Exposure to particulate air pollution increases respiratory and cardiovascular morbidity and mortality, especially in elderly, possibly through inflammation and vascular dysfunction.
We examined potential beneficial effects of indoor air filtration in the homes of elderly, including people taking vasoactive drugs.Forty-eight nonsmoking subjects (51 to 81 years) in 27 homes were included in this randomized, double-blind, crossover intervention study with consecutive two-week periods with or without the inclusion of a high-efficiency particle air filter in re-circulating custom built units in their living room and bedroom. We measured blood pressure, microvascular and lung function and collected blood samples for hematological, inflammation, monocyte surface and lung cell damage markers before and at day 2, 7 and 14 during each exposure scenario.
The particle filters reduced the median concentration of PM2.5 from approximately 8 to 4 µg/m3 and the particle number concentration from 7669 to 5352 particles/cm3. No statistically significant effects of filtration as category were observed on microvascular and lung function or the biomarkers of systemic inflammation among all subjects, or in the subgroups taking (n = 11) or not taking vasoactive drugs (n = 37). However, the filtration efficacy was variable and microvascular function was within 2 days significantly increased with the actual PM2.5 decrease in the bedroom, especially among 25 subjects not taking any drugs.
Substantial exposure contrasts in the bedroom and no confounding by drugs appear required for improved microvascular function by air filtration, whereas no other beneficial effect was found in this elderly population.
Cites: Am J Physiol Heart Circ Physiol. 2008 Feb;294(2):H944-5318083905
Cites: Occup Environ Med. 2008 May;65(5):319-2417704195
Cardiovascular disease (CVD) is the number one cause of death globally and evidence is steadily increasing on the role of non-traditional risk factors such as meteorology and air pollution. Nevertheless, many research gaps remain, such as the association between these non-traditional risk factors and subtypes of CVD, such as acute myocardial infarction (AMI). The objective of this study was to investigate the association between daily ambient temperature and AMI hospitalisations using a case-crossover design in Gothenburg, Sweden (1985-2010). A secondary analysis was also performed for out-of-hospital ischemic heart disease (IHD) deaths. Susceptible groups by age and sex were explored. The entire year as well as the warm (April-September) and cold periods (October-March) were considered. In total 28,215 AMI hospitalisations (of 22,475 people) and 21,082 out-of-hospital IHD deaths occurred during the 26-year study period. A linear exposure-response corresponding to a 3% and 7% decrease in AMI hospitalisations was observed for an inter-quartile range (IQR) increase in the 2-day cumulative average of temperature during the entire year (11°C) and the warm period (6°C), respectively, with and without adjustment for PM10, NO2, NOx or O3. No heat waves occurred during the warm period. No evidence of an association in the cold period nor any association between temperature and IHD deaths in the entire year, warm or cold periods--with and without adjusting for PM10, NO2, NOx or O3 was found. No susceptible groups, based on age or sex, were identified either. The inverse association between temperature and AMI hospitalisations (entire year and warm period) in Gothenburg is in accordance with the majority of the few other studies that investigated this subtype of CVD.
There are relatively few studies on the association between disturbances in drinking water services and symptoms of gastrointestinal (GI) illness. Health Call Centres data concerning GI illness may be a useful source of information. This study investigates if there is an increased frequency of contacts with the Health Call Centre (HCC) concerning gastrointestinal symptoms at times when there is a risk of impaired water quality due to disturbances at water works or the distribution network. The study was conducted in Gothenburg, a Swedish city with 0.5 million inhabitants with a surface water source of drinking water and two water works. All HCC contacts due to GI symptoms (diarrhoea, vomiting or abdominal pain) were recorded for a three-year period, including also sex, age, and geocoded location of residence. The number of contacts with the HCC in the affected geographical areas were recorded during eight periods of disturbances in the water works (e.g. short stops of chlorine dosing), six periods of large disturbances in the distribution network (e.g. pumping station failure or pipe breaks with major consequences), and 818 pipe break and leak repairs over a three-year period. For each period of disturbance the observed number of calls was compared with the number of calls during a control period without disturbances in the same geographical area. In total about 55, 000 calls to the HCC due to GI symptoms were recorded over the three-year period, 35 per 1000 inhabitants and year, but much higher (>200) for children
The association between exposure during handling of sewage and compost and the serum concentration of inflammatory biomarkers was studied.
A total of 44 workers exposed to sewage dust, 47 workers exposed to compost dust and 38 referents from the administrative staff participated. Microbial aerosols were collected by personal inhalable samplers. The concentrations of bacterial cells, spores from fungi and bacteria (actinomycetes) and endotoxins were determined by fluorescence and scanning electron microscopy and the Limulus assay. Fibrinogen, D-dimer, ICAM-1, VCAM-1 and IL-6 were determined by ELISA and C-reactive protein (CRP) by HS-MicroCRP assay in blood samples collected post-shift.
