Urban residential greenness and adiposity: A cohort study in Stockholm County.

BACKGROUND: Increasing evidence suggests that exposure to residential greenness is associated with positive health outcomes among urban populations. However, few studies have considered effects on adiposity development in a longitudinal setting. OBJECTIVES: This study aimed to explore the association between long-term exposure to urban residential greenness and markers of adiposity. METHODS: A cohort of 5126 adults from five municipalities in Stockholm County was examined clinically at baseline (1992-1998) and follow-up (2002-2006) after on average nine years. Time-weighted average exposure to urban greenness was estimated by Normalized Difference Vegetation Index (NDVI) within 100 m, 250 m, and 500 m buffers around the residential addresses of each participant. Multiple linear and Poisson regression models were used to estimate associations between greenness and change in weight and waist circumference as well as risk of overweight, obesity and central obesity. Co-exposures to air pollution, traffic noise and distance to water were also examined. RESULTS: In women, higher levels of residential greenness were associated with a reduced increase in waist circumference during follow-up (ß = -0.11 cm/year, 95% CI -0.14; -0.08 per one interquartile range increase in NDVI) and decreased risk for central obesity (IRR = 0.88: 95% CI 0.79; 0.99) in the 500 m buffer. No associations were observed for men or with regard to weight development or the risk of developing overweight or obesity. Exposure to low NDVI levels in combination with high NOx from road traffic and transportation noise as well as long distance to water rendered statistically significant increases in waist circumference in both sexes. CONCLUSION: Higher long-term exposure to greenness was associated with a reduced increase in waist circumference and lower risk of central adiposity in women but not in men. In both sexes, low NDVI exposure in combination with other environmental risk factors appeared particularly harmful.

Exposure to grass pollen--but not birch pollen--affects lung function in Swedish children.

Allergic response to pollen is increasing worldwide, leading to high medical and social costs. However, the effect of pollen exposure on lung function has rarely been investigated. Over 1800 children in the Swedish birth cohort BAMSE were lung-function- and IgE-tested at the age of 8 and 16 years old. Daily concentrations for 9 pollen types together with measurements for ozone, NO2 , PM10 , PM2.5 were estimated for the index day as well as up to 6 days before the testing. Exposure to grass pollen during the preceding day was associated with a reduced forced expiratory volume in 8-yr-olds; -32.4 ml; 95% CI: -50.6 to -14.2, for an increase in three pollen counts/m³. Associations appeared stronger in children sensitized to pollen allergens. As the grass species flower late in the pollen season, the allergy care routines might be weakened during this period. Therefore, allergy information may need to be updated to increase awareness among grass pollen-sensitized individuals.

Interaction between smoking and the interleukin-6 gene affects systemic levels of inflammatory biomarkers.

BACKGROUND: Smoking is associated with a systemic inflammatory response. However, the role of genetic predisposition is not well known. We assessed whether circulatory acute phase reactants were associated with smoking and whether or not the association was modified by the major cytokine gene of the acute phase reaction, interleukin-6 (IL-6). METHODS: In total, 1,003 postmyocardial infarction patients were recruited in six European cities and six repeated clinical examinations performed. C-reactive protein (CRP), interleukin 6 (IL-6), and fibrinogen levels were assayed at 5,659 subject visits. Genotyping of single nucleotide polymorphisms was performed in the IL-6 gene. RESULTS: Cumulative smoking (pack-years) and time since smoking cessation were strongly associated with blood levels of all three inflammatory markers. Among subjects without any respiratory disorder, these associations remained statistically significant for CRP and IL-6. A polymorphism in the IL-6 gene (rs2069840) showed an interaction with smoking on CRP (p < .001) and IL-6 (p = .049) peripheral levels. CONCLUSIONS: These results indicate a potential role of the IL-6 gene in the inflammatory response associated with smoking and suggest rs2069840 polymorphism deserves attention.

Associations of long- and short-term air pollution exposure with markers of inflammation and coagulation in a population sample.

