Cadmium Concentrations In Air Research Articles

Chronic Cadmium Intoxication and Renal Injury Among Workers of a Small-scale Silver Soldering Company.

BackgroundCadmium exposure may induce chronic intoxication with renal damage. Silver soldering may be a source of cadmium exposure.MethodsWe analyzed working environment measurement data and periodic health screening data from a small-scale silver soldering company with ten workers. Concentrations of cadmium in air from working environment measurement data were obtained. Concentrations of blood and urinary cadmium, urine protein, and urine β2-microglobulin (β2M) were obtained. The generalized linear model was used to identify the association between blood and urine cadmium and urine β2M concentrations. Clinical features of chronic cadmium intoxication focused with toxicological renal effects were described.ResultsThe mean duration of work was 8.5 years (standard deviation [SD] = 6.9, range = 3–20 years). Cadmium concentrations in air were ranged from 0.006 to 0.015 mg/m3. Blood cadmium concentration was elevated in all ten workers, with a highest level of 34.6 μg/L (mean = 21.288 μg/L, SD = 11.304, range = 9.641–34.630 μg/L). Urinary cadmium concentration was elevated in nine workers, with a highest level of 62.9 μg/g Cr (mean = 22.151 μg/g creatinine, SD = 19.889, range = 3.228–62.971 μg/g creatinine). Urine β2M concentration was elevated in three workers. Urinary cadmium concentration was positively associated with urine protein concentration (beta coefficient = 10.27, 95% confidence interval = [4.36, 16.18]). Other clinical parameters were compatible with renal tubular damage.ConclusionCadmium intoxication may occur at quite low air concentrations. Exposure limit may be needed to be lowered.

Assessment of long-term exposure to airborne dioxin and cadmium concentrations in the Lyon metropolitan area (France)

Identifying the long-term effects of airborne pollutants requires the computation of the spatial and temporal variability of their concentration in air to estimate the exposure of the population. To estimate exposure levels of individuals in a breast cancer case control study nested in a national prospective cohort, we determine here the differential impact of a variety of cadmium and dioxin sources on urban air over a large urban area and over a period of almost 20years.To that end, we couple an emission model, to estimate dioxin and cadmium atmospheric annual releases, with an urban dispersion model in order to compute pollutant concentration fields at a fine temporal (1h) and spatial (25m) resolution. The reliability of the modelling chain is compared to two types of measurement: i) localized industrial emissions and ii) dioxin and cadmium air monitoring data (from 2007 to 2008), collected at a fixed station, placed in the city centre, as well as at three mobile short-term dioxin monitoring stations, located in the suburbs (the latter providing dioxin data, only). Comparisons between measured and estimated emissions show non-negligible difference, with a correlations for dioxin (rs=0.42) and cadmium (rs=0.41). Despite this, mean values between estimated emissions and emission measurements are close to each other, in particular for cadmium. Weekly average modelled concentrations show an overall good agreement with weekly average measured concentrations in spring and summer but are generally lower than monitored data in winter due to peak concentrations from diffuse sources representing an important proportion of emissions in 2007/2008. The model provides better results for cadmium than for dioxin. Despite the relevant errors in the model predictions, the model meets the validation criteria, defined by Chang and Hanna for an urban dispersion model.Simulation scenarios of air pollutant concentrations, reconstructed over the last 20years, show the effects of the variability of the pollutant sources over time with decreasing levels of dioxin and cadmium concentrations in air. This is primarily due to the reduction in localized industrial releases, which results in a general trend of homogenization of the exposure of the population.The model further allows us to dissociate the contribution of different types of pollutant sources on the population exposure. The impact on local concentrations due to industrial emissions, which were originally responsible for the major impact on air quality, is shown to drop over the years by 99% and 92% for dioxin and cadmium, respectively. Today, the major contributions are due to diffuse miscellaneous sources in the case of dioxin and to traffic-related emissions for cadmium.Average modelled concentrations at the study subjects' residential locations range from 10.2 to 82.1fg-TEQ/m3 for dioxin and 0.10 to 1.6ng/m3 for cadmium and are comparable with data from the literature.The study results will be essential to increase the accuracy of the assessment of long-term airborne dioxin and cadmium exposure and improve the results of epidemiological studies.

Occupational exposure to heavy metals: DNA damage induction and DNA repair inhibition prove co-exposures to cadmium, cobalt and lead as more dangerous than hitherto expected.

