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OBJECTIVE: To investigate the risk of congenital anomalies in relation to an index of geographic density of landfill sites across 5x5 km grid squares in England. METHODS: 2 km zones were constructed in a geographical information system around 8804 landfill sites, including 607 that handled special (hazardous) wastes, and intersected with postcode coordinates of over 10 million births (136,821 with congenital anomalies), 1983-98. A landfill exposure index was calculated to represent the geographic density of landfill sites within 2 km of births for each 5x5 km grid square, calculated separately for landfill sites handling special, and non-special or unknown, waste. For each group of landfills, the index was classified into four categories of intensity, and risks for the second, third and top categories were compared to the bottom category, comprising areas with no such landfill sites within 2 km (index of zero). We used hierarchical logistic regression modelling in a Bayesian framework, with adjustment for potential confounding. RESULTS: For special waste sites, adjusted odds ratios were significant for the third category of the landfill exposure index for all anomalies combined and cardiovascular defects (OR 1.08 (95% credible interval 1.02 to 1.13) and 1.16 (1.00 to 1.33), respectively) and for hypospadias and epispadias for the third and top categories (OR 1.11 (1.02 to 1.21) and 1.12 (1.02 to 1.22), respectively). After adjustment, there were no excess risks in relation to sites handling non-special or unknown waste types. CONCLUSIONS: There was a weak spatial association between risk of certain congenital anomalies and geographic density of special (hazardous) waste sites at the level of 5x5 km grid squares. Exposure pathways and mechanisms to help interpret these findings are not well-established.

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The aim was to assess how urinary creatinine is affected by age, gender, body size and meat intake, and to determine to what extent such factors might affect the creatinine adjustment of urinary cadmium. The study was based on three Swedish studies: (1) 67 non-smoking women aged 20-50 years (24-h urine samples); (2) 289 men and 434 women aged 16-81 years (spot urine samples); and (3) 98 men and 105 women aged 19-72 years (spot urine samples). The effects of age, body surface area (as an indicator of muscle mass), and meat intake on urinary creatinine and cadmium were analysed using multiple regression analyses. Gender- and age-related variations in urinary creatinine and cadmium adjusted for creatinine or specific gravity were compared by ANOVA or ANCOVA. In the multiple regression analyses, body surface area, gender, age and meat intake were the major determinants of urinary creatinine. Urinary cadmium adjusted for creatinine and specific gravity were also dependent on body size, gender and age. Urinary cadmium adjusted for creatinine was 15-92% higher in women or older individuals than in men or younger individuals. Women or older individuals had -3 to 79% higher urinary cadmium adjusted for specific gravity than men or younger individuals had, and such a difference between