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Background and Aims: Despite firm evidence for an association between long-term ambient air pollution exposure and cardiovascular morbidity and mortality, results from epidemiological studies on the association between air pollution exposure and atherosclerosis have not been consistent. We investigated associations between long-term low-level air pollution exposure and coronary atherosclerosis., Methods: We performed a cross-sectional analysis in the large Swedish CArdioPulmonary bioImaging Study (SCAPIS, n = 30 154), a random general population sample. Concentrations of total and locally emitted particulate matter <2.5 μm (PM 2.5 ), <10 μm (PM 10 ), and nitrogen oxides (NO x ) at the residential address were modelled using high-resolution dispersion models. We estimated associations between air pollution exposures and segment involvement score (SIS), coronary artery calcification score (CACS), number of non-calcified plaques (NCP), and number of significant stenoses, using ordinal regression models extensively adjusted for potential confounders., Results: Median 10-year average PM 2.5 exposure was 6.2 μg/m 3 (range 3.5-13.4 μg/m 3 ). 51 % of participants were women and 51 % were never-smokers. None of the assessed pollutants were associated with a higher SIS or CACS. Exposure to PM 2.5 was associated with NCP (adjusted OR 1.34, 95 % CI 1.13, 1.58, per 2.05 μg/m 3 ). Associations with significant stenoses were inconsistent., Conclusions: In this large, middle-aged general population sample with low exposure levels, air pollution was not associated with measures of total burden of coronary atherosclerosis. However, PM 2.5 appeared to be associated with a higher prevalence of non-calcified plaques. The results suggest that increased risk of early-stage atherosclerosis or rupture, but not increased total atherosclerotic burden, may be a pathway for long-term air pollution effects on cardiovascular disease., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: Lead exposure is associated with cardiovascular disease. Atherosclerosis has been hypothesized to be one of the underlying mechanisms behind this association., Aim: To investigate whether lead exposure is associated with an increased risk of atherosclerosis in the carotid arteries in a large Swedish population-based cohort., Methods: We performed a cross-sectional study using data from the population-based Swedish CardioPulmonary bioImage Study (SCAPIS), including 5622 middle-aged men and women, enrolled 2013-2018. Blood lead (B-Pb), measured by inductively coupled plasma mass spectrometry, was used as exposure biomarker. The presence of atherosclerotic plaque in the carotid arteries (yes/no), total plaque area (mm 2 ) and the presence of large plaques (>25 mm 2 ) were determined by ultrasonography. Associations between B-Pb and the different outcomes were analysed using Poisson and linear regression models, adjusted for potential confounders., Results: Atherosclerotic plaque was present in 57% of the individuals, for whom the median total plaque area was 16 mm 2 (range: 0.2-222). The median B-Pb concentration was 14 μg/L (range: 0.75-203). After adjusting for potential confounders, individuals in the fourth quartile of B-Pb (Q4) had a prevalence ratio (PR) for plaque of 1.08 (95% CI: 1.01, 1.16) when compared with the first quartile (Q1). A 10 μg/L increase in B-Pb concentrations was associated with an increase of 0.92 mm 2 (95% CI: 0.14, 1.71) in total plaque area. The PR for large plaque was 1.09 (95% CI: 0.84, 1.42 for Q4 vs Q1)., Conclusions: This study shows an association between B-Pb and atherosclerosis in the carotid arteries providing some support for the hypothesis that atherosclerosis is one of the mechanisms underlying the association between lead exposure and cardiovascular disease., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Background Colon cancer incidence is rising globally, and factors pertaining to urbanization have been proposed involved in this development. Traffic noise may increase colon cancer risk by causing sleep disturbance and stress, thereby inducing known colon cancer risk-factors, e.g. obesity, diabetes, physical inactivity, and alcohol consumption, but few studies have examined this. Objectives The objective of this study was to investigate the association between traffic noise and colon cancer (all, proximal, distal) in a pooled population of 11 Nordic cohorts, totaling 155,203 persons. Methods We identified residential address history and estimated road, railway, and aircraft noise, as well as air pollution, for all addresses, using similar exposure models across cohorts. Colon cancer cases were identified through national registries. We analyzed data using Cox Proportional Hazards Models, adjusting main models for harmonized sociodemographic and lifestyle data. Results During follow-up (median 18.8 years), 2757 colon cancer cases developed. We found a hazard ratio (HR) of 1.05 (95% confidence interval (CI): 0.99-1.10) per 10-dB higher 5-year mean time-weighted road traffic noise. In sub-type analyses, the association seemed confined to distal colon cancer: HR 1.06 (95% CI: 0.98-1.14). Railway and aircraft noise was not associated with colon cancer, albeit there was some indication in sub-type analyses that railway noise may also be associated with distal colon cancer. In interaction-analyses, the association between road traffic noise and colon cancer was strongest among obese persons and those with high NO 2 -exposure. Discussion A prominent study strength is the large population with harmonized data across eleven cohorts, and the complete address-history during follow-up. However, each cohort estimated noise independently, and only at the most exposed façade, which may introduce exposure misclassification. Despite this, the results of this pooled study suggest that traffic noise may be a risk factor for colon cancer, especially of distal origin., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Long-term exposure to air pollution is associated with cardiovascular events. A main suggested mechanism is that air pollution accelerates the progression of atherosclerosis, yet current evidence is inconsistent regarding the association between air pollution and coronary artery and carotid artery atherosclerosis, which are well-established causes of myocardial infarction and stroke. We studied associations between low levels of long-term air pollution, coronary artery calcium (CAC) score, and the prevalence and area of carotid artery plaques, in a middle-aged population-based cohort. The Swedish CArdioPulmonary bioImage Study (SCAPIS) Gothenburg cohort was recruited during 2013-2017 and thoroughly examined for cardiovascular risk factors, including computed tomography of the heart and ultrasonography of the carotid arteries. In 5070 participants (age 50-64 years), yearly residential exposures to air pollution (PM 2.5 , PM 10 , PM coarse , NO x , and exhaust-specific PM 2.5 1990-2015) were estimated using high-resolution dispersion models. We used Poisson regression to examine associations between long-term (26 years' mean) exposure to air pollutants and CAC score, and prevalence of carotid artery plaques, adjusted for potential confounders. Among