Co-exposure to cadmium, cobalt, lead and other heavy metals occurs in many occupational settings, such as pigment and batteries production, galvanization and recycling of electric tools. However, little is known about interactions between several heavy metals. In the present study we determined DNA single strand break (DNA-SSB) induction and repair capacity for 8-oxoguanine in mononuclear blood cells of 78 individuals co-exposed to cadmium (range of concentrations in air: 0.05-138.00 micro g/m(3)), cobalt (range: 0-10 micro g/m(3)) and lead (range: 0-125 micro g/m(3)). Exposure to heavy metals was determined in air, blood and urine. Non-parametric correlation analysis showed a correlation between cadmium concentrations in air with DNA-SSB (P = 0.001, R = 0.371). Surprisingly, cobalt air concentrations correlated even better (P < 0.001, R = 0.401), whereas lead did not correlate with DNA-SSB. Logistic regression analysis including 11 possible parameters of influence resulted in a model showing that cobalt in air, cadmium in air, cadmium in blood and lead in blood influence the level of DNA-SSB. The positive result with cobalt was surprising, since exposure levels were much lower compared with the TRK-value of 100 micro g/m(3). To examine, whether the positive result with cobalt is stable, we applied several logistic regression models with two blocks, where all factors except cobalt were considered preferentially. All strategies resulted in the model described above. Logistic regression analysis considering also all possible interactions between the relevant parameters of influence finally resulted in the following model: Odds ratio = 1.286(Co in air) x 1.040(Cd in air) x 3.111(Cd in blood) x 0.861(Pb in air) x 1.023(Co in air x Pb in air). This model correctly predicts an increased level of DNA-SSB in 91% of the subjects in our study. One conclusion from this model is the existence of more than multiplicative effects for co-exposures of cadmium, cobalt and lead. For instance increasing lead air concentrations from 1.6 to 50 micro g/m(3) in the presence of constant exposures to cobalt and cadmium (8 micro g/m(3) and 3.8 micro g/m(3)) leads to an almost 5-fold increase in the odds ratio, although lead alone does not increase DNA-SSB. The mechanism behind these interactions might be repair inhibition of oxidative DNA damage, since a decrease in repair capacity will increase susceptibility to reactive oxygen species generated by cadmium or cobalt. Indeed, repair of 8-oxoguanine decreased with increasing exposures and inversely correlated with the level of DNA-SSB (P = 0.001, R = -0.427). Protein expression patterns of individuals exposed to cobalt concentrations of approximately 10 micro g/m(3) were compared with those of unexposed individuals using two-dimensional gel electrophoresis. Qualitative and apparent quantitative alterations in protein expression were selective and certainly occurred in <0.1% of all proteins. In conclusion, the hazard due to cobalt exposure - that has been classified only as IIB by the IARC - seems to be underestimated, especially when individuals are co-exposed to cadmium or lead. Co-exposure may cause genotoxic effects, even if the concentrations of individual heavy metals do not exceed TRK-values.

Concentrations of cadmium in air and urine in an alkaline battery works.

Concentrations of cadmium in air are available for exposed workers in an alkaline battery factory from 1965, and of cadmium in urine concentrations from rather later. Using simple statistical methods annual data sets have been analysed by department, job or other classification. Summary results of concentrations of cadmium in air from 1965 and in urine from 1970 are examined, and show a steady annual reduction. No attempt is made to relate changes in concentrations to changes in manufacturing practice or control measures, although the effects of one major change are noted. Relations between concentrations of cadmium in air and in urine since 1970 are reported. Those between cadmium in air and recent concentrations of cadmium in blood and of beta 2-microglobulin in urine are commented on. The kinetics of cadmium absorption, partition and excretion are not considered in any depth.

Forecast of cadmium impact on the environment using environmental models

A study of the pathway of cadmium in the European Community (EC) has led to the development of a time-dependent computer model that relates past and present environmental cadmium levels to the inputs of cadmium. Information on the origin and movement of environmental cadmium through the different compartments of the biosphere has been obtained from a literature study and has been used to simulate the pathway of cadmium in the EC. The model is used to investigate the future evolution of the average cadmium concentrations in air, soil, and sediments in the EC, based on assumptions for the future evolution of consumption and for possible environmental policies to be adopted. The results are averages taken over the whole Community, which implies that no local pollution can be obtained from this model that only indicates the possible future trend.