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

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 <0.18 µg/L, Cd-Q2 0.18-0.28 µg/L, Cd-Q3 0.28-0.51 µg/L, and Cd-Q4 >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.

Cancer incidence in Swedish oil refinery workers exposed to benzene.

BACKGROUND: Oil refinery workers are exposed to benzene, which is a well-known cause of leukaemia, but results on leukaemia in oil refinery workers have been mixed, and the data on workers' exposure is limited. Oil refinery workers are also exposed to asbestos and several studies have shown increased risk of mesothelioma. AIM: The objective was to investigate cancer incidence, especially leukaemia, at low to moderate exposure to benzene in an update of a previous study of employees at three Swedish oil refineries. METHODS: Cancer incidence was followed up in 2264 men (1548 refinery operators) employed at three oil refineries in Sweden for at least one year. Job types and employment times were collected from complete company files. A retrospective assessment of the benzene exposure was performed by occupational hygienists in collaboration with the refineries using historic measurements as well as detailed information on changes in the industrial hygiene and technological developments. Cases of cancer were retrieved by a linkage with the Swedish Cancer Register through 35-47 years of follow-up and standardized incidence ratios (SIR) with 95% confidence intervals (CI) were calculated. RESULTS: In total, 258 tumors had occurred versus 240 expected (SIR 1.07; 95% CI 0.95-1.21). There were 10 cases of leukaemia, all in refinery operators (SIR 2.4; 95% CI 1.18-4.51). There were three cases of pleural mesothelioma, two of which in refinery operators. The mean estimated cumulative benzene exposure for the cases of leukaemia was 7.9 ppm-years (median 4.9, range 0.1-31.1). DISCUSSION: The study suggests that low to moderate average cumulative benzene exposure increases the risk of leukaemia. Limitations include the modest number of cases and potential misclassification of exposure. CONCLUSION: The present study indicated an increased risk of leukaemia in male oil refinery workers with low to moderate exposure to benzene.

Risk of hypertension from exposure to road traffic noise in a population-based sample.

OBJECTIVES: To assess the association between hypertension and traffic noise. METHODS: The prevalence and incidence of hypertension were examined in a Swedish municipality partly affected by noise from a highway (20,000 vehicles/24 h) and a railway (200 trains/24 h). A-weighed 24 h average sound levels (L(Aeq,24h)) from road and railway traffic were calculated at each residential building using a geographical information system and a validated model. Physician-diagnosed hypertension, antihypertensive medication and background factors were evaluated in 1953 individuals using postal questionnaires (71% response rate). Prevalence ratios and odds ratios (ORs) were calculated for different noise categories. Based on year of moving into the residence and year of diagnosis, person-years and incidence rates of hypertension were estimated, as well as relative risks including covariates, using Poisson and Cox regression. RESULTS: When road traffic noise, age, sex, heredity and body mass index were included in logistic regression models, and allowing for >10 years of latency, the OR for hypertension was 1.9 (95% CI 1.1 to 3.5) in the highest noise category (56-70 dBA) and 3.8 (95% CI 1.6 to 9.0) in men. The incidence rate ratio was increased in this group of men, and the relative risk of hypertension in a Poisson regression model was 2.9 (95% CI 1.4 to 6.2). There were no clear associations in women or for railway noise. CONCLUSIONS: The study shows a positive association between residential road traffic noise and hypertension among men, and an exposure-response relationship. While prevalence ratios were increased, findings were more pronounced when incidence was assessed.

Inorganic arsenic in food products on the Swedish market and a risk-based intake assessment.