BACKGROUND: Exposure to elevated levels of ambient air pollutants can lead to adverse cardiovascular effects. Potential mechanisms include systemic inflammation and perturbation of the coagulation balance. OBJECTIVES: To investigate long- and short-term effects of air pollution exposure on serum levels of inflammatory (IL-6, TNF-alpha and CRP) and coagulation (fibrinogen and PAI-1) markers relevant for cardiovascular pathology. METHODS: The study group consisted of a population sample of 1028 men and 508 women aged 45-70 years from Stockholm. Long-term air pollution exposure was assessed using spatial modelling of traffic-related NO(2) and heating-related SO(2) emissions at each subject's residential addresses over retrospective periods of 1, 5 and 30 years. Short-term exposure was assessed as averages of rooftop measurements over 12-120 h before blood sampling. RESULTS: Long-term exposures to both traffic-NO(2) and heating-SO(2) emissions showed consistent associations with IL-6 levels. 30-year average traffic-NO(2) exposure was associated with a 64.5% (95% CI 6.7% to 153.8%) increase in serum IL-6 per 28.8 microg/m(3) (corresponding to the difference between the 5th and 95th percentile exposure value), and 30-year exposure to heating-SO(2) with a 67.6% (95% CI 7.1% to 162.2%) increase per 39.4 microg/m(3) (5th-95th percentile value difference). The association appeared stronger in non-smokers, physically active people and hypertensive subjects. We observed positive non-significant associations of inflammatory markers with NO(2) and PM(10) during 24 h before blood sampling. Short-term exposure to O(3) was associated with increased, and SO(2) with decreased, fibrinogen levels. CONCLUSIONS: Our results suggest that exposure to moderate levels of air pollution may influence serum levels of inflammatory markers.

Bacteria and mould components in house dust and children's allergic sensitisation.

It has been suggested that early childhood exposure to microbial agents decreases the risk of allergies in children. The current authors studied the association between microbial agents in house dust and allergic sensitisation in children aged 2-4 yrs. Nested case-control studies were performed within ongoing birth cohort studies in Germany, the Netherlands and Sweden and approximately 180 sensitised and 180 nonsensitised children were selected per country. Levels of bacterial endotoxin, beta(1,3)-glucans and fungal extracellular polysaccharides (EPS) were measured in dust samples from the children's mattresses and the living-room floors. Combined across countries, higher amounts of mattress dust and higher mattress dust loads of endotoxin, beta(1,3)-glucans and EPS were associated with a significantly decreased risk of sensitisation to inhalant allergens. After mutual adjustment, only the protective effect of the amount of mattress dust remained significant (odds ratio (95% confidence interval) 0.57(0.39-0.84)). Higher amounts of mattress dust may decrease the risk of allergic sensitisation to inhalant allergens. The effect might be partly attributable to endotoxin, beta(1,3)-glucans and extracellular polysaccharides, but could also reflect (additional) protective effects of (microbial) agents other than the ones measured. It is not possible to distinguish with certainty which component relates to the effect, since their levels are highly correlated.

Determinants of house dust endotoxin in three European countries - the AIRALLERG study.

UNLABELLED: The comparison of endotoxin levels between study populations and countries is limited as a result of differences in sampling, extraction, and storage procedures. The objective of this study is to assess the levels and determinants of endotoxin in mattress and living room floor dust samples from three European countries, namely, Germany, the Netherlands, and Sweden, using a standardized sampling, storage, and analysis protocol. The mattress and living room floor dust was collected from the homes of 1065 German, Dutch, and Swedish (pre-)school children. All the samples were collected in the cool season and analyzed for endotoxin in a central laboratory. The determinants were assessed by a standardized questionnaire. The endotoxin concentrations in mattress and living room floor dust were found to be the highest in German homes and lowest in the Swedish ones. Differences between the geometric means were small (factor 1.1-1.7). Most of the associations between endotoxin concentrations and potential determinants were not statistically significant and heterogeneous across countries. However, keeping pets and having more than four persons living in the home were consistently associated with up to 1.7-fold higher endotoxin concentrations in mattress and floor dust. Furthermore, having carpets or rugs, and opening the windows frequently was associated with up to 3.4-fold and 1.3-fold higher endotoxin concentrations in living room floor dust, respectively. The proportion of variance explained by the questionnaire variables was generally low. In conclusion, the data on housing characteristics did not accurately predict the endotoxin concentrations in house dust, and could only partly explain the differences between countries. PRACTICAL IMPLICATIONS: The differences between the endotoxin concentrations in German, Dutch, and Swedish homes are small. House dust endotoxin concentrations are associated with a number of housing factors, such as pet-ownership, floor cover, number of persons living in the home, and ventilation. The variability of the endotoxin levels between homes and countries can only be partly explained by these factors.