The exposure to dust ranged from 0.02 to 11 mg/m(3), endotoxins from 1 to 3160 EU/m(3) and bacteria from 0 to 209 × 10(6) cells/m(3). Fungal (0-41 × 10(6) spores/m(3)) and actinomycetes spores (0-590 × 10(6) actinomycetes spores/m(3)) were observed only at compost plants. The exposed workers had significantly higher fibrinogen (arithmetic mean 3.3 mg/ml) and CRP (geometric mean 1.5 mg/L) compared to the referents (2.8 and 1.0 mg/L, respectively). The serum concentration of CRP was negatively associated with forced expiratory volume in one second (FEV1) in % of predicted. Exposure to inhalable dust and bacteria was positively associated with the serum concentration of ICAM-1.
This study suggests that exposure to bacteria and dust when handling sewage and compost may initiate an inflammation shown by an increase in serum concentration of ICAM-1. The higher concentrations of fibrinogen and CRP in exposed workers compared to the referents may reflect a low-grade systemic inflammation.
Cadmium exposure may increase the risk of cardiovascular disease. The only published longitudinal study on cadmium and incident cardiovascular disease was performed in American Indians with relatively high cadmium exposure.
Our aim was to examine the association between blood cadmium at baseline and incident cardiovascular events in a population-based study of Swedish men and women with cadmium levels similar to those of most European and U.S.
A Swedish population-based cohort (n = 6,103, age 46-67 years) was recruited between 1991 and 1994. After we excluded those with missing data on smoking, 4,819 participants remained. Acute coronary events, other major cardiac events, stroke, and cardiovascular mortality were followed until 2010. Associations with blood cadmium (estimated from cadmium in erythrocytes) were analyzed using Cox proportional hazards regression including potential confounders and important cardiovascular risk factors.
Hazard ratios for all cardiovascular end points were consistently increased for participants in the 4th blood cadmium quartile (median, 0.99 ?g/L). In models that also included sex, smoking, waist circumference, education, physical activity, alcohol intake, serum triglycerides, HbA1c, and C-reactive protein, the hazard ratios comparing the highest and lowest quartiles of exposure were 1.8 (95% CI: 1.2, 2.7) for acute coronary events, and 1.9 (1.3, 2.9) for stroke. Hazard ratios in never-smokers were consistent with these estimates.
Blood cadmium in the highest quartile was associated with incident cardiovascular disease and mortality in our population-based samples of Swedish adults. The consistent results among never-smokers are important because smoking is a strong confounder. Our findings suggest that measures to reduce cadmium exposures are warranted, even in populations without unusual sources of exposure.
Barregard L, Sallsten G, Fagerberg B, Born? Y, Persson M, Hedblad B, Engstr?m G. 2016. Blood cadmium levels and incident cardiovascular events during follow-up in a population-based cohort of Swedish adults: the Malm? Diet and Cancer Study. Environ Health Perspect 124:594-600; http://dx.doi.org/10.1289/ehp.1509735.
Cites: Am J Epidemiol. 2010 Sep 15;172(6):671-8120693268
Cites: Environ Health Perspect. 2013 Feb;121(2):187-9123128055
Cites: Int J Cardiol. 2013 Jul 15;167(1):146-5022244480
Epidemiological studies indicate that cadmium exposure through diet and smoking is associated with increased risk of cardiovascular disease. There are few data on the relationship between cadmium and plaques, the hallmark of underlying atherosclerotic disease.
To examine the association between exposure to cadmium and the prevalence and size of atherosclerotic plaques in the carotid artery.
A population sample of 4639 Swedish middle-aged women and men was examined in 1991-1994. Carotid plaque was determined by B-mode ultrasound. Cadmium in blood was analyzed by inductively coupled plasma mass spectrometry.
Comparing quartile 4 with quartile 1 of blood cadmium, the odds ratio (OR) for prevalence of any plaque was 1.9 (95% confidence interval 1.6-2.2) after adjustment for sex and, age; 1.4 (1.1-1.8) after additional adjustment for smoking status; 1.4 (1.1-1.7) after the addition of education level and life style factors; 1.3 (1.03-1.8) after additional adjustment for risk factors and predictors of cardiovascular disease. No effect modification by sex was found in the cadmium-related prevalence of plaques. Similarly, ORs for the prevalence of small and large plaques were after full adjustment 1.4 (1.0-2.1) and 1.4 (0.9-2.0), respectively. The subgroup of never smokers showed no association between cadmium and atherosclerotic plaques.
These results extend previous studies on cadmium exposure and clinical cardiovascular events by adding data on the association between cadmium and underlying atherosclerosis in humans. The role of smoking remains unclear. It may both cause residual confounding and be a source of pro-atherogenic cadmium exposure.