Inorganic arsenic (iAs) and total arsenic (tAs) were determined in common food from the Swedish market. Special focus was on rice, fish and shellfish products. For the speciation of iAs the European standard EN:16802 based on anion exchange chromatography coupled to ICP-MS was used. The two market basket food groups cereals (including rice), and sweets and condiments (a mixed group of sugar, sweets, tomato ketchup and dressings), contained the highest iAs levels (means 9 and 7 µg iAs/kg), whereas other food groups, including fish, did not exceed 2 µg iAs/kg. Varying levels of iAs were found in separate samples of tomato ketchup, 2.4-26 µg/kg, and is suggested to be one reason of the rather high average level of iAs in the food group sweets and condiments. Some specific food products revealed iAs levels much higher, i.e. rice crackers 152 and Norway lobster 89 µg iAs/kg. The intake of iAs via food was estimated by data from two national consumption surveys, performed in 2010-11 (1797 adults) and 2003 (2259 children). The estimated median iAs intakes in adults and children were 0.047 and 0.095 µg/kg body weight and day, respectively. The iAs intake for rice eaters was about 1.4 times higher than for non-rice eaters. Validation of the consumption survey-based iAs intake, using food purchase and market basket data mainly from 2015, resulted in a per capita intake of a similar magnitude, i.e. 0.056 µg/kg body weight and day. The estimated cancer risk for adults using low-dose linear extrapolation is <1 per 100,000 per year.

Experimental exposure to wood smoke: effects on airway inflammation and oxidative stress.

BACKGROUND: Particulate air pollution affects cardiovascular and pulmonary disease and mortality. A main hypothesis about the mechanisms involved is that particles induce inflammation in lower airways, systemic inflammation and oxidative stress. OBJECTIVES: To examine whether short-term exposure to wood smoke in healthy subjects affects markers of pulmonary inflammation and oxidative stress. METHODS: 13 subjects were exposed first to clean air and then to wood smoke in a chamber during 4-hour sessions, 1 week apart. The mass concentrations of fine particles at wood smoke exposure were 240-280 mug/m(3), and number concentrations were 95 000-180 000/cm(3), about half of the particles being ultrafine (<100 nm). Blood and breath samples were taken before and at various intervals after exposure to wood smoke and clean air and examined for exhaled nitric oxide and Clara cell protein in serum and urine, and malondialdehyde in exhaled breath condensate. RESULTS: Exposure to wood smoke increased alveolar nitric oxide 3 hours post-exposure while malondialdehyde levels in breath condensate were higher both immediately after and 20 hours after exposure. Serum Clara cell protein was increased 20 hours after exposure. CONCLUSIONS: Wood smoke at levels that can be found in smoky indoor environments caused an inflammatory response and signs of increased oxidative stress in the respiratory tract, especially in the lower airways.

Gamma radiation doses to people living in Western Sweden.

Indoor environments contribute to gamma radiation in the general population. The aims of the present study were to investigate average gamma radiation doses in a rural and an urban area of Sweden, compare indoor dose rates with personal exposure, and study the effects of building characteristics on radiation levels. Radiation was measured with thermoluminescence dosimeters (TLDs). Repeated measurements were performed with TLDs worn by participants (n=46) and placed in their dwellings. Personal dose rates were 0.092microSv/h (rural) and 0.096microSv/h (urban). The mean effective gamma dose rates in dwellings were 0.091microSv/h (rural) and 0.11microSv/h (urban), which are higher than the world average. Dose rates in apartments were higher than in detached houses and higher for concrete than wooden dwellings. Personal dose rates were strongly associated with dwelling dose rates (r(p)=0.68, p<0.01) and could be modelled. Within-participant variability was low.

Childhood tuberculosis and exposure to indoor air pollution: a systematic review and meta-analysis.

BACKGROUND: Indoor air pollution (IAP) from environmental tobacco smoke (ETS) and biomass fuel smoke (BMS) poses respiratory health risks, with children and women bearing the major burden. OBJECTIVES: We used a systematic review and meta-analysis to investigate the relation between childhood tuberculosis (TB) and exposure to ETS and BMS. METHODS: We searched three databases for epidemiological studies that investigated the association of childhood TB with exposure to ETS and BMS. We calculated pooled estimates and heterogeneity for studies eligible for inclusion in the meta-analysis and stratified studies on ETS by outcome. RESULTS: Five case-control and three cross-sectional studies were eligible for inclusion in the meta-analysis and quality assessment. Pooled effect estimates showed that exposure to ETS is associated with tuberculous infection and TB disease (OR 1.9, 95%CI 1.4-2.9) among exposed compared to non-exposed children. TB disease in ETS studies produced a pooled OR of 2.8 (95%CI 0.9-4.8), which was higher than the OR for tuberculous infection (OR 1.9, 95%CI 0.9-2.9) for children exposed to ETS compared to non-exposed children. Studies on BMS exposure were too few and too small to permit a conclusion. CONCLUSION: Exposure to ETS increases the risk of childhood TB disease or tuberculous infection.

