| 1. |
- Bergdahl, Ingvar A., et al.
(författare)
-
Non-renal effects and the risk assessment of environmental cadmium exposure.
- 2014
-
Ingår i: Environmental health perspectives. - : Environmental Health Perspectives. - 1552-9924 .- 0091-6765. ; 122:5, s. 431-8
-
Tidskriftsartikel (refereegranskat)abstract
- Exposure to cadmium (Cd) has long been recognized as a health hazard, both in industry and in general populations with high exposure. Under the currently prevailing health risk assessment, the relationship between urinary Cd (U-Cd) concentrations and tubular proteinuria is used. However, doubts have recently been raised regarding the justification of basing the risk assessment on this relationship at very low exposure.
|
|
| 2. |
|
|
| 3. |
- Bergemalm, Daniel, 1977-, et al.
(författare)
-
Systemic Inflammation in Preclinical Ulcerative Colitis
- 2021
-
Ingår i: Gastroenterology. - : AGA Institute. - 0016-5085 .- 1528-0012. ; 161:5, s. 1526-1539.e9
-
Tidskriftsartikel (refereegranskat)abstract
- Background & Aims: Preclinical ulcerative colitis is poorly defined. We aimed to characterize the preclinical systemic inflammation in ulcerative colitis, using a comprehensive set of proteins.Methods: We obtained plasma samples biobanked from individuals who developed ulcerative colitis later in life (n = 72) and matched healthy controls (n = 140) within a population-based screening cohort. We measured 92 proteins related to inflammation using a proximity extension assay. The biologic relevance of these findings was validated in an inception cohort of patients with ulcerative colitis (n = 101) and healthy controls (n = 50). To examine the influence of genetic and environmental factors on these markers, a cohort of healthy twin siblings of patients with ulcerative colitis (n = 41) and matched healthy controls (n = 37) were explored.Results: Six proteins (MMP10, CXCL9, CCL11, SLAMF1, CXCL11 and MCP-1) were up-regulated (P < .05) in preclinical ulcerative colitis compared with controls based on both univariate and multivariable models. Ingenuity Pathway Analyses identified several potential key regulators, including interleukin-1β, tumor necrosis factor, interferon-gamma, oncostatin M, nuclear factor-κB, interleukin-6, and interleukin-4. For validation, we built a multivariable model to predict disease in the inception cohort. The model discriminated treatment-naïve patients with ulcerative colitis from controls with leave-one-out cross-validation (area under the curve = 0.92). Consistently, MMP10, CXCL9, CXCL11, and MCP-1, but not CCL11 and SLAMF1, were significantly up-regulated among the healthy twin siblings, even though their relative abundances seemed higher in incident ulcerative colitis.Conclusions: A set of inflammatory proteins are up-regulated several years before a diagnosis of ulcerative colitis. These proteins were highly predictive of an ulcerative colitis diagnosis, and some seemed to be up-regulated already at exposure to genetic and environmental risk factors.
|
|
| 4. |
|
|
| 5. |
-
Handbook on the toxicology of metals
- 2007. - 3
-
Samlingsverk (redaktörskap) (övrigt vetenskapligt/konstnärligt)abstract
- Handbook of the Toxicology of Metals is the standard reference work for physicians, toxicologists and engineers in the field of environmental and occupational health. This new edition is a comprehensive review of the effects on biological systems from metallic elements and their compounds. An entirely new structure and illustrations represent the vast array of advancements made since the last edition. Special emphasis has been placed on the toxic effects in humans with chapters on the diagnosis, treatment and prevention of metal poisoning. This up-to-date reference provides easy access to a broad range of basic toxicological data and also gives a general introduction to the toxicology of metallic compounds.
|
|
| 6. |
- Liang, Yihuai, et al.
(författare)
-
Renal function after reduction in cadmium exposure : an eight-year follow-up of residents in cadmium-polluted areas
- 2012
-
Ingår i: Journal of Environmental Health Perspectives. - : National Institute of Environmental Health Sciences. - 0091-6765 .- 1552-9924. ; 120:2, s. 223-228
-
Tidskriftsartikel (refereegranskat)abstract
- Background and objective: Long-term exposure to cadmium (Cd) causes renal dysfunction, but its change with exposure is unknown. We aimed at assessing the evolution of Cd-induced renal effects after a reduction in dietary exposure to Cd in rice.Methods: 412 residents in previously Cd-polluted and non-polluted areas were examined twice: in 1998 and 2006. Changes in blood Cd, urinary Cd, and kidney function (N-acetyl-β-D-glucosaminidase = NAG, β2-microglobulin, and albumin in urine) were measured. Results: In the most polluted area, mean blood Cd was 8.9 μg/L in 1998 and 3.3 μg/L in 2006, and urinary Cd was 11.6 and 9.0 μg/g creatinine in 1998 and 2006, respectively. Urinary albumin in 1998 increased with urinary Cd but no such exposure-response appeared for 2006 albumin versus urinary Cd 1998, indicating recovery. Other biomarkers of kidney function were also elevated in 1998. Partial recovery was observed for NAG, among women, and suggested for β2-microglobulin, among young individuals. The probability of having a β2-microglobulin above the 95th percentile in 2006 was high in those with an elevated β2-microglobulin in 1998 (odds ratio: 24.8, 95% CI: 11.2-55.3), whereas corresponding estimates for albumin and NAG were 3.0 (1.2-7.5) and 2.6 (1.6-4.4), respectively.Conclusions: Results suggest that a Cd-mediated increase in urinary albumin excretion is reversible upon substantial reduction of exposure. For the markers of tubular effects, a tendency towards improvement, but not complete recovery, was observed. Data from repeated observations suggests that β2-microglobulin may be more informative than NAG as an indicator for the individual's future tubular function.
