbidities or sociodemographic covariates.
This study suggests that long-term exposure to PM2.5 may contribute to the development of diabetes.
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Cites: Circulation. 2012 Feb 14;125(6):767-7222219348
This study aims to (i) evaluate relative risks, excess fraction of cases, and rate advancement periods for total hip replacement (THR) due to primary osteoarthritis in relation to lifelong cumulative physical workload and (2) describe temporal trends in the proportion employed in the most highly exposed industries from 1986-2006.
In a cohort study of the Danish working population, we assessed cumulative physical workload by combining year-by-year register information on employment industry with an industry exposure matrix that provided point scores (0-2) of physical workload. Cumulative physical workload was expressed as point-years corresponding to the pack-year concept of smoking. We retrieved register information on first-time THR during 1996-2006 and used a logistic regression technique to fit discrete time hazards models adjusting for age and other factors. We calculated excess fraction of cases and rate advancement periods.
Total numbers of point-years ranged from 0-86. For men, an exposure-response relation was observed reaching an odds ratio of 1.33 [95% confidence interval (95% CI) 1.17-1.53] for the highest exposure category (35-86 point-years) compared to 0 point-years. The excess fraction of cases was 18%, and THR took place up to 3.4 years earlier with increasing exposure. For women, no exposure-response relation was found.
At the population level, cumulative physical workload increased the risk of THR among men, with surgery being performed slightly earlier in life. The proportion employed in the most highly exposed industries remained constant.
Socioeconomic differences in morbidity and mortality, particularly across educational groups, are widening. Differential exposures to behavioural risk factors have been shown to play an important mediating role on the social inequality in chronic diseases such as heart disease, cerebrovascular disease, chronic obstructive pulmonary disease, and lung cancer. However, much less attention has been given to the potential role of interaction, where the same level of exposure to a behavioural risk factor has different effect across socioeconomic groups, creating subgroups that are more vulnerable than others. In this thesis, Paper 1 describes the unique cohort consortium which was established by pooling and harmonising prospective data from existing cohort studies in Denmark. This consortium generated a large study population with long follow-up sufficient to study power demanding questions of mechanisms underlying social inequalities in chronic disease outcomes. In Paper 2 on incidence of coronary heart disease, smoking and body mass index partially mediated the observed educational differences. This result suggested that some of the social inequality in coronary heart disease may be enhanced by differential exposure to behavioural risk factors (i.e. smoking and obesity). In Paper 3 on incidence of stroke, an observed interaction between education and smoking indicated that participants, particularly men, with low level of education may be more vulnerable to the effect of smoking than those with high level of education in terms of ischemic stroke. Finally, Paper 4 revealed that behavioural risk factors, primarily smoking, explained a considerable part of the educational differences in cause-specific mortality. Further, this paper added important knowledge about the considerable part of the mediated effect, which could be due to interaction between education and smoking. In conclusion, the research in this thesis is a practical implementation of contemporary statistical methodology, the additive hazards models, in which the potential role of behavioural risk factors can be regarded not only as mediation but also as interaction with the effect of socioeconomic position on chronic disease outcomes. The results support that two central mechanisms, differential exposure and differential vulnerability to behavioural risk factors, particularly smoking; have contributed substantially to the social inequality in chronic disease outcomes in Denmark. These mechanism are not mutually exclusive and should be regarded simultaneously. However, the findings could be non-causal associations due to, for instance, psychosocial or environmental factors. Nevertheless, research on social inequality in chronic disease outcomes should regard not only that the smoking prevalence is higher in lower socioeconomic groups (differential exposure), but also that health consequences of being a smoker seem to be worse in these subgroups (differential vulnerability).
Established causes of diabetes do not fully explain the present epidemic. High-level arsenic exposure has been implicated in diabetes risk, but the effect of low-level arsenic exposure in drinking water remains unclear.
We sought to determine whether long-term exposure to low-level arsenic in drinking water in Denmark is associated with an increased risk of diabetes using a large prospective cohort.
During 1993-1997, we recruited 57,053 persons. We followed each cohort member for diabetes occurrence from enrollment until 31 December 2006. We traced and geocoded residential addresses of the cohort members and used a geographic information system to link addresses with water-supply areas. We estimated individual exposure to arsenic using all addresses from 1 January 1971 until the censoring date. Cox proportional hazards models were used to model the association between arsenic exposure and diabetes incidence, separately for two definitions of diabetes: all cases and a more strict definition in which cases of diabetes based solely on blood glucose results were excluded.
Over a mean follow-up period of 9.7 years for 52,931 eligible participants, there were a total of 4,304 (8.1%) diabetes cases, and 3,035 (5.8%) cases of diabetes based on the more strict definition. The adjusted incidence rate ratios (IRRs) per 1-µg/L increment in arsenic levels in drinking water were as follows: IRR = 1.03 (95% CI: 1.01, 1.06) and IRR = 1.02 (95% CI: 0.99, 1.05) for all and strict diabetes cases, respectively.