Variability in airborne and biological measures of exposure to mercury in the chloralkali industry: implications for epidemiologic studies.

Exposure assessment is a critical component of epidemiologic studies, and more sophisticated approaches require that variation in exposure be considered. We examined the intra- and interindividual sources of variation in exposure to mercury vapor as measured in air, blood, and urine among four groups of workers during 1990-1997 at a Swedish chloralkali plant. Consistent with the underlying kinetics of mercury in the body, the variability of biological measures was dampened considerably relative to the variation in airborne levels. Owing to the effects of intraindividual variation, estimating workers' exposures from a few measurements can attenuate measures of effect. To examine such effects on studies relating long-term exposure to a continuous health outcome, we evaluated the utility of each exposure measure by comparing the necessary sample sizes required for accurate estimation of a slope coefficient obtained from a regression analysis. No single measure outperformed the others for all groups of workers. However, when workers were evaluated together, creatinine-corrected urinary mercury better discriminated workers' exposures than airborne or blood mercury levels. Thus, pilot studies should be conducted to examine variability in both air and biomonitoring data because quantitative information about the relative magnitude of the intra- and interindividual sources of variation feeds directly into our efforts to design an optimal sampling strategy when evaluating health risks associated with occupational or environmental contaminants.

Cadmium, mercury, and lead in kidney cortex of the general Swedish population: a study of biopsies from living kidney donors.

Cadmium, mercury, and lead concentrations were determined in deep-frozen kidney cortex biopsies taken from 36 living, healthy Swedish kidney donors (18 males and 18 females), who were 30-71 (mean 53) years of age. Information about occupation, smoking, the presence of dental amalgam, and fish consumption could be obtained for 27 of the donors. The samples (median dry weight 0.74 mg) were analyzed using inductively coupled plasma mass spectrometry, and the results were transformed to wet-weight concentrations. The median kidney Cd was 17 micrograms/g (95% confidence interval, 14-23 micrograms/g), which was similar in males and females. In 10 active smokers, the median kidney Cd was 24 micrograms/g, and in 12 who never smoked, it was 17 micrograms/g. The median kidney Hg was 0.29 micrograms/g, with higher levels in females (median 0.54 micrograms/g) than in males (median 0.16 micrograms/g). Subjects with amalgam fillings had higher kidney Hg (median 0.47 micrograms/g, n = 20) than those without dental amalgam (median 0.15 micrograms;g/g, n = 6), but kidney Hg was below the detection limit in some samples. Nearly half of the samples had kidney Pb below the detection limit. The median kidney Pb was estimated as 0. 14 micrograms/g. This is the first study of heavy metals in kidney cortex of living, healthy subjects, and the results are relatively similar to those of a few previous autopsy studies, indicating that results from autopsy cases are not seriously biased in relation to kidney metal concentrations in the general population. Cd concentrations in those who never smoked were relatively high, indicating considerable Cd intake from the diet in Sweden. The effect of dental amalgam on kidney Hg was as expected, although the reason for the difference in Hg levels between males and females is unclear.

Long-term use of nicotine chewing gum and mercury exposure from dental amalgam fillings.

In experimental studies, chewing gum has been shown to increase the release rate of mercury vapor from dental amalgam fillings. The aim of the present study was to investigate the influence of long-term frequent chewing on mercury levels in plasma and urine. Mercury levels in plasma (P-Hg) and urine (U-Hg), and urinary cotinine were examined in 18 subjects who regularly used nicotine chewing gum, and in 19 referents. Age and number of amalgam surfaces were similar in the two groups. Total mercury concentrations in plasma and urine were determined by means of cold vapor atomic absorption spectrometry. Urinary cotinine was determined by gas chromatography-mass spectrometry. The chewers had been using 10 (median) pieces of gum per day for the past 27 (median) months. P-Hg and U-Hg levels were significantly higher in the chewers (27 nmol/L and 6.5 nmol/mmol creatinine) than in the referents (4.9 nmol/L and 1.2 nmol/mmol creatinine). In both groups, significant correlations were found between P-Hg or U-Hg on the one hand and the number of amalgam surfaces on the other. In the chewers, no correlations were found between P-Hg or U-Hg and chewing time per day or cotinine in urine. Cotinine in urine increased with the number of pieces of chewing gum used. The impact of excessive chewing on mercury levels was considerable.

