Impact of consumption of freshwater fish on mercury levels in hair, blood, urine, and alveolar air

Human exposure to methylmercury occurs mainly via consumption of fish. The aim of the study was to investigate the influence of freshwater fish consumption on mercury levels in hair, blood, urine, and end-exhaled air. Twenty subjects without dental amalgam fillings were recruited from sport-fishing societies. They ranged in age from 61 to 87 yr. Six individuals ate freshwater fish at least once a week and were categorized as high consumers. Eight individuals were classified as medium consumers and ate freshwater fish at least once a month but less than once a week. Six individuals were categorized as low consumers and had not eaten freshwater fish in the past 3 mo. Among the high consumers, median concentrations of mercury were 8.6 mug/L in blood, 2.4 mug/g in hair, 10 mug/L in end-exhaled air, and 1.1 mug/g creatinine in urine. The relationship between freshwater fish consumption and mercury was significant in all biological media. The high-consumption group had much higher mercury levels in blood (9-fold), hair (7-fold), alveolar air (3-fold), and urine (15-fold) than the low-consumption group. The latter finding may be explained by demethylation of methylmercury in the body. The ratio between mercury concentration in blood and hair was 1:270. This implies that the typical blood-hair ratio of 1:250, specified by the World Health Organization (WHO) in 1990, is valid also for exposure to low amounts of methylmercury

Influence of solvent exposure and aging on cognitive functioning: an 18 year follow up of formerly exposed floor layers and their controls

Objectives: To extend our knowledge of how exposure to neurotoxic substances during working life affects cognitive functioning in the long term. Does long term occupational exposure to organic solvents lead to aggravated cognitive impairment later in life? Methods: A follow up was conducted of floor layers exposed to solvents and their unexposed referents (carpenters) 18 years after the baseline assessment. The pattern of cognitive changes in the two groups was compared, with the same 10 neuropsychological tests from the test battery for investigating functional disorders (TUFF) that were used at baseline. The study included 41 floor layers and 40 carpenters. A medical examination focused on health at the present and during the past 18 years. An extensive exposure assessment made in the initial study included questionnaires, interviews, and measurements. Additional exposure during the follow up period was minor, as explored in interviews at follow up. Results: The entire group of floor layers did not deteriorate significantly more over time than did the carpenters. However, among the oldest subjects (>60 years), only floor layers showed decline in visual memory. Moreover, the most highly exposed floor layers deteriorated significantly more than their referents in visual memory and perceptual speed, and they tended to display larger decrements in motor speed. Significant dose effect relations were found; higher cumulative exposure was associated with decrements in visual episodic memory, perceptual speed and attention, and visuospatial skill. Conclusions: The hypothesis that floor layers would deteriorate more in cognitive performance than their unexposed referents over a period of 18 years was partly supported by the results of this study. The results are consistent with the view that the negative effects of exposure to solvents may interact with the normal aging process, primarily at heavy exposure

Increased blood cadmium levels were not associated with increased fracture risk but with increased total mortality in women : the Malmö Diet and Cancer Study

Summary: This study aimed to investigate if high levels of blood cadmium at baseline were associated with increased fracture risk during follow-up in middle-aged women. No increased fracture risk was observed during follow-up, but women with higher levels of cadmium had an increased overall mortality. Introduction: Exposure to high levels of cadmium has been associated with an increased fracture risk. The aim was to investigate a perceived association between low levels of blood cadmium (B-Cd) at baseline and risk of first incident fracture. Methods: From the population-based Malmö Diet and Cancer Study Cardiovascular cohort, 2920 middle-aged women with available background questionnaire and B-Cd measurements were included. Women were divided into quartiles (Q) according to their cadmium levels (Cd-Q1 0.51 μg/L). National registries were analysed for prospective risk of fractures or death. Associations between B-Cd and fracture risk were assessed by survival analysis (Cox regression analysis). Results: In total, 998 first incident fractures occurred in women during a follow-up lasting 20.2 years (median) (12.5–21.2 years) (25th–75th percentile). Women in Cd-Q4 were more often current smokers than in Cd-Q1 78.4 vs. 3.3% (p < 0.001) and the number of cigarettes smoked per day correlated with B-Cd (r = 0.49; p < 0.001). The risk of fracture was not associated with baseline B-Cd in adjusted models. The hazard ratio (HR) Cd-Q4 vs. Cd-Q1 was 1.06 (95% confidence interval (CI) 0.89–1.27). In the multivariate Cox regression, independent variables for increased fracture risk were history of gastric ulcer and increasing age, whereas increasing body mass index (BMI) lowered fracture risk. Overall mortality was significantly higher for women with high B-Cd, HR 2.06 (95% CI 1.57–2.69). Conclusions: Higher blood levels of cadmium did not increase fracture risk in middle-aged women but reduced overall survival

8-isoprostane in exhaled breath condensate after experimental exposure to wood smoke in humans