|
|
| 7. |
|
|
| 8. |
- Nordberg, Gunnar F., et al.
(författare)
-
Introduction-General Considerations and International Perspectives
- 2007. - 3
-
Ingår i: Handbook on the Toxicology of Metals, 3rd Edition. - San Diego : Elsevier. - 9780123694133 ; , s. 1-9
-
Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
- This introductory chapter is composed of two parts. The first section is a brief history of the science of the toxicology of metals by the late Dr. Lars Friberg. He delineates the early realization of the need for international cooperation and consensus that have guided seminal studies related to environmental and occupational toxicology. In this spirit, he initiated work on the first edition of the Handbook of Toxicology of Metals that included contributors from around the world. The second section takes up some current concerns related to the toxicology of metals. It highlights such concerns in relation to the current status of the scientific understanding to date of the metals included and discussed fully in the chapters of the Handbook. Furthermore, it draws attention to future directions in generating new knowledge to fill gaps in the continued quest to assemble the knowledge base necessary for the protection of human health from adverse consequences related to exposure to metals.
|
|
| 9. |
- Nordberg, G F, et al.
(författare)
-
Metal Exposures in Occupational and Environmental Settings
- 2015
-
Ingår i: International Commission on Occupational Health Newsletter. - 1795-0260. ; 13:1, s. 12-14
-
Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- The use of metals has expanded substantially in the last century and gives rise to widespread exposure of humans. It has long been recognized that metals are important toxic agents that may cause acute and chronic poisoning in metal workers and population groups with high exposures. In recent years evidence has been presented indicating that low level exposures to metallic compounds contribute to the occurrence of several common diseases. The World Health Organization (WHO, 2009) has estimated that on a Global basis, 143,000 deaths and nearly 9 million disability-adjusted life years (DALYs; i.e. years of healthy life lost) were caused by lead exposure in 2004. Although lead exposure in the general population of many countries has decreased since 2004 because of the continued phase-out of lead in gasoline, several recent epidemiological studies support the notion that low-exposure effects of lead occur in addition to those considered by the WHO (2009). It is therefore quite possible that the present global burden of disease caused by lead exposure is the same or greater than the one estimated in 2004.In addition to the estimates of lead-related disease and mortality, there are other well documented effects that were not included in the WHO estimates of the global burden of disease. This organization further summarized data indicating 9100 deaths and 125,000 DALYs per year in Bangladesh from arsenic in drinking water and that mercury exposure (mainly methylmercury) through fish consumption causes cognitive deficits and mild retardation in a considerable number of children. An increased incidence of myocardial infarction has been reported in populations with a high intake of methylmercury from fish and a low intake of polyunsaturated fatty acids. The public health impact of this observation of interaction between a nutritional factor and a toxic metal compound may be considerable. There is evidence for a role for relatively low occupational exposure to manganese as well as exposure in the general environment as a contributory factor to the increasing prevalence of Parkinson disease and there is a potentially great importance of metal exposure in early life as a risk factor for neurodegenerative disorders later in life. Recent epidemiological evidence indicates a role for cadmium in the general environment in increasing the occurrence of renal effects and osteoporosis, as well as cardiovascular diseases. There is no doubt thus that exposure to toxic metals and their compounds represents important causal factors contributing to the global burden of disease. Deficient dietary intake of essential metals in food in a global perspective was estimated by the WHO (2009) to cause 433,000 deaths and 15,580,000 DALYs from zinc deficiency and 273,000 deaths and 19,734,000 DALYs per year from iron deficiency.In view of the considerable global burden of disease caused by metals there is an obvious need for preventive action.
|
|
| 10. |
- Nordberg, Gunnar F., et al.
(författare)
-
Preface
- 2007. - 3
-
Ingår i: Handbook on the Toxicology of Metals, 3rd Edition. - San Diego : Elsevier. - 9780123694133 ; , s. V-V
-
Bokkapitel (övrigt vetenskapligt/konstnärligt)
|
|