participants with carotid artery plaques, we also examined the association with plaque area using linear regression. Mean exposure to PM 2.5 was low by international standards (8.5 μg/m 3 ). There were no consistent associations between long-term total PM 2.5 exposure and CAC score or presence of carotid artery plaques, but an association between total PM 2.5 and larger plaque area in participants with carotid plaques. Associations with traffic-related air pollutants were consistently positive for both a high CAC score and bilateral carotid artery plaques. These associations were independent of road traffic noise. We found stronger associations among men and participants with cardiovascular risk factors. The results lend some support to atherosclerosis as a main modifiable pathway between low levels of traffic-related ambient air pollution and cardiovascular disease, especially in vulnerable individuals., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Lead is a non-essential toxic trace element. Lead in blood (BPb) is the most common biomarker of lead exposure but lead in urine (UPb) has also been used. There is, however, limited data on the variability of UPb in the general population and the association with BPb., Objectives: Our aims were to assess variability of lead in repeated blood and urine samples. The diurnal variation of UPb was also examined as well as associations with BPb., Methods: We established an openly available biobank including 60 healthy non-smoking individuals, 29 men and 31 women, 21-64 years of age (median 31 years), with repeated sampling of blood and urine. Timed urine samples were collected at six fixed time points in two 24 h periods, about one week apart, and adjusted for creatinine and specific gravity (SG). BPb and UPb were analyzed by inductively coupled plasma mass spectrometry. The within- and between-individual variabilities and intra-class correlation coefficients (ICCs; ratios of the between-individual to total observed variances) were calculated using mixed-effects models., Results: The ICCs for UPb samples were mostly above 0.5, when adjusted for creatinine or SG, and higher for overnight samples compared with daytime samples. The highest ICCs were obtained for BPb (ICC = 0.97) and for urine samples corrected for dilution by SG or creatinine. The ICC was 0.66 for overnight samples adjusted for creatinine. High correlations with BPb were found for 24 h UPb (r s  = 0.77) and overnight samples, e.g. r s  = 0.74 when adjusted for SG. There was diurnal variation of UPb with lowest excretion rate in overnight samples. There was also a significant association between the Pb excretion rate and urinary flow rate., Conclusions: In addition to BPb, UPb adjusted for creatinine or SG seems to be a useful biomarker for exposure assessment in epidemiological studies., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Lead (Pb), cadmium (Cd) and mercury (Hg) are all nephrotoxic metals, and a large part of the body burden of Cd and Hg is found in the kidneys. There are, however, few studies on associations between exposure to these toxic metals and renal biopsy findings, and none at low-level exposure., Aim: To examine the hypothesis that low-level concentration of Pb, Cd or Hg in the kidneys is associated with histopathological changes in the kidneys., Methods: We determined concentrations of Pb, Cd and Hg in kidney, blood and urine in 109 healthy kidney donors, aged 24-70 years. The renal biopsies were scored according to the Banff classification regarding tubular atrophy, interstitial fibrosis, glomerulosclerosis, arteriosclerosis, and arteriolohyalinosis. Kidney function was assessed based on glomerular filtration rate (GFR) as well as urinary excretion of albumin, low molecular weight proteins, kidney injury molecule 1 and N-acetylglucose aminidase. Associations between metal concentrations and histopathological changes, were assessed in models also including age, sex and smoking., Results: The median kidney concentrations of Pb, Cd and Hg were 0.08, 13 and 0.21 μg/g, respectively. There were signs of tubular atrophy in 63%, interstitial fibrosis in 21%, glomerulosclerosis in 71%, arteriosclerosis in 47%, and arteriolohyalinosis in 36% of the donors, but, as could be expected, the histopathological findings were limited, mostly Banff grade 1. In models adjusted for age, sex and smoking, kidney Cd was positively associated with tubular atrophy (p = 0.03) and possibly with arteriolohyalinosis (p = 0.06). Kidney Hg was associated with arteriosclerosis (p = 0.004)., Discussion and Conclusions: The results suggest that even low levels of Cd in the kidney can induce a mild degree of tubular atrophy. This is in line with previous findings at high-level Cd exposure. The association between kidney Hg and renal arteriosclerosis was unexpected, and may be a chance finding., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Cadmium is a toxic metal and exposure is mainly from diet and tobacco smoke. Cadmium is accumulated in blood vessels and may reduce synthesis of procollagen and inhibit proliferation of vascular smooth muscle cells. High blood cadmium has been associated with increased risk of myocardial infarction, stroke and unruptured intracranial aneurysms. We examined whether blood cadmium increase the risk of subarachnoid haemorrhage (SAH)., Methods: The Malmö Diet and Cancer cohort (n = 28,449) was examined in 1991-1996 and blood samples were taken. Incidence of SAH was followed up to 2014. Cadmium was measured in stored blood samples from incident SAH cases and matched controls (n = 93 vs n = 276) and odds ratio (OR) for SAH was assessed in a nested case control design., Results: Subjects with cadmium concentration in the highest quartile had increased risk of SAH compared to those in the first quartile (OR: 3.22, 95%CI: 1.67-6.22). However, after adjusting for smoking, results were weakened and non-significant (OR: 1.57, 95%CI: 0.51-4.80)., Conclusions: Cadmium concentration was associated with increased risk of SAH but this association was largely explained by smoking. Whether cadmium in tobacco may contribute to the vascular pathology and increased risk of SAH in smokers should be further studied., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Exposure to high levels of road traffic noise at the most exposed building facade is increasing, both due to urbanization and due to overall traffic increase. This study investigated how different noise reduction measures would influence the noise exposure on a city-wide scale in Gothenburg, a city in Sweden with approximately 550,000 inhabitants. Noise exposure was estimated under several different scenarios for the period 2015-2035, using the standardized Nordic noise prediction method together with traffic flow measurements and population statistics. The scenarios were based on reducing speed limits, reducing traffic flows, introducing more electrically powered vehicles and introducing low-noise tires and pavements. The most effective measures were introducing low-noise tires or pavements, which in comparison to business as usual produced between 13% and 29% reduction in the number of inhabitants exposed above 55 dB equivalent level., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)

