Selling smokeless tobacco (snus) in Finland is illegal, yet one-third of all males aged 16 to 18 years have tried it. A regular snus user can receive a daily dose of 60 to 150 milligrams of nicotine and become heavily addicted. The first--and easily detectable--lesions appear in the oral mucosa and gingiva. Long-time followup studies of snus use from a young age are, however, still lacking. Evidence exists of increased risk for fatal cardiovascular diseases and increased risk for injuries. Risk for oral cancer is debated, with more studies showing an increased risk than showing no risk; risk also exists for cancer of esophagus, stomach and pancreas. A new and alarming finding among female users is increased risk for preterm birth, preeclampsia and neonatal apnea.
There is some evidence linking air pollution to cardiovascular morbidity. Our aim was to examine whether there is a correlation between air pollution and cardiovascular morbidity in the city of Trondheim, Norway.
We compared the mean daily number of admissions for cardiovascular disease to the St. Olav University hospital on days with relatively low and high levels of PM10 (1993-2001), PM2,5, NO, NO2, SO2, O3, toluene and paraxylene (1998-2001). A time series analysis was carried out to see how day-to-day variations in concentrations of air pollutants correlated with the number of hospitalizations for cardiovascular disease.
In the bivariate analysis, the mean daily number of hospitalizations was found to be significantly higher (p
The concentration-response relationship between daily ambient inhalable particle (particulate matter less than or equal to 10 micro m; PM(10)) concentrations and daily mortality typically shows no evidence of a threshold concentration below which no relationship is observed. However, the power to assess a relationship at very low concentrations of PM(10) has been limited in studies to date. The concentrations of PM(10) and other air pollutants in Vancouver, British Columbia, Canada, from January 1994 through December 1996 were very low: the 50th and 90th percentiles of daily average PM(10) concentrations were 13 and 23 micro g/m(3), respectively, and 27 and 39 ppb, respectively, for 1-hr maximum ozone. Analyses of 3 years of daily pollution (PM(10), ozone, sulfur dioxide, nitrogen dioxide, and carbon monoxide) concentrations and mortality counts showed that the dominant associations were between ozone and total mortality and respiratory and cardiovascular mortality in the summer, and between nitrogen dioxide and total mortality in the winter, although some association with PM(10) may also have been present. We conclude that increases in low concentrations of air pollution are associated with increased daily mortality. These findings may support the notion that no threshold pollutant concentrations are present, but they also raise concern that these effects may not be effects of the measured pollutants themselves, but rather of some other factor(s) present in the air pollution-meteorology mix.
Cites: J Air Waste Manag Assoc. 2000 Jul;50(7):1184-9810939211
Cites: Am J Epidemiol. 2000 Sep 1;152(5):397-40610981451
Cites: J Air Waste Manag Assoc. 2000 Aug;50(8):1481-50011002609
PURPOSE: Polycystic ovaries and menstrual disturbances seem to be common among women taking valproate for epilepsy. The purpose of the present study was to assess the frequency of valproate-related metabolic and endocrine disorders in different groups of women with epilepsy. SUBJECTS AND METHODS: Seventy-two women with epilepsy and 52 control subjects from centers in three European countries (Finland, Norway, and the Netherlands) participated in the study. Thirty-seven of the women with epilepsy were taking valproate monotherapy and 35 carbamazepine monotherapy. RESULTS: The frequency of polycystic ovaries or hyperandrogenism, or both, among valproate-treated women with epilepsy was 70% (26 of 37) compared with 19% (10 of 52) among control subjects (P
Non-therapeutic use of anabolic androgenic steroids (AAS) has been associated with various adverse effects; one of the most serious being direct cardiovascular effects with unknown long-term consequences. Therefore, large studies of the association between AAS and cardiovascular outcomes are warranted. We investigated cardiovascular morbidity and mortality in individuals who tested positive for AAS.
Between 2002 and 2009, a total of 2013 men were enrolled in a cohort on the date of their first AAS test. Mortality and morbidity after cohort entry was retrieved from national registries. Of the 2013 individuals, 409 (20%) tested positive for AAS. These men had twice the cardiovascular morbidity and mortality rate as those with negative tests (adjusted hazard ratio (aHR) 2.0; 95% confidence interval (CI) 1.2-3.3). Compared to the Swedish population, all tested men had an increased risk of premature death from all causes (standardized mortality ratio for AAS-positive: 19.3, 95% CI 12.4-30.0; for AAS-negative: 8.3, 95% CI 6.1-11.0).
Non-therapeutic exposure to AAS appears to be an independent risk factor for cardiovascular morbidity and premature death.
It is generally believed that long-term use of antipsychotics increases mortality and, especially, the risk of cardiovascular death. However, there are no solid data to substantiate this view.