Cadmium is a non-essential toxic metal with multiple adverse health effects. Cadmium has been shown to be associated with cardiovascular diseases, but few studies have investigated heart failure (HF) and none of them reported atrial fibrillation (AF). We examined whether cadmium exposure is associated with incidence of HF or AF.
A prospective, observational cohort study with a 17-year follow-up.
The city of Malmö, Sweden.
Blood cadmium levels were measured in 4378 participants without a history of HF or AF (aged 46-67 years, 60% women), who participated in the Malmö Diet and Cancer (MDC) study during 1992-1994.
Incidence of HF and AF were identified from the Swedish hospital discharge register.
143 participants (53% men) were diagnosed with new-onset HF and 385 individuals (52% men) were diagnosed with new-onset AF during follow-up for 17 years. Blood cadmium in the sex-specific 4th quartile of the distribution was significantly associated with incidence of HF. The (HR, 4th vs 1st quartile) was 2.64 (95% CI 1.60 to 4.36), adjusted for age, and 1.95 (1.02 to 3.71) after adjustment also for conventional risk factors and biomarkers. The blood cadmium level was not significantly associated with risk of incident AF.
Blood cadmium levels in the 4th quartile were associated with increased incidence of HF in this cohort with comparatively low exposure to cadmium. Incidence of AF was not associated with cadmium.
There is currently widespread exposure to the toxic metal cadmium through the diet as well as through smoking, and it has been suggested that cadmium exposure may increase the risk of cardiovascular disease. Here we examined whether cadmium exposure is associated with prevalence and growth of atherosclerotic plaques in the carotid arteries.
The analyses were performed in a screening-based cohort of 64-year-old Caucasian women with stratified, random selection to groups with normal glucose tolerance, impaired glucose tolerance and diabetes (n = 599). We measured cadmium concentrations in blood and urine at baseline. In addition, we performed ultrasound examination to determine the prevalence and area of atherosclerotic plaques in the carotid arteries and assessed smoking history and other cardiovascular risk factors at baseline and at a follow-up examination after a mean of 5.4 years.
At baseline, blood cadmium levels were associated with increased risk of plaque and a large plaque area after adjustment for confounders. In women who had never smoked, blood cadmium levels correlated positively with plaque area at baseline. The occurrence of large plaques and the change in plaque area at follow-up were associated with blood and creatinine-corrected urinary cadmium concentrations at baseline after adjustment for confounders. Blood and urine cadmium levels added information to established cardiovascular risk factors in predicting progress of atherosclerosis.
We have shown that cadmium levels in blood and urine are independent factors associated with the development of atherosclerotic plaques at baseline as well as prospectively. This novel observation emphasizes the need to consider cadmium as a pro-atherogenic pollutant.
Diet and smoking are the main sources of cadmium exposure in the general population. Cadmium increases the risk of cardiovascular diseases, and experimental studies show that it induces inflammation. Blood cadmium levels are associated with macrophages in human atherosclerotic plaques. Soluble urokinase-type plasminogen activator receptor (suPAR) is an emerging biomarker for cardiovascular events related to inflammation and atherosclerotic plaques. The aim was to examine whether blood cadmium levels are associated with circulating suPAR and other markers of inflammation.
A population sample of 4648 Swedish middle-aged women and men was examined cross-sectionally in 1991-1994. Plasma suPAR was assessed by ELISA, leukocytes were measured by standard methods, and blood cadmium was analysed by inductively coupled plasma mass spectrometry. Prevalent cardiovascular disease, ultrasound-assessed carotid plaque occurrence, and several possible confounding factors were recorded.
After full adjustment for risk factors and confounding variables, a 3-fold increase in blood cadmium was associated with an 10.9% increase in suPAR concentration (p
Cadmium in urine is positively associated with urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) concentrations, a sensitive marker of oxidative DNA damage. We determined whether kidney concentrations of cadmium, mercury, and lead, which may generate oxidative DNA damage, were associated with urinary 8-oxodG or not.
8-OxodG was measured in separate 24 h and overnight urine samples from Swedish healthy adult kidney donors (N = 152) using LC-MS/MS. Concentrations of metals were measured in kidney biopsies (N = 109) by ICP-MS.
The median 8-oxodG concentrations (adjusted to specific gravity) in 24 h and overnight samples were 13.5 and 15.3 nmol/L; 8-oxodG excretion rates in 24 h and overnight samples were 0.93 and 0.86 nmol/h. In multivariable linear regression analyses, we did not find any association between 8-oxodG concentrations or rates and elements in the kidney. The 24-h 8-oxodG concentrations were positively associated with serum ferritin (ß = 0.048, p