Background and Aims: Long-term exposure to air pollution increases cardiopulmonary morbidity and mortality, but it is not clear which components of air pollution are the most harmful, nor which time window of exposure is most relevant. Further studies at low exposure levels have also been called for. We analyzed two Swedish cohorts to investigate the effects of total and source-specific particulate matter (PM) on incident cardiovascular disease for different time windows of exposure., Methods: Two cohorts initially recruited to study predictors of cardiovascular disease (the PPS cohort and the GOT-MONICA cohort) were followed from 1990 to 2011. We collected data on residential addresses and assigned each individual yearly total and source-specific PM and Nitrogen Oxides (NO x ) exposures based on dispersion models. Using multivariable Cox regression models with time-dependent exposure, we studied the association between three different time windows (lag 0, lag 1-5, and exposure at study start) of residential PM and NO x exposure, and incidence of ischemic heart disease, stroke, heart failure and atrial fibrillation., Results and Discussion: During the study period, there were 2266 new-onset cases of ischemic heart disease, 1391 of stroke, 925 of heart failure and 1712 of atrial fibrillation. The majority of cases were in the PPS cohort, where participants were older. Exposure levels during the study period were moderate (median: 13µg/m 3 for PM 10 and 9µg/m 3 for PM 2.5 ), and similar in both cohorts. Road traffic and residential heating were the largest local sources of PM air pollution, and long distance transportation the largest PM source in total. In the PPS cohort, there were positive associations between PM in the last five years and both ischemic heart disease (HR: 1.24 [95% CI: 0.98-1.59] per 10µg/m 3 of PM 10 , and HR: 1.38 [95% CI: 1.08-1.77] per 5µg/m 3 of PM 2.5 ) and heart failure. In the GOT-MONICA cohort, there were positive but generally non-significant associations between PM and stroke (HR: 1.48 [95% CI: 0.88-2.49] per 10µg/m 3 of PM 10 , and HR: 1.50 [95% CI: 0.90-2.51] per 5µg/m 3 of PM 2.5 , in the last five years). Effect estimates were stronger for women, non-smokers, and higher socioeconomic classes. Exposure in the last five years seemed to be more strongly associated with outcomes than other exposure time windows. Associations between source-specific PM air pollution and outcomes were mixed and generally weak. High correlations between the main pollutants limited the use of multi-pollutant models., Conclusions: The main PM air pollutants were associated with ischemic heart disease and stroke (in women) at the relatively low exposure levels in Gothenburg, Sweden. The associations tended to be stronger for women than for men, for non-smokers than for smokers, and for higher socioeconomic classes than for lower. The associations could not be attributed to a specific PM source or type, and differed somewhat between the two cohorts. The results of this study confirm that further efforts to reduce air pollution exposure should be undertaken in Sweden to reduce the negative health effects in the general population., (Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.)

Introduction: Elevated levels of indoor air pollutants may cause cardiopulmonary disease such as lower respiratory infection, chronic obstructive lung disease and lung cancer, but the association with tuberculosis (TB) is unclear. So far the risk estimates of TB infection or/and disease due to indoor air pollution (IAP) exposure are based on self-reported exposures rather than direct measurements of IAP, and these exposures have not been validated., Objective: The aim of this paper was to characterize and develop predictive models for concentrations of three air pollutants (PM 10 , NO 2 and SO 2 ) in homes of children participating in a childhood TB study., Methods: Children younger than 15 years living within the eThekwini Municipality in South Africa were recruited for a childhood TB case control study. The homes of these children (n=246) were assessed using a walkthrough checklist, and in 114 of them monitoring of three indoor pollutants was also performed (sampling period: 24h for PM 10 , and 2-3 weeks for NO 2 and SO 2 ). Linear regression models were used to predict PM 10 and NO 2 concentrations from household characteristics, and these models were validated using leave out one cross validation (LOOCV). SO 2 concentrations were not modeled as concentrations were very low., Results: Mean indoor concentrations of PM 10 (n=105) , NO 2 (n=82) and SO 2 (n=82) were 64μg/m 3 (range 6.6-241); 19μg/m 3 (range 4.5-55) and 0.6μg/m 3 (range 0.005-3.4) respectively with the distributions for all three pollutants being skewed to the right. Spearman correlations showed weak positive correlations between the three pollutants. The largest contributors to the PM 10 predictive model were type of housing structure (formal or informal), number of smokers in the household, and type of primary fuel used in the household. The NO 2 predictive model was influenced mostly by the primary fuel type and by distance from the major roadway. The coefficients of determination (R 2 ) for the models were 0.41 for PM 10 and 0.31 for NO 2 . Spearman correlations were significant between measured vs. predicted PM 10 and NO 2 with coefficients of 0.66 and 0.55 respectively., Conclusion: Indoor PM 10 levels were relatively high in these households. Both PM 10 and NO 2 can be modeled with a reasonable validity and these predictive models can decrease the necessary number of direct measurements that are expensive and time consuming., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Background and Aims: Diet and smoking expose the general population to cadmium (Cd), which is a toxic metal that accumulates in the arterial wall. In experimental studies, Cd causes reductions in proliferation of smooth muscle cells and cellular synthesis of procollagen. The aim of this study was to examine whether blood Cd levels, a valid measure of Cd exposure, are associated with increased risk of abdominal aortic aneurysm (AAA)., Methods: All middle-aged men and women enrolled in the Malmö Diet and Cancer study (n = 30 447) were followed from the baseline examination in 1991-1996 through 2009. A total of 297 cases with AAA and two randomly selected control subjects for each case, matched for age and sex, were included. Blood Cd was analysed by inductively coupled plasma mass spectrometry. Diagnoses of AAA, thoracic aortic aneurysm and aortic dissection were obtained from registers., Results: Increased blood Cd was associated with increased risk of incident AAA after adjustment for smoking and other established risk factors for AAA. The highest tertile of blood Cd concentrations had a rate ratio of 2.5 (95% confidence interval 1.3, 5.0) for incident AAA. Concentration of blood Cd (log transformed) was not associated with AAA in never-smokers (n = 24)., Conclusions: Blood Cd levels corresponding to the upper tertile of the distribution in the age- and sex-matched control group were associated with a 2.5-fold increase in rate ratio for incident AAA. This relationship was not found in the small group of never-smokers., (Copyright © 2017. Published by Elsevier B.V.)