Exposure to mercury vapor and impact on health in the dental profession in Sweden.

Possible adverse effects of mercury exposure in dentistry have been discussed in several studies. The objective of the present study was to carry out detailed measurements of mercury exposure in the dental profession in Sweden, and to search for adverse health effects from such exposure. We examined 22 dentists and 22 dental nurses, working in teams, at six Swedish dental clinics. Measurements of air mercury, performed with personal, active air samplers, showed a median air Hg of 1.8 micrograms/m3 for the dentists, and 2.1 micrograms/m3 for the dental nurses. Spot measurements with a direct reading instrument displayed temporarily elevated air Hg, especially during the preparation and application of amalgam. The average concentration of mercury in whole blood (B-Hg) was 18 nmol/L, in plasma (P-Hg) 5.1 nmol/L, and in urine (U-Hg) 3.0 nmol/mmol creatinine. Possible effects on the central nervous system (CNS) were registered with three questionnaires: Q16, Eysenck Personality Inventory (EPI), and the Profile of Mood Scales (POMS). In the Q16, the number of symptoms was statistically significantly higher in the dentistry group compared with an age- and gender-matched control group (n = 44). The urinary excretion of albumin and urinary activity of the tubular enzyme N-acetyl-beta-glucose-aminidase (NAG) did not differ between the two groups. The results confirm that exposure to mercury in the dental profession in Sweden is low. The air Hg levels were mainly influenced by the method of amalgam preparation and inserting, and by the method of air evacuation during drilling and polishing.

In vivo XRF analysis of mercury: the relation between concentrations in the kidney and the urine.

The objective of this study was to determine the concentrations of mercury in organs of occupationally exposed workers using in vivo x-ray fluorescence analysis. Twenty mercury exposed workers and twelve occupationally unexposed referents participated in the study. Their mercury levels in kidney, liver and thyroid were measured using a technique based on excitation with partly plane polarized photons. The mercury levels in blood and urine were determined using atomic absorption spectrophotometry. The detection limit for mercury in the kidney was exceeded in nine of the exposed workers, but in none of the referents. The mean kidney mercury concentration (including estimates below the detection limits) was 24 micrograms g-1 in the exposed workers, and 1 microgram g-1 in the referents. The association between mercury in the kidney and in urine was statistically significant, but it was unclear whether the relation was linear. The measurements on liver (n = 10) and thyroid (n = 8) in the exposed workers showed mercury levels below the detection limit. The study shows that it is now possible to measure the mercury concentrations in kidneys of occupationally exposed persons, using in vivo x-ray fluorescence. The estimated concentrations are in reasonable agreement with the limited human autopsy data, and the results of animal studies.

Variability in the quantification of abrasion on the Bruxcore device.

The rate of abrasion of dental surfaces during short periods of time is difficult to measure clinically, but one quantifiable method is the use of the Bruxcore bruxism monitoring device. The aim of this study was to estimate the interobserver and intraobserver variation in the Bruxcore system using different reading methods. Fifteen volunteers used individually fabricated Bruxcore devices during 4 consecutive nights, and this procedure was repeated after 6 weeks. The abraded areas of the 30 Bruxcore devices were measured by two observers on two occasions and with three methods: microscope without a reference scale; microscope with a reference scale; and a computer-aided system. Intraobserver variation was small (5%), but interobserver variation was statistically significant for all three methods. The computer-aided system was superior to the other two methods. The interaction between Bruxcore values and observers was statistically significant for the microscope methods but not for the computer method. This was a desired property, indicating stability of the computer-aided method over the range of Bruxcore values observed. Small measurement errors, independent of the size of the measurements, can be expected using a trained observer and a computer-aided method for reading the Bruxcore bruxism monitoring device.

Biological monitoring of exposure to mercury vapor.