Long-term exposure to low-level arsenic in drinking water may contribute to the development of diabetes.
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Maternal smoking during pregnancy is associated with significant infant morbidity and mortality, and may influence later disease risk. One mechanism by which smoking (and other environmental factors) might have long-lasting effects is through epigenetic modifications such as DNA methylation.
We conducted an epigenome-wide association study (EWAS) investigating alterations in DNA methylation in infants exposed in utero to maternal tobacco smoke, using the Norway Facial Clefts Study.
The Illumina HumanMethylation450 BeadChip was used to assess DNA methylation in whole blood from 889 infants shortly after delivery. Of 889 mothers, 287 reported smoking-twice as many smokers as in any previous EWAS of maternal smoking. CpG sites related to maternal smoking during the first trimester were identified using robust linear regression.
We identified 185 CpGs with altered methylation in infants of smokers at genome-wide significance (q-value
Hospital readmissions are increasingly used as a quality indicator with a belief that they are a marker of poor care and have led to financial penalties in UK and USA. Risk scoring systems, such as LACE and HOSPITAL, have been proposed as tools for identifying patients at high risk of readmission but have not been validated in international populations.
To perform an external independent validation of the HOSPITAL and LACE scores.
An unplanned secondary cohort study.
Patients admitted to the medical admission unit at the Hospital of South West Jutland (10/2008-2/2009; 2/2010-5/2010) and the Odense University Hospital (6/2009-8/2011) were analysed. Validation of the scores using 30 day readmissions as the endpoint was performed.
A total of 19?277 patients fulfilled the inclusion criteria. Median age was 67 (range 18-107) years and 8977 (46.6%) were female. The LACE score had a discriminatory power of 0.648 with poor calibration and the HOSPITAL score had a discriminatory power of 0.661 with poor calibration. The HOSPITAL score was significantly better than the LACE score for identifying patients at risk of 30 day readmission (P?
Previous findings on the association between stress during pregnancy and pregnancy loss are inconsistent. We aimed to estimate this association using a large prospective cohort.
This population-based study included all 1 303 660 clinically recognised pregnancies in Denmark between 1995 and 2008. We categorised women as exposed to severe stress if they lost a child, sibling or parent during pregnancy. Cox Proportional Hazards models were used to study the association between exposure and rate of fetal death, starting with the follow-up on the day of completion of week 4 of pregnancy. In an attempt to control for unknown potential confounders, we also designed a pregnancy-matched analysis in which each woman had her own baseline risk of pregnancy loss and controls therefore for genetic and time-stable environmental factors.
A total of 146 031 pregnancies ended in clinically recognised fetal loss (11.2%) and a total of 10 808 (0.8%) women were categorised as exposed. The overall risk of pregnancy loss was similar in the exposed and unexposed (aHR=1.05, 95% CI 0.95 to 1.15). Results from the pregnancy-matched analysis (performed in 423 women) showed stronger and significant associations (aHR=1.83, 95% CI 1.49 to 2.25). All the analyses indicated a stronger effect of bereavement when the mother lost a child or when the death was unexpected.
Our main results suggested no strong association between severe stress during pregnancy and risk of pregnancy loss. Results from the pregnancy-matched analyses considered information from a selected and small group of women for whom there may exist a stronger association between stress during pregnancy and pregnancy loss. The fact that an unexpected death or the loss of a child had a stronger effect in both analyses may indicate that severe stressful situations increase the risk of pregnancy loss.
Our aim was to assess the mortality of fishermen and fishermen's wives in Finland, presuming that the mortality reflects their high consumption of contaminated fish.
All Finnish fishermen, registered since 1980, were identified from the Professional Fishermen Register (N = 6410), and the fishermen's wives from the national population register (N = 4260). The cohorts were individually linked with cause-of-death data until 2005 at Statistics Finland. The follow-up started in the year after the first registration as a fisherman and at marriage (if later) for the wives. The standardized mortality ratios (SMRs) were calculated based on the national mortality rates. In addition, blood samples and food frequency questionnaire data were collected from a volunteer sample.
The average fish consumption and serum concentrations of fish-derived fatty acids and environmental contaminants were higher among the fishermen and their wives than among the general population from the same region. The fishermen and their wives had lower mortality from all causes (SMR 0.78, 95% confidence interval (CI) 0.73-0.82, and 0.84, 0.76-0.93, respectively), and ischaemic heart diseases (0.73, 0.65-0.81, and 0.65, 0.50-0.83) than the general population. Mortality from cerebrovascular diseases and malignant neoplasms was decreased among the fishermen (0.67, 0.52-0.85, and 0.90, 0.80-1.01), but not among the wives. In addition, the fishermen's mortality from water transport accidents was extremely high (8.31, 5.65-11.79).
The fishermen and their wives had lower mortality from many natural causes. The high intakes of environmental contaminants in fish were not seen as excess mortality.