Background: 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., Methods: 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., Results: 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<0.001). In never-smokers, a 3-fold increase in blood cadmium was associated with a 3.7% increase in suPAR concentration (p<0.01) after full adjustment. Blood cadmium was not associated with C-reactive protein, white blood cell count and Lp-PLA2 but with neutrophil/lymphocyte ratio in one of two statistical models., Conclusions: Exposure to cadmium was associated with increased plasma suPAR in the general population, independently of smoking and cardiovascular disease. These results imply that cadmium is a possible cause for raised levels of this inflammatory marker., (Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Environmental lead exposure is a possible causative factor for increased blood pressure and hypertension, but large studies at low-level exposure are scarce, and results inconsistent., Objective: We aimed to examine the effects of environmental exposure to lead in a large population-based sample., Methods: We assessed associations between blood lead and systolic/diastolic blood pressure and hypertension in 4452 individuals (46-67 years) living in Malmö, Sweden, in 1991-1994. Blood pressure was measured using a mercury sphygmomanometer after 10min supine rest. Hypertension was defined as high systolic (≥140mmHg) or diastolic (≥90mmHg) blood pressure and/or current use of antihypertensive medication. Blood lead was calculated from lead in erythrocytes and haematocrit. Multivariable associations between blood lead and blood pressure or hypertension were assessed by linear and logistic regression. Two-thirds of the cohort was re-examined 16 years later., Results: At baseline, mean blood pressure was 141/87mmHg, 16% used antihypertensive medication, 63% had hypertension, and mean blood lead was 28µg/L. Blood lead in the fourth quartile was associated with significantly higher systolic and diastolic blood pressure (point estimates: 1-2mmHg) and increased prevalence of hypertension (odds ratio: 1.3, 95% confidence interval: 1.1-1.5) versus the other quartiles after adjustment for sex, age, smoking, alcohol, waist circumference, and education. Associations were also significant with blood lead as a continuous variable. Blood lead at baseline, having a half-life of about one month, was not associated with antihypertensive treatment at the 16-year follow-up., Conclusions: Low-level lead exposure increases blood pressure and may increase the risk of hypertension., (Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.)

Background and Aims: The general population is exposed to cadmium through diet and smoking. Cadmium is pro-atherogenic and pro-inflammatory in experimental and observational studies. Cadmium levels in blood and carotid plaque endarterectomies correlate. Cadmium concentrations are much higher in plaque-areas that most frequently rupture. Here we investigated if blood cadmium concentrations are associated with macrophage density and the accumulation of CD14 as indicator of macrophage activation by lipopolysaccharide (LPS) in endarterectomies from patients with symptomatic carotid plaques., Methods: Endarterectomies from ninety nine patients were fixed in formalin, embedded in paraffin, serially sectioned and stained for assessment of morphology. As predefined, the two section levels with most prevalent plaque rupture were used for further analyses. Macrophages were assessed as area of staining for CD68 (%). Blood cadmium was measured with ICP-MS., Results: The CD68 median [25,75 percentiles] from the average of both sections were higher in cadmium tertile 3 than in tertile 1 (9.8 [4.9,16.1] % and 3.8 (0.6,12.4) %, p = 0.017). This difference remained in a multiple linear regression analysis with (10)log meanCD68 as dependent variable and adjustment for sex, age, smoking, statin treatment, index event, time between event and surgery (beta coefficient 0.44 [95% CI 0.05-0.87]. CD14 was not associated with blood cadmium., Conclusions: The results showed that blood cadmium was associated with proinflammatory macrophage density in the sections of carotid plaques with most frequent rupture, previously shown to contain most cadmium. No association between cadmium and LPS-mediated macrophage-activation was found. Cadmium exposure may promote plaque inflammation., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Background: Chronic kidney disease is common among sugarcane workers in Central America. The main risk factor seems to be repeated high-intensity work in hot environments. Several cross-sectional studies have been performed but few longitudinal studies., Objectives: The aim of the study was to examine whether kidney function changes over a few months of work during the harvest period., Methods: A group of male sugarcane cutters in Nicaragua (N=29, aged 17-38 years) was examined with renal biomarkers before and after shift on the first day at the start of harvest, on the sixth day during acclimatization, and then in mid-harvest 9 weeks later. A reference group (N=25, mainly office workers) was examined with the same biomarkers at start of harvest, and then at end of harvest 5 months later., Results: The pre-shift renal function decreased significantly during 9 weeks of work in the cane cutters. Mean serum creatinine increased (20%), mean estimated glomerular filtration rate decreased (9%, 10mL/min), serum urea N (BUN) increased (41%), and mean urinary neutrophil gelatinase-associated lipocalin (NGAL) increased (four times). The cane cutters also developed cross-shift increases in these biomarkers, in particular serum creatinine and BUN, and in urinary uric acid. The longitudinal decrease in eGFR tended to be associated with the cross-shift increase in serum creatinine., Conclusions: There was a remarkable decrease of glomerular kidney function, after only 9 weeks of harvest. The cross-shift increase in serum creatinine may be caused by dehydration (pre-renal dysfunction), and when repeated on a daily basis this may cause permanently reduced GFR., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Background: The Global Burden of Disease, Injuries, and Risk Factor study 2013 (GBD 2013) is the first of a series of annual updates of the GBD. Risk factor quantification, particularly of modifiable risk factors, can help to identify emerging threats to population health and opportunities for prevention. The GBD 2013 provides a timely opportunity to update the comparative risk assessment with new data for exposure, relative risks, and evidence on the appropriate counterfactual risk distribution., Methods: Attributable deaths, years of life lost, years lived with disability, and disability-adjusted life-years (DALYs) have been estimated for 79 risks or clusters of risks using the GBD 2010 methods. Risk-outcome pairs meeting explicit evidence criteria were assessed for 188 countries for the period 1990-2013 by age and sex using three inputs: risk exposure, relative risks, and the theoretical minimum risk exposure level (TMREL). Risks are organised into a hierarchy with blocks of behavioural, environmental and occupational, and metabolic risks at the first level of the hierarchy. The next level in the hierarchy includes nine clusters of related risks and two individual risks, with more detail provided