Comparison of parental reports of smoking and residential air nicotine concentrations in children.

BACKGROUND: Using questionnaires to assess children's residential exposure to environmental tobacco smoke (ETS) may result in misclassification from recall and response bias. Questionnaire data have frequently been validated against urinary cotinine measurements, but rarely against actual measurements of residential air nicotine. OBJECTIVE: To compare questionnaire reported smoking with air nicotine concentrations in a large population of children and with urinary cotinine levels in a subpopulation; and to assess the potential impact of the symptom status of the children on the agreement between different measures of exposure. METHODS: The authors assessed residential exposure to ETS in 347 German, 335 Dutch, and 354 Swedish preschool and schoolchildren by questionnaire and air nicotine measurements, and in a subset of 307 German children by urinary cotinine measurements. They then compared the different measures of ETS exposure. RESULTS: In all countries, air nicotine concentrations increased with increasing questionnaire reported smoking in a dose-response fashion. Specificity and negative predictive values of questionnaire reports for nicotine concentrations were excellent. Sensitivity and positive predictive values were moderate to good. Excluding occasional smokers, the overall percentage of homes misclassified was 6.9%, 6.7%, and 5.1% in Germany, the Netherlands, and Sweden, respectively. Similar results were found for the agreement of urinary cotinine concentrations with questionnaire reports and air nicotine levels. There was no indication of underreporting by parents of symptomatic children. CONCLUSION: Despite some misclassification, questionnaire reports are an inexpensive and valid estimate of residential ETS exposure among preschool and school children.

Exposure to traffic related air pollutants: self reported traffic intensity versus GIS modelled exposure.

BACKGROUND: In epidemiological studies of the potential health effects of traffic related air pollution, self reported traffic intensity is a commonly used, but rarely validated, exposure variable. METHODS: As part of a study on the impact of Traffic Related Air Pollution on Childhood Asthma (TRAPCA), data from 2633 and 673 infants from the Dutch and the German-Munich cohorts, respectively, were available. Parents subjectively assessed traffic intensity at the home address. Objective exposures were estimated by a combination of spatial air pollution measurements and geographic information system (GIS) based modelling using an identical method for both cohorts. RESULTS: The agreement rates between self reported and GIS modelled exposure--accumulated over the three strata of self assessed traffic intensity--were 55-58% for PM(2.5), filter absorbance (PM(2.5) abs), and nitrogen dioxide in Munich and 39-40% in the Netherlands. Of the self reported low traffic exposed group, 71-73% in Munich and 45-47% in the Netherlands had low modelled exposure to these three air pollutants. Of the self assessed high exposed subgroups in Munich (15% of the total population) and the Netherlands (22% of the total population), only 22-33% and 30-32% respectively had high modelled exposure to the three air pollutants. The subjective assessments tend to overestimate the modelled estimates for PM(2.5) and NO2 in both study areas. When analysis was restricted to the portion of the Dutch cohort living in non-urban areas, the agreement rates were even lower. CONCLUSIONS: Self reported and modelled assessment of exposure to air pollutants are only weakly associated.

Traffic-related air pollution and respiratory health during the first 2 yrs of life.