We identified all individuals in Sweden with schizophrenia diagnoses before year 2006 (N = 21 492), aged 17-65 years, and persons with first-episode schizophrenia during the follow-up 2006-2010 (N = 1230). Patient information was prospectively collected through nationwide registers. Total and cause-specific mortalities were calculated as a function of cumulative antipsychotic exposure from January 2006 to December 2010.
Compared with age- and gender-matched controls from the general population (N = 214920), the highest overall mortality was observed among patients with no antipsychotic exposure (hazard ratio [HR] = 6.3, 95% CI: 5.5-7.3), ie, 0.0 defined daily dose (DDD)/day, followed by high exposure (>1.5 DDD/day) group (HR = 5.7, 5.2-6.2), low exposure (
Self-reported data on the municipality of residence were used to assess long-term exposure to outdoor air pollution from 1980 to 2002 in the longitudinal Canadian National Population Health Survey. Exposure to carbon monoxide, nitrogen dioxide, ozone, sulfur dioxide, and particulate matter was determined using data obtained from fixed-site air pollution monitors operated principally in urban areas. Four different methods of attributing pollution exposure were used based on residence in (1) 1980, (2) 1994, (3) 1980 and 1994, and (4) at all locations between 1980 and 2002. Between 1,693 and 4,274 of 10,515 members of the cohort could be assigned exposures to individual pollutants using these methods. On average, subjects spent 71.4% of the 1980-2002 period in the census subdivision where they lived in 1980. A single exposure measure in 1980 or 1994 or a mean of the two measures was highly correlated (r>0.7, P
Clinical guidelines have been criticized for encouraging the use of ß-blockers in noncardiac surgery despite weak evidence. Relevant clinical trials have been small and have not convincingly demonstrated an effect of ß-blockers on hard end points (ie, perioperative myocardial infarction, ischemic stroke, cardiovascular death, and all-cause death).
To assess the association of ß-blocker treatment with major cardiovascular adverse events (MACE) and all-cause mortality in patients with ischemic heart disease undergoing noncardiac surgery. DESIGN, SETTING, PARTICIPANTS, AND EXPOSURE: Individuals with ischemic heart disease with or without heart failure (HF) and with and without a history of myocardial infarction undergoing noncardiac surgery between October 24, 2004, and December 31, 2009, were identified from nationwide Danish registries. Adjusted Cox regression models were used to calculate the 30-day risks of MACE (ischemic stroke, myocardial infarction, or cardiovascular death) and all-cause mortality associated with ß-blocker therapy.
Thirty-day risk of MACE and all-cause mortality.
Of 28,263 patients with ischemic heart disease undergoing surgery, 7990 (28.3%) had HF and 20,273 (71.7%) did not. ß-Blockers were used in 4262 (53.3%) with and 7419 (36.6%) without HF. Overall, use of ß-blockers was associated with a hazard ratio (HR) of 0.90 (95% CI, 0.79-1.02) for MACE and 0.95 (0.85-1.06) for all-cause mortality. Among patients with HF, use of ß-blockers was associated with a significantly lower risk of MACE (HR, 0.75; 95% CI, 0.70-0.87) and all-cause mortality (0.80; 0.70-0.92), whereas among patients without HF, there was no significant association of ß-blocker use with MACE (1.11; 0.92-1.33) or mortality (1.15; 0.98-1.35) (P
A number of serious cardiovascular safety concerns related to the use of atypical antipsychotics, compared with no use, have emerged, but nearly all reports are from studies of older patients. We aimed to compare the risk of cardiovascular events between the three most commonly used atypical antipsychotics in young and middle-aged adults.
We conducted a nationwide register-based cohort study in Denmark, 1997-2011, including adults aged 18-64 years, who started treatment with oral or intramuscular olanzapine (n = 15,774), oral quetiapine (n = 18,717), and oral or intramuscular risperidone (n = 14,134). The primary outcome was any major cardiovascular event (composite of cardiovascular mortality, acute coronary syndrome, or ischemic stroke) within 1 year following treatment initiation. Cox regression was used to estimate hazard ratios (HRs) while on current antipsychotic monotherapy in the outpatient setting, adjusting for an outcome-specific disease risk score.
The crude rate of any major cardiovascular event was 5.3 per 1,000 person-years among olanzapine users, 3.4 in quetiapine users, and 5.2 in risperidone users. Compared with risperidone, the risk of any major cardiovascular event was not significantly different in olanzapine users (HR 0.90, 95 % confidence interval [CI] 0.53-1.52) and quetiapine users (HR 0.79, 95 % CI 0.45-1.39). The absolute risk difference per 1,000 person-years on treatment was -0.5 (95 % CI -2.4 to 2.7) events for olanzapine and -1.1 (95 % CI -2.9 to 2.0) events for quetiapine.
Among young and middle-aged outpatients, the risk of acute major cardiovascular events was similar with use of olanzapine, quetiapine, and risperidone. Although moderate relative differences cannot be ruled out, any differences are small in absolute terms.