at levels 3 and 4 of the hierarchy. Compared with GBD 2010, six new risk factors have been added: handwashing practices, occupational exposure to trichloroethylene, childhood wasting, childhood stunting, unsafe sex, and low glomerular filtration rate. For most risks, data for exposure were synthesised with a Bayesian meta-regression method, DisMod-MR 2.0, or spatial-temporal Gaussian process regression. Relative risks were based on meta-regressions of published cohort and intervention studies. Attributable burden for clusters of risks and all risks combined took into account evidence on the mediation of some risks such as high body-mass index (BMI) through other risks such as high systolic blood pressure and high cholesterol., Findings: All risks combined account for 57·2% (95% uncertainty interval [UI] 55·8-58·5) of deaths and 41·6% (40·1-43·0) of DALYs. Risks quantified account for 87·9% (86·5-89·3) of cardiovascular disease DALYs, ranging to a low of 0% for neonatal disorders and neglected tropical diseases and malaria. In terms of global DALYs in 2013, six risks or clusters of risks each caused more than 5% of DALYs: dietary risks accounting for 11·3 million deaths and 241·4 million DALYs, high systolic blood pressure for 10·4 million deaths and 208·1 million DALYs, child and maternal malnutrition for 1·7 million deaths and 176·9 million DALYs, tobacco smoke for 6·1 million deaths and 143·5 million DALYs, air pollution for 5·5 million deaths and 141·5 million DALYs, and high BMI for 4·4 million deaths and 134·0 million DALYs. Risk factor patterns vary across regions and countries and with time. In sub-Saharan Africa, the leading risk factors are child and maternal malnutrition, unsafe sex, and unsafe water, sanitation, and handwashing. In women, in nearly all countries in the Americas, north Africa, and the Middle East, and in many other high-income countries, high BMI is the leading risk factor, with high systolic blood pressure as the leading risk in most of Central and Eastern Europe and south and east Asia. For men, high systolic blood pressure or tobacco use are the leading risks in nearly all high-income countries, in north Africa and the Middle East, Europe, and Asia. For men and women, unsafe sex is the leading risk in a corridor from Kenya to South Africa., Interpretation: Behavioural, environmental and occupational, and metabolic risks can explain half of global mortality and more than one-third of global DALYs providing many opportunities for prevention. Of the larger risks, the attributable burden of high BMI has increased in the past 23 years. In view of the prominence of behavioural risk factors, behavioural and social science research on interventions for these risks should be strengthened. Many prevention and primary care policy options are available now to act on key risks., Funding: Bill & Melinda Gates Foundation., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Background: The Global Burden of Disease Study 2013 (GBD 2013) aims to bring together all available epidemiological data using a coherent measurement framework, standardised estimation methods, and transparent data sources to enable comparisons of health loss over time and across causes, age-sex groups, and countries. The GBD can be used to generate summary measures such as disability-adjusted life-years (DALYs) and healthy life expectancy (HALE) that make possible comparative assessments of broad epidemiological patterns across countries and time. These summary measures can also be used to quantify the component of variation in epidemiology that is related to sociodemographic development., Methods: We used the published GBD 2013 data for age-specific mortality, years of life lost due to premature mortality (YLLs), and years lived with disability (YLDs) to calculate DALYs and HALE for 1990, 1995, 2000, 2005, 2010, and 2013 for 188 countries. We calculated HALE using the Sullivan method; 95% uncertainty intervals (UIs) represent uncertainty in age-specific death rates and YLDs per person for each country, age, sex, and year. We estimated DALYs for 306 causes for each country as the sum of YLLs and YLDs; 95% UIs represent uncertainty in YLL and YLD rates. We quantified patterns of the epidemiological transition with a composite indicator of sociodemographic status, which we constructed from income per person, average years of schooling after age 15 years, and the total fertility rate and mean age of the population. We applied hierarchical regression to DALY rates by cause across countries to decompose variance related to the sociodemographic status variable, country, and time., Findings: Worldwide, from 1990 to 2013, life expectancy at birth rose by 6·2 years (95% UI 5·6-6·6), from 65·3 years (65·0-65·6) in 1990 to 71·5 years (71·0-71·9) in 2013, HALE at birth rose by 5·4 years (4·9-5·8), from 56·9 years (54·5-59·1) to 62·3 years (59·7-64·8), total DALYs fell by 3·6% (0·3-7·4), and age-standardised DALY rates per 100 000 people fell by 26·7% (24·6-29·1). For communicable, maternal, neonatal, and nutritional disorders, global DALY numbers, crude rates, and age-standardised rates have all declined between 1990 and 2013, whereas for non-communicable diseases, global DALYs have been increasing, DALY rates have remained nearly constant, and age-standardised DALY rates declined during the same period. From 2005 to 2013, the number of DALYs increased for most specific non-communicable diseases, including cardiovascular diseases and neoplasms, in addition to dengue, food-borne trematodes, and leishmaniasis; DALYs decreased for nearly all other causes. By 2013, the five leading causes of DALYs were ischaemic heart disease, lower respiratory infections, cerebrovascular disease, low back and neck pain, and road injuries. Sociodemographic status explained more than 50% of the variance between countries and over time for diarrhoea, lower respiratory infections, and other common infectious diseases; maternal disorders; neonatal disorders; nutritional deficiencies; other communicable, maternal, neonatal, and nutritional diseases; musculoskeletal disorders; and other non-communicable diseases. However, sociodemographic status explained less than 10% of the variance in DALY rates for cardiovascular diseases; chronic respiratory diseases; cirrhosis; diabetes, urogenital, blood, and endocrine diseases; unintentional injuries; and self-harm and interpersonal violence. Predictably, increased sociodemographic status was associated with a shift in burden from YLLs to YLDs, driven by declines in YLLs and increases in YLDs from musculoskeletal disorders, neurological disorders, and mental and substance use disorders. In most country-specific estimates, the increase in life expectancy was greater than that in HALE. Leading causes of DALYs are highly variable across countries., Interpretation: Global health is improving. Population growth and ageing have driven up numbers of DALYs, but crude rates have remained relatively constant, showing that progress in health does not mean fewer demands on health systems. The notion of an epidemiological transition--in which increasing sociodemographic status brings structured change in disease burden--is useful, but there is tremendous variation in burden of disease that is not associated with sociodemographic status. This further underscores the need for country-specific assessments of DALYs and HALE to