Biological monitoring of mercury in whole blood (B-Hg) or urine (U-Hg) can be used to assess exposure to mercury vapor if the kinetics and other sources of variation are taken into account. Its rapid rise postexposure makes B-Hg a good indicator of recent exposure peaks, while U-Hg (corrected for urinary flow rate) reflects average long-term exposure. However, high intraindividual variation sometimes requires the average of several U-Hg determinations. In the general population, methylmercury from fish and mercury from dental amalgam influence B-Hg and U-Hg, respectively, and must be considered if other exposures are being monitored. The quantitative relations between mercury in biological fluids and critical organs are poorly understood. Monitoring U-Hg is useful for assessing the risk of adverse effects and the need for preventive measures. At average U-Hg levels of about 50 micrograms.g creatinine-1 (28 nmol.mmol creatinine-1) the prevalence of symptoms and slight objective changes in the central nervous system and the excretion of certain urinary proteins are increased.

Polyneuropathy possibly caused by 30 years of low exposure to n-hexane.

A slowly developing, mainly sensory, polyneuropathy was found in a 60-year-old man exposed to n-hexane (10-100 mg/m3) for 30 years in a mountain fuel stockpile. The nerve damage was verified by electromyography and sural nerve biopsy, and it is proposed that also a low-grade, but prolonged, exposure to n-hexane may cause polyneuropathy.

Effects of occupational exposure to mercury vapor on lymphocyte micronuclei.

For 26 chloralkali workers exposed to inorganic mercury and 26 age-matched, occupationally unexposed referents, the frequency and size distribution of micronuclei were determined in peripheral lymphocytes stimulated with either phytohemagglutinin or pokeweed mitogen. For the exposed workers the mean concentrations of mercury in urine, plasma, and erythrocytes were 16 nmol/mmol of creatinine, 48 nmol/l, and 78 nmol/l, respectively, and their mean exposure time was 10 years. Neither the frequency nor the size of micronuclei was significantly different in the two groups; nor were there any correlations to current mercury levels. However, in the exposed group, and with phytohemagglutinin as the mitogen, a statistically significant correlation between previous exposure to mercury (cumulative exposure or number of blood mercury peaks) and the frequency of micronuclei was found. This association was also present when the effects of age and smoking were allowed for, and it may indicate an accumulation of cytogenetic effects in T-lymphocytes.

Cerebrospinal fluid proteins in men with chronic encephalopathy after exposure to organic solvents.

Cerebrospinal fluid was examined for 23 patients with chronic toxic encephalopathy after heavy exposure to organic solvents and 23 healthy age-matched referents. No differences were found between the patients and referents with respect to the levels of albumin, immunoglobulin, prealbumin, alpha-1-antitrypsin, beta-2-microglobulin, haptoglobin, or the astroglial cell proteins S100 and glial fibrillary acidic protein in the cerebrospinal fluid. The albumin ratio was normal for both the patients and the referents. The patient group had had heavy exposure to organic solvents, but its members had not been exposed for at least one year before the study. It was concluded that, if exposure to organic solvents affects proteins in cerebrospinal fluid, such effects are probably reversible.

Levels of selenium and antioxidative enzymes following occupational exposure to inorganic mercury.

Levels of selenium and mercury in blood and urine were analysed in 37 male workers exposed to elemental mercury vapour in a chloralkali plant and in 39 unexposed controls of the same age. Mean urinary Hg was 223 nmol l-1 (15 nmol/mmol creatinine) in the exposed group and 26 nmol l-1 (2.0 nmol/mmol creatinine) in the controls. Mean blood and plasma Hg levels were 46 and 36 nmol l-1, respectively, in the exposed group, as compared with 17 and 7 nmol l-1 in the controls. The concentrations of Se in plasma and erythrocytes did not differ between the two groups. Urinary Se levels were, however, slightly but significantly lower in the exposed group (median values 23 vs 29 nmol/mmol creatinine), and there was a negative correlation between urinary Se and plasma Hg in the exposed group. This may be due to a retention of Se in the kidneys. In a subgroup of exposed workers and controls, glutathione peroxidase, superoxide dismutase and catalase were also analysed. No differences were found between the groups with respect to these antioxidative enzymes. The effect on Se status of moderate Hg exposure seems to be of minor clinical importance.