As part of an international collaborative study on the impact of Traffic-Related Air Pollution on Childhood Asthma (TRAPCA), the health effects associated with long-term exposure to particles with a 50% cut-off aerodynamic diameter of 2.5 microm (PM2.5), PM2.5 absorbance, and nitrogen dioxide (NO2) were analysed. The German part of the TRAPCA study used data from subpopulations of two ongoing birth cohort studies (German Infant Nutrition Intervention Programme (GINI) and Influences of Lifestyle Related Factors on the Human Immune System and Development of Allergies in Children (LISA)) based in the city of Munich. Geographic information systems (GIS)-based exposure modelling was used to estimate traffic-related air pollutants at the birth addresses of 1,756 infants. Logistic regression was used to analyse possible health effects and potential confounding factors were adjusted for. The ranges in estimated exposures to PM2.5, PM2.5 absorbance, and NO2 were 11.9-21.9 microg m(-3), 1.38-4.39 x 10(-5) m(-1), and 19.5-66.9 microg x m3, respectively. Significant associations between these pollutants and cough without infection (odds ratio (OR) (95% confidence interval (CI)): 1.34 (1.11-1.61), 1.32 (1.10-1.59), and 1.40 (1.12-1.75), respectively) and dry cough at night (OR (95% CI): 1.31 (1.07-1.60), 1.27 (1.04-1.55), and 1.36 (1.07-1.74), respectively) in the first year of life were found. In the second year of life, these effects were attenuated. There was some indication of an association between traffic-related air pollution and symptoms of cough. Due to the very young age of the infants, it was too early to draw definitive conclusions from this for the development of asthma.

Using geographic information systems to assess individual historical exposure to air pollution from traffic and house heating in Stockholm.

A specific aim of a population-based case-control study of lung cancer in Stockholm, Sweden, was to use emission data, dispersion models, and geographic information systems (GIS) to assess historical exposure to several components of ambient air pollution. Data collected for 1,042 lung cancer cases and 2,364 population controls included information on residence from 1955 to the end of follow-up for each individual, 1990-1995. We assessed ambient air concentrations of pollutants from road traffic and heating throughout the study area for three points in time (1960, 1970, and 1980) using reconstructed emission data for the index pollutants nitrogen oxides (NO(x)/NO(2)) and sulfur dioxide together with dispersion modeling. NO(2) estimates for 1980 compared well with actual measurements, but no independently measured (study-external) data were available for SO(2), precluding similar validation. Subsequently, we used linear intra- and extrapolation to obtain estimates for all other years 1955-1990. Eleven thousand individual addresses were transformed into geographic coordinates through automatic and manual procedures, with an estimated error of < 100 m for 90% of the addresses. Finally, we linked annual air pollution estimates to annual residence coordinates, yielding long-term residential exposure indices for each individual. There was a wide range of individual long-term average exposure, with an 11-fold interindividual difference in NO(2) and an 18-fold difference in SO(2). The 30-year average for all study subjects was 20 microg/m(3) NO(2) from traffic and 53 microg/m(3) SO(2) from heating. The results indicate that GIS can be useful for exposure assessment in environmental epidemiology studies, provided that detailed geographically related exposure data are available for relevant time periods.

Exposure to chemical agents in Swedish aluminum foundries and aluminum remelting plants--a comprehensive survey.

Secondary aluminum melting is mainly performed in sand, die, and static die-casting foundries and remelting plants. In seven Swedish foundries and two remelting plants, the exposure and area concentrations of total dust, metals, organic gases, and vapors were determined mainly as daily, time-weighted averages (TWAs). For most combinations of jobs and agents, the exposure levels were well below the current threshold limits suggested by the American Conference of Governmental Industrial Hygienists (ACGIH). However, high exposure levels of mineral oil mist (geometric mean [GM] = 0.6 mg/m3) were observed in the die-casting process, with a maximum of 4 mg/m3. The findings were similar for total dust (GM = 5.1 mg/m3) and crystalline quartz (GM = 0.05 mg/m3) during molding operations in the sand foundries, maximum air concentrations being 31 mg/m3 and 0.22 mg/m3, respectively. Other agents which occasionally reached high exposure levels included furfuryl alcohol (up to 23 mg/m3 during furan binder use in sand foundries), aniline (up to 2.6 mg/m3 during thermal degradation of cold-box binders), and dimethylethylamine (up to 9 mg/m3) in the cold-box process used in static die-casting and sand foundries. The average aluminum exposure levels (GM = 0.043 mg/m3) were low in all foundries, individual values not exceeding 0.94 mg/m3. The exposures to metals were below 10 percent of their threshold limits. Similarly low levels were detected of polyaromatic hydrocarbons, phenol, formaldehyde, methylenebisphenyl diisocyanate, and phenylisocyanate. In the aluminum remelting plants, a few high exposure levels of total dust (GM = 1.4 mg/m3) up to 8 mg/m3 were detected in furnace workers. Aluminum and other metals were well below 10 percent of their threshold limits, with the exception of a few high concentrations of manganese, up to 0.14 mg/m3. The between-worker variability (GSDB) in the foundries for total dust, aluminum, and oil mist were on the order of 3-4. The heterogenicity of secondary aluminum melting requires assessment of a wide variety of chemical agents. For certain exposures, technical and medical monitoring programs are still needed.