appropriately inform health policy decisions and attendant actions., Funding: Bill & Melinda Gates Foundation., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Background and Aims: Exposure to air pollution has been linked to total and cardiopulmonary mortality. However, few studies have examined the effects of exposure over decades, or which time windows of long term exposure are most relevant. We investigated the long term effects of residential air pollution on total and cause-specific mortality and incidence of myocardial infarction in a well-characterized cohort of men in Sweden., Methods: A cohort of 7494 men in Gothenburg was examined in 1970-1973 and followed subsequently to determine predictors of cardiovascular disease. We collected data on residential address and cause-specific mortality for the years 1973-2007. Each individual was assigned yearly nitrogen oxides (NOx) exposure based on dispersion models. Using multivariable Cox regression and generalized additive models with time-dependent exposure, we studied the association between three different time windows of residential NOx exposure, and selected outcomes., Results: In the years 1973-2007, a total of 5669 deaths, almost half of which were due to cardiovascular diseases, occurred in the cohort. Levels of NOx exposure decreased during the study period, from a median of 38 µg/m(3) in 1973 to 17 µg/m(3) in 2007. Total non-accidental mortality was associated with participants' NOx exposure in the last year (the year of outcome) (HR 1.03, 95% CI 1.01-1.05, per 10 µg/m(3)), with the mean NOx exposure during the last 5 years, and with the mean NOx exposure since enrolment (HR 1.02, 95% CI 1.01-1.04 for both). The associations were similar (HR 1.01-1.03), but generally not statistically significant, for cardiovascular, ischemic heart disease, and acute myocardial infarction mortality, and weaker for cerebrovascular and respiratory mortality. There was no association between NOx exposure and incident myocardial infarction., Discussion and Conclusions: Long term residential exposure to NOx at these relatively low exposure levels in Gothenburg was associated with total non-accidental mortality. The association was as strong for NOx exposure in the last year as for longer exposure windows. The effect was near linear, and only marginally affected by confounders and effect modifiers. The improved air quality in Gothenburg has by these estimates led to a 6% decrease in excess non-accidental mortality during the study period., (Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: An epidemic of progressive kidney failure afflicts sugarcane workers in Central America. Repeated high-intensity work in hot environments is a possible cause., Objectives: To assess heat stress, dehydration, biomarkers of renal function and their possible associations. A secondary aim was to evaluate the prevalence of pre-shift renal damage and possible causal factors., Methods: Sugarcane cutters (N=189, aged 18-49 years, 168 of them male) from three regions in El Salvador were examined before and after shift. Cross-shift changes in markers of dehydration and renal function were examined and associations with temperature, work time, region, and fluid intake were assessed. Pre-shift glomerular filtration rate was estimated (eGFR) from serum creatinine., Results: The mean work-time was 4 (1.4-11) hours. Mean workday temperature was 34-36 °C before noon, and 39-42 °C at noon. The mean liquid intake during work was 0.8L per hour. There were statistically significant changes across shift. The mean urine specific gravity, urine osmolality and creatinine increased, and urinary pH decreased. Serum creatinine, uric acid and urea nitrogen increased, while chloride and potassium decreased. Pre-shift serum uric acid levels were remarkably high and pre-shift eGFR was reduced (<60 mL/min) in 23 male workers (14%)., Conclusions: The high prevalence of reduced eGFR, and the cross-shift changes are consistent with recurrent dehydration from strenuous work in a hot and humid environment as an important causal factor. The pathophysiology may include decreased renal blood flow, high demands on tubular reabsorption, and increased levels of uric acid., (Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: 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., Objectives: To examine the association between exposure to cadmium and the prevalence and size of atherosclerotic plaques in the carotid artery., Methods: 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., Results: 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., Conclusions: 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., (Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: It has been proposed that diabetic patients are more sensitive to the nephrotoxicity of cadmium (Cd) compared to non-diabetics, but few studies have examined this in humans, and results are inconsistent., Aim: To test the hypothesis that women with type 2 diabetes mellitus (DM) or impaired glucose tolerance (IGT) have higher risk of kidney damage from cadmium compared to women with normal glucose tolerance (NGT)., Methods: All 64-year-old women in Gothenburg, Sweden, were invited to a screening examination including repeated oral glucose tolerance tests. Random samples of women with DM, IGT, and NGT were recruited for further clinical examinations. Serum creatinine was measured and used to calculate estimated glomerular filtration rate (eGFR). Albumin (Alb) and retinol-binding protein (RBP) were analyzed in a 12h urine sample. Cadmium in blood (B-Cd) and urine (U-Cd) was determined using inductively coupled plasma mass spectrometry. Associations between markers of kidney function (eGFR, Alb, and RBP) and quartiles of B-Cd and U-Cd were evaluated in models, including also blood pressure and smoking habits., Results: The mean B-Cd (n=590) was 0.53 µg/L (median 0.34 µg/L). In multivariable models, a significant interaction was seen between high B-Cd (upper quartile, >0.56 µg/L) and DM (point estimate +0.40 mg Alb/12h, P=0.04). In stratified analyzes, the effect of high B-Cd on Alb excretion was significant in women with DM (53% higher Alb/12h, P=0.03), but not in women with IGT or NGT. Models with urinary albumin adjusted for creatinine showed similar results. In women with DM, the multivariable odds ratio (OR) for microalbuminuria (>15 mg/12h) was increased in the highest quartile of B-Cd vs. B-Cd quartiles 1-3 in women with DM (OR 4.2, 95% confidence interval 1.1-12). No such effect was found in women with IGT or NGT. There were no associations between B-Cd and eGFR or excretion of RBP, and no differences between women with DM, IGT, or NGT regarding effect of B-Cd on eGFR or RBP., Conclusion: The present study provides support for the hypothesis that women with DM have higher risk of renal glomerular damage from cadmium exposure compared to women without DM., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Background: Cadmium is a wide-spread pollutant. Observational studies suggest associations between cadmium and prevalence of type 2 diabetes. Experimental studies indicate that cadmium may cause impaired insulin production., Objectives: To examine whether cadmium exposure is associated with impaired glucose tolerance and type 2 diabetes and impaired pancreatic beta-cell function., Methods: Oral glucose tolerance tests were used in a screening