Wood smoke, a well-known indoor and outdoor air pollutant, may cause adverse health effects through oxidative stress. In this study 8-isoprostane, a biomarker of oxidative stress, was measured in exhaled breath condensate (EBC) and urine before and after experimental exposure to wood smoke. The results were compared with measurements of other biomarkers of oxidative stress and inflammation. Thirteen subjects were exposed first to clean air and then, after 1 week, to wood smoke in an exposure chamber during 4-hour sessions. Exhaled breath condensate, exhaled nitric oxide, blood and urine were sampled before and at various intervals after exposure to wood smoke and clean air. Exhaled breath condensate was examined for 8-isoprostane and malondialdehyde (MDA), while exhaled air was examined for nitric oxide, serum for Clara cell protein (CC16) and urine for 8-isoprostane. 8-isoprostane in EBC did not increase after wood smoke exposure and its net change immediately after exposure was inversely correlated with net changes in MDA (r(s)= -0.57, p= 0.041) and serum CC16 (S-CC16) (r(p)= -0.64, p= 0.020) immediately after the exposure. No correlation was found between 8-isoprostane in urine and 8-isoprostane in EBC. In this study controlled wood smoke exposure in healthy subjects did not increase 8-isoprostane in EBC

8-isoprostane in exhaled breath condensate after experimental exposure to wood smoke in humans

Wood smoke, a well-known indoor and outdoor air pollutant, may cause adverse health effects through oxidative stress. In this study 8-isoprostane, a biomarker of oxidative stress, was measured in exhaled breath condensate (EBC) and urine before and after experimental exposure to wood smoke. The results were compared with measurements of other biomarkers of oxidative stress and inflammation. Thirteen subjects were exposed first to clean air and then, after 1 week, to wood smoke in an exposure chamber during 4-hour sessions. Exhaled breath condensate, exhaled nitric oxide, blood and urine were sampled before and at various intervals after exposure to wood smoke and clean air. Exhaled breath condensate was examined for 8-isoprostane and malondialdehyde (MDA), while exhaled air was examined for nitric oxide, serum for Clara cell protein (CC16) and urine for 8-isoprostane. 8-isoprostane in EBC did not increase after wood smoke exposure and its net change immediately after exposure was inversely correlated with net changes in MDA (r(s)= -0.57, p= 0.041) and serum CC16 (S-CC16) (r(p)= -0.64, p= 0.020) immediately after the exposure. No correlation was found between 8-isoprostane in urine and 8-isoprostane in EBC. In this study controlled wood smoke exposure in healthy subjects did not increase 8-isoprostane in EBC

Are urinary PAHs biomarkers of controlled exposure to diesel exhaust?

Urinary polycyclic aromatic hydrocarbons (PAHs) were evaluated as possible biomarkers of exposure to diesel exhaust (DE) in two controlled-chamber studies. We report levels of 14 PAHs from 28 subjects in urine that were collected before, immediately after and the morning after exposure. Using linear mixed-effects models, we tested for effects of DE exposure and several covariates (time, age, gender and urinary creatinine) on urinary PAH levels. DE exposures did not significantly alter urinary PAH levels. We conclude that urinary PAHs are not promising biomarkers of short-term exposures to DE in the range of 106-276 mu g/m(3)

Mortality from cardiovascular diseases and exposure to inorganic mercury

OBJECTIVE—To study the mortality from cardiovascular and other chronic non-neoplastic diseases after long term exposure to inorganic mercury. Limited information is available on the effect of chronic exposure to mercury on the cardiovascular system.
METHODS—The mortality was studied among 6784 male and 265 female workers from four mercury mines and mills in Spain, Slovenia, Italy, and the Ukraine. Workers were employed between 1900 and 1990; the follow up period lasted from the 1950s to the 1990s. The mortality of the workers was compared with national reference rates.
RESULTS—Among men, there was a slight increase in overall mortality (standardised mortality ratio (SMR) 1.08, 95% confidence interval (95% CI) 1.04 to 1.12). An increased mortality was found from hypertension (SMR 1.46, 95% CI 1.08 to 1.93), heart diseases other than ischaemic (SMR 1.36, 95% CI 1.20 to 1.53), pneumoconiosis (SMR 27.1, 95% CI 23.1 to 31.6), and nephritis and nephrosis (SMR 1.55, 95% CI 1.13 to 2.06). The increase in mortality from cardiovascular diseases was not consistent among countries. Mortality from hypertension and other heart diseases increased with estimated cumulative exposure to mercury; mortality from ischaemic heart disease and cerebrovascular diseases increased with duration of employment, but not with estimated exposure to mercury. Results among women were hampered by few deaths.
CONCLUSION—Despite limited quantitative data on exposure, possible confounding, and likely misclassification of disease, the study suggests a possible association between employment in mercury mining and refining and risk in some groups of cardiovascular diseases.


Keywords: epidemiology; inorganic mercury; mining; cardiovascular disease