Urban air pollution and lung cancer in Stockholm.

We conducted a population-based case-control study among men 40-75 years of age encompassing all cases of lung cancer 1985-1990 among stable residents of Stockholm County 1950-1990. Questionnaires to subjects or next-of-kin (primarily wives or children) elicited information regarding smoking and other risk factors, including occupational and residential histories. A high response rate (>85%) resulted in 1,042 cases and 2,364 controls. We created retrospective emission databases for NOx/NO2 and SO2 as indicators of air pollution from road traffic and heating, respectively. We estimated local annual source-specific air pollution levels using validated dispersion models and we linked these levels to residential addresses using Geographical Information System (GIS) techniques. Average traffic-related NO2 exposure over 30 years was associated with a relative risk (RR) of 1.2 (95% confidence interval 0.8-1.6) for the top decile of exposure, adjusted for tobacco smoking, socioeconomic status, residential radon, and occupational exposures. The data suggested a considerable latency period; the RR for the top decile of average traffic-related NO2 exposure 20 years previously was 1.4 (1.0-2.0). Little association was observed for SO2. Occupational exposure to asbestos, diesel exhaust, and other combustion products also increased the risk of lung cancer. Our results indicate that urban air pollution increases lung cancer risk and that vehicle emissions may be particularly important.

Historical exposure to inorganic mercury at the smelter works of Abbadia San Salvatore, Italy.

Metallic mercury production from cinnabar ore may result in high exposures to inorganic mercury, that are difficult to assess separately from the exposures originating from underground extraction, and previously have only been scantily described. We retrieved and analysed the air and biological mercury determinations on workers involved in the smelting process of the Abbadia San Salvatore mine (Monte Amiata, Italy). Native mercury was not present in the ore, and the exposure in the underground extraction was low. The smelter operated from 1897 to 1983. Blood and urine (24/h urine collections and concentration samples) had been sampled in 1968 to 1982, and analysed for mercury by atomic absorption spectrophotometry, and relate to all subjects. Exposure to mercury in air had been determined in a small set of personal samples in 1982. The data relate to all jobs in the smelter process, and all jobs entailed substantial exposure to mercury. The overall distribution of breathing zone air, blood and urinary levels is right-skewed and similar to the log-normal distribution (air, median 48 micrograms/m3, n = 49; blood, arithmetic mean AM 49 micrograms/L; geometric mean GM 26 micrograms/L, n = 192; urinary excretion, AM 140 micrograms/24 h, GM 78 micrograms/24 h, n = 839; and urinary concentration, AM 160 micrograms/L, GM 83 micrograms/L, n = 632). Air, blood and urinary values show a high ratio of the between- and within-job variance, indicating differences in exposure by job. Cinnabar pigment production, of which the exposure has not been characterised previously, was the job with the highest air (AM 160 micrograms/m3) and urinary levels (excretion AM 690 micrograms/24 h; concentration AM 1100 micrograms/L). Other jobs with high urinary levels were soot purification, laboratory work, and bottling. Cleaning of condensers showed the highest blood level (AM 280 micrograms/L). There is a downwards time trend in mercury concentration in blood and in urine. The corresponding trend is not seen for urinary excretion levels, the reason for this being unclear. Roasters, which is the most frequently monitored group, show however a decreasing trend in all sets of data (e.g. the mean of urinary excretion decreased from 300 micrograms/24 h in 1968/69 to 50 micrograms/24 h in 1980/81). The mercury exposure experienced by the smelters of Abbadia San Salvatore is in line with the few available data on workers from other mercury mines and smelters, and our data confirm the high exposure levels in this occupational group, in particular at cinnabar pigment production, soot purification, and condenser cleaning.

Mortality and cancer incidence in Swedish battery workers exposed to cadmium and nickel.