examination of 64-year old women (n=2595) to identify all with diabetes, impaired (IGT) and normal (NGT) glucose tolerance. Random samples of women with type 2 diabetes (n=215), IGT (n=207) and NGT (n=194) were recruited in a cross-sectional examination including measurement of pancreatic insulin production (acute insulin response) and insulin sensitivity (homeostasis model assessment). Cadmium concentrations were measured in blood and urine. A follow-up examination was performed after 5.4 years with assessment of new cases with diabetes or impaired glucose tolerance., Results: At baseline, neither blood nor urinary cadmium concentrations showed any statistically significant differences between women with type 2 diabetes, IGT or NGT. The prospective analysis included 68 cases with incident diabetes, 58 with IGT and 118 women with NGT and no associations with cadmium levels at baseline were observed. Blood and urinary cadmium at baseline were not associated with insulin production, blood glucose, HbA1c, or changes in HbA1c during follow-up., Conclusions: This is the first study of cadmium and diabetes with detailed data on pancreatic beta-cell function, insulin sensitivity and glucose tolerance. Cadmium exposure was not associated with increased risk of type 2 diabetes or IGT., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Emissions from petrochemical industries may contain suspected or established carcinogens. As increased incidence of cancer in residential areas close to petrochemical industries has been reported in the literature, we conducted a study of cancer incidence in Stenungsund, Sweden, where petrochemical industries were established in the mid 1960s. A number of cancer cases in the central parts of Stenungsund were collected from the regional cancer registry for each year between 1974 and 2005. In addition to the total number of cases, the numbers of leukemia, lymphoma, liver cancer, lung cancer, and brain cancer were also collected. Expected numbers for each year were calculated based on age- and sex-specific incidence rates in reference areas. Levels of carcinogenic volatile hydrocarbons (VOC) were estimated from measurements and emission data. A dispersion model was used to classify Stenungsund into a "low" and "high" ethylene level area. Standardized Incidence Ratio (SIR) for all cancer for the entire period was 1.02 (95% CI 0.97-1.08). The occurrence of leukemia, lymphoma, and cancer in the central nervous system was slightly lower than expected for the entire period. SIR for lung cancer was 1.37 (95% CI 1.10-1.69), and SIR for liver cancer was 1.50 (0.82-2.53). VOC levels were low. Taking estimated exposure and demographic factors into account, our assessment is that occurrence of cancer was not affected by industrial emissions in any of the studied sites., (Copyright 2010 Elsevier B.V. All rights reserved.)

Sweden has only just begun remediation of its many contaminated sites, a process that will cost an estimated SEK 60,000 million (USD 9100 million). Although the risk assessment method, carried out by the Swedish EPA, is driven by health effects, it does not consider actual exposure. Instead, the sites are assessed based on divergence from guideline values. This paper uses an environmental medicine approach that takes exposure into account to analyse how cancer risks on and near arsenic-contaminated sites are implicitly valued in the remediation process. The results show that the level of ambition is high. At 23 contaminated sites, the cost per life saved varies from SEK 287 million to SEK 1,835,000 million, despite conservative calculations that in fact probably underestimate the costs. It is concluded that if environmental health risks are to be reduced, there are probably other areas where economic resources can be used more cost-effectively.

Background: Most current knowledge on kidney concentrations of nephrotoxic metals like cadmium (Cd), mercury (Hg), or lead (Pb) comes from autopsy studies. Assessment of metal concentrations in kidney biopsies from living subjects can be combined with information about exposure sources like smoking, diet, and occupation supplied by the biopsied subjects themselves., Objectives: To determine kidney concentrations of Cd, Hg, and Pb in living kidney donors, and assess associations with common exposure sources and background factors., Methods: Metal concentrations were determined in 109 living kidney donors aged 24-70 years (median 51), using inductively coupled plasma-mass spectrometry (Cd and Pb) and cold vapor atomic fluorescence spectrometry (Hg). Smoking habits, occupation, dental amalgam, fish consumption, and iron stores were evaluated., Results: The median kidney concentrations were 12.9microg/g (wet weight) for cadmium, 0.21microg/g for mercury, and 0.08microg/g for lead. Kidney Cd increased by 3.9microg/g for a 10 year increase in age, and by 3.7microg/g for an extra 10 pack-years of smoking. Levels in non-smokers were similar to those found in the 1970s. Low iron stores (low serum ferritin) in women increased kidney Cd by 4.5microg/g. Kidney Hg increased by 6% for every additional amalgam surface, but was not associated with fish consumption. Lead was unaffected by the background factors surveyed., Conclusions: In Sweden, kidney Cd levels have decreased due to less smoking, while the impact of diet seems unchanged. Dental amalgam is the main determinant of kidney Hg. Kidney Pb levels are very low due to decreased exposure.

Objectives: To assess the incidence of leukaemia in an area downwind of a large oil refinery emitting carcinogenic volatile organic compounds (VOCs) including benzene., Methods: Using a dispersion model and the prevailing wind direction, two parishes with about 5000 inhabitants were a priori considered to be exposed to VOCs from the refinery. Numbers of observed and expected leukaemia cases in 1975-2004 were calculated using regional sex- and age-specific incidence rates. In addition, five nearby parishes (12000 inhabitants), considered unaffected by the emissions, served as a local reference area. Based on emission data, dispersion modelling and VOC measurements, the refinery's contribution to the population's exposure to carcinogenic VOCs was estimated. Published "unit risks" for carcinogenic VOCs were used to estimate the expected excess leukaemia risk., Results: The incidence of leukaemia in the "exposed parishes" was significantly increased in 1975-2004 (33 cases v. 22 expected cases), owing to an increase in the last 10-year period, from 1995 to 2004 (19 cases v. 8.5 expected cases). The leukaemia incidence in the local control area was normal (50 cases v. 56 expected cases). The estimated contribution from the refinery to VOC concentrations was, however, only about 2 microg/m(3) (yearly average) for benzene, 2 microg/m(3) for ethylene, 0.5 microg/m(3) for 1,3-butadiene and 5 microg/m(3) for propene. Calculations of expected excess risk using published risk estimates would indicate a much lower excess risk in the exposed parishes., Conclusions: Using risk estimates extrapolated from high-level exposure, we would not expect an increase of leukaemia at low exposure to VOC emissions. Nevertheless, the clear elevation of leukaemia in the priori selected, exposed parishes was remarkable. Our finding may reflect a causal association due to emissions, but it could also be due to unknown confounding, or chance.