OBJECTIVE: To follow up cancer incidence and mortality in a group of Swedish battery workers exposed to nickel hydroxide and cadmium oxide. METHODS: 869 workers, employed at least one year between the years 1940 and 1980 were followed up until 1992. Vital status and causes of death were obtained from the Swedish cause of death registry. Cancer morbidity was retrieved from the Swedish cancer registry. Regional reference rates were used to compute the expected numbers of deaths and cancers. RESULTS: Up to 31 December, 1992, a total of 315 deaths (292 in men and 23 in women) had occurred in the cohort. For men, the overall standardised mortality ratio (SMR) was 106 (95% confidence interval (95% CI) 93.7 to 118) and for women 83.8 (95% CI 53.1 to 126). The SMRs for total cancer mortality were 125 (95% CI 98.2 to 157) for men and 69.5 (95% CI 25.5 to 151) for women. The SMR for lung cancer in men was 176 (95% CI 101 to 287). No lung cancers were found among female workers. Up to 31 December, 1991, a total of 118 cancers had occurred in the cohort. A significantly increased standardised incidence ratio (SIR) was found for cancer of the nose and nasal sinuses in men, three cases v 0.36 expected, yielding an SIR of 832 (95% CI 172 to 2430). Applying a 10 year latency period in cohort members exposed to > or = 1000 micrograms cadmium/m3, the SIR was 1107 (95% CI 134 to 4000). Similarly, for cohort members exposed to 2000 micrograms nickel/m3, the SIR was 1080 (95% CI 131 to 3900). CONCLUSION: There was an increased overall risk for lung cancer, but no exposure-response relation between cumulative exposure to cadmium or nickel and risk of lung cancer. There was a highly significant increased risk of cancer of the nose and nasal sinuses, which may be caused by exposure to nickel or cadmium or a combination of both exposures.

Cancer occurrence among European mercury miners.

OBJECTIVES: To study the carcinogenicity of inorganic mercury in humans. METHODS: We studied the mortality from cancer among 6784 male and 265 female workers of four mercury mines and mills in Spain, Slovenia, Italy and the Ukraine. Workers were employed between the beginning of the century and 1990; the follow-up period lasted from the 1950s to the 1990s. We compared the mortality of the workers with national reference rates. RESULTS: Among men, there was no overall excess cancer mortality; an increase was observed in mortality from lung cancer (standardized mortality ratio [SMR] 1.19, 95 percent confidence interval [CI] 1.03-1.38) and liver cancer (SMR 1.64, CI 1.18-2.22). The increase in lung cancer risk was restricted to workers from Slovenia and the Ukraine: no relationship was found with duration of employment or estimated mercu ry exposure. The increase in liver cancer risk was present both among miners and millers and was stronger in workers from Italy and Slovenia: there was a trend with estimated cumulative exposure but not with duration of employment, and the excess was not present in a parallel analysis of cancer incidence among workers from Slovenia. No increase was observed for other types of cancer, including brain and kidney tumours. Among female workers (Ukraine only), three deaths occurred from ovarian cancer, likely representing an excess. CONCLUSIONS: Exposure to inorganic mercury in mines and mills does not seem strongly associated with cancer risk, with the possible exception of liver cancer; the increase in lung cancer may be explained by co-exposure to crystalline silica and radon.

In vivo analysis of cadmium in battery workers versus measurements of blood, urine, and workplace air.

OBJECTIVES: To measure in vivo the cadmium concentrations in kidney cortex (kidney-Cd) and in superficial liver tissue (liver-Cd) of nickel cadmium battery workers, and to compare the results with other commonly used estimates of cadmium exposure (current concentrations of cadmium in blood (B-Cd) and urine (U-Cd)) or repeated measurements of cadmium in workplace air (CumAir-Cd). METHODS: The study comprised 30 workers with a range of duration of exposure of 11-51 years. 13 subjects were currently employed, whereas the other 17 had a median period without occupational exposure of eight years before the measurements. The in vivo measurements were made with an x ray fluorescence technique permitting average detection limits of 30 and 3 micrograms cadmium per g tissue in kidney and liver, respectively. RESULTS: 19 of 30 (63%) people had kidney-Cd and 13 of 27 (48%) had liver-Cd above the detection limits. Kidney-Cd ranged from non-detectable to 350 micrograms/g and liver-Cd from non-detectable to 80 micrograms/g. The median kidney-Cd and liver-Cd were 55 micrograms/g and 3 micrograms/g, respectively. Kidney-Cd correlated significantly with B-Cd (r, 0.49) and U-Cd (r, 0.70), whereas liver-Cd correlated significantly with U-Cd (r, 0.58). Neither kidney-Cd nor liver-Cd correlated with the CumAir-Cd. The prevalence of beta 2-microglobulinurea increased with increased liver-Cd. CONCLUSIONS: Current U-Cd can be used to predict the kidney-Cd and liver-Cd measured in vivo. In vivo measurements of kidney-Cd and liver-Cd were not shown to correlate with the individual cadmium exposure estimates, obtained by integration of the cadmium concentration in workplace air. There may be several reasons for this, including uncertainties in the estimate of the individual cumulative exposures as well as in the in vivo measurements. There was a suggestion of a relation between liver-Cd and tubular proteinuria.