The EPA reference dose for methylmercury (MeHg) was established using data from populations with greater exposures than those typical of the US. Few data are available on potential adverse health effects at lower levels. We examined relationships between hair mercury (Hg) levels and neuropsychological outcomes in a population of US children. This study included data from 355 children ages 6-10 enrolled in the New England Children's Amalgam Trial. Data on total hair Hg levels, sociodemographic information and neuropsychological function were collected. We evaluated associations between hair Hg and neuropsychological test scores with linear regression methods and used generalized additive models to determine the shape of associations that departed from linearity. Models controlled for relevant covariates, including the potential beneficial effects of consuming fish. In adjusted models, we observed no significant linear relationships between hair Hg level and any test score. Significant departures from linearity were identified for WIAT Math Reasoning and WRAMVA Visual-Motor Composite scores. The association was positive for hair Hg levels below 0.5 microg/g and negative for levels between 0.5 and 1.0 microg/g. Overall, test scores of children with hair Hg levels 1.0 microg/g appeared to be lower than those of children with levels < 1.0 microg/g, but few children had levels in this upper range and these differences did not reach statistical significance. Hair Hg levels below 1.0 microg/g in US school-age children were not adversely related to neuropsychological function.

Particulate matter from wood smoke may cause health effects through generation of oxidative stress with resulting damage to DNA. We investigated oxidatively damaged DNA and related repair capacity in peripheral blood mononuclear cells (PBMC) and measured the urinary excretion of repair products after controlled short-term exposure of human volunteers to wood smoke. Thirteen healthy adults were exposed first to clean air and then to wood smoke in a chamber during 4h sessions, 1 week apart. Blood samples were taken 3h after exposure and on the following morning, and urine was collected after exposure, from bedtime until the next morning. We measured the levels of DNA strand breaks (SB), oxidized purines as formamidopyrimidine-DNA-glycosylase (FPG) sites and activity of oxoguanine glycosylase 1 (hOGG1) in PBMC by the comet assay, whereas mRNA levels of hOGG1, nucleoside diphosphate linked moiety X-type motif 1 (hNUDT1) and heme oxygenase 1 (hHO1) were determined by real-time RT-PCR. The excretion of 8-oxo-7,8-dihydro-oxoguanine (8-oxoGua) and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in urine was measured by high performance liquid chromatography purification followed by gas chromatography with mass spectrometry. The morning following exposure to wood smoke the PBMC levels of SB were significantly decreased and the mRNA levels of hOGG1 significantly increased. FPG sites, hOGG1 activity, expression of hNUDT1 and hHO1, urinary excretion of 8-oxodG and 8-oxoGua did not change significantly. Our findings support that exposure to wood smoke causes systemic effects, although we could not demonstrate genotoxic effects, possibly explained by enhanced repair and timing of sampling.

Unlabelled: Children may be at particular risk from toxic effects of mercury (Hg). Previous studies of hair (organic) and urine (inorganic) Hg levels in US children were unable to assess Hg levels while accounting for exposure to amalgam dental restorations. This analysis describes, over a 5-year period, levels and correlates/predictors of scalp hair (H-Hg) and urinary (U-Hg) mercury in 534 New England Children's Amalgam Trial (NECAT) participants, aged 6-10 years and without exposure to dental amalgam at baseline., Results: Mean H-Hg levels were between 0.3 and 0.4 microg/g over 5 years. 17-29% of children had H-Hg levels > or = 0.5 microg/g, and 5.0 to 8.5% of children had levels > or = 1 microg/g, in any given study year. In adjusted models, fish consumption frequency was the most robust predictor of high H-Hg. U-Hg mean levels were between 0.7 and 0.9 microg/g creatinine over two years. The percentage of those with U-Hg > or 2.3 microg/g creatinine ranged from 4% to 6%. Number of amalgam restorations had a significant dose-response relationship with U-Hg level. Daily gum chewing in the presence of amalgam was associated with high U-Hg.

As part of the European Mercury Emissions from Chlor Alkali Plants (EMECAP) project, we tested the hypothesis that contamination of ambient air with mercury around chlor alkali plants using mercury cells would increase the internal dose of mercury in people living close to the plants. Mercury in urine (U-Hg) was determined in 225 individuals living near a Swedish or an Italian chlor alkali plant, and in 256 age- and sex-matched individuals from two reference areas. Other factors possibly affecting mercury exposure were examined. Emissions and concentrations of total gaseous mercury (TGM) around the plants were measured and modeled. No increase in U-Hg could be demonstrated in the populations living close to the plants. This was the case also when the comparison was restricted to subjects with no dental amalgam and low fish consumption. The emissions of mercury to air doubled the background level, but contributed only about 2 ng/m(3) to long-term averages in the residential areas. The median U-Hg levels in subjects with dental amalgam were 1.2 microg/g creatinine (micro/gC) in Italy and 0.6 microg/gC in Sweden. In individuals without dental amalgam, the medians were 0.9 microg/gC and 0.2 microg/gC, respectively. The number of amalgam fillings, as well as chewing, fish consumption, and female sex were associated with higher U-Hg. The difference between the countries is probably due to higher fish consumption in Italy, demethylated methyl mercury (MeHg) being partly excreted in urine. Post hoc power calculations showed that if the background mercury exposure is low it may be possible to demonstrate an increase in U-Hg of as little as about 10 ng/m(3) as a contribution to ambient mercury from a point source.