Exposure to styrene and mortality from nervous system diseases and mental disorders.

Chronic low-dose exposure to solvents has been associated in epidemiologic studies with chronic neurotoxicity, but the evidence is not consistent. Styrene causes acute disturbances in the central and peripheral nervous systems. To determine if exposure to styrene may contribute to chronic diseases of the central nervous system, the authors examined mortality from nervous system diseases, mental disorders, and suicide in relation to styrene exposure in an international historical cohort study. The cohort involved 35,443 workers employed during 1945-1991 in the reinforced plastics industry, where high exposures to styrene occur. Indicators of exposure were reconstructed through job histories and environmental and biologic monitoring data. Poisson regression was used for internal comparisons. Mortality from diseases of the central nervous system (27 deaths) increased with time since first exposure, duration of exposure, average level of exposure, and cumulative exposure to styrene. A quadratic model described best the dose-response shape for cumulative exposure and duration of exposure with the highest risks at around 300 ppm-years and 5 years, respectively, and a subsequent decrease in risk in the highest exposure categories. Mortality from epilepsy increased monotonically with all styrene exposure indicators, while associations for degenerative diseases of the central nervous system were generally weaker. Mortality from mental disorders and suicide decreased with increasing duration of exposure and cumulative exposure, while there was no trend with time since first exposure and average exposure to styrene. These findings suggest that, in addition to the known acute effects, exposure to styrene may contribute to chronic diseases of the central nervous system.

Exposure to styrene and mortality from nonmalignant respiratory diseases.

A cohort of 34,560 men and 6128 women employed in 660 European factories manufacturing reinforced plastic products, followed up originally to assess the risk of cancer, was used to assess the risk of non-malignant respiratory diseases associated with exposure to styrene. Mortality from pneumonia was associated with intensity of exposure to styrene, but this may have been due to chance. Mortality from bronchitis, emphysema, and asthma was not associated with styrene exposure.

Exposure to styrene and mortality from nonmalignant diseases of the genitourinary system.

OBJECTIVES: A historical cohort study was carried out to investigate mortality from nonmalignant diseases of the genitourinary system among workers in the reinforced plastics industry, where high workroom concentrations of styrene are encountered. METHODS: The external comparisons in this report were based on an average of 12.6 years of retrospective follow-up of 35 443 workers who were first employed in the reinforced plastics industry during 1945-1991 and were known to have been exposed to styrene in their work. For the internal comparisons, 2641 subjects with incomplete occupational histories were excluded, leaving 32 802 subjects. Previous individual exposure histories to styrene were reconstructed through job histories and environmental and biological monitoring data. RESULTS: Mortality from nonmalignant diseases of the genitourinary system (N = 20) was associated with average exposure to styrene (P for trend 0.05). Weaker increasing trends in risk were seen for time since first exposure and cumulative exposure, while no increase was identified for duration of exposure. There was a significant increasing trend in mortality from nephritis and nephrosis (N = 5), associated with an increasing average level of exposure to styrene (P for trend 0.03). No clear trend was observed for time since first exposure, duration of exposure, or cumulative exposure. CONCLUSIONS: In this large cohort study of workers exposed to styrene, mortality from nonmalignant diseases of the genitourinary system increased as the average intensity of exposure increased. This finding indicates that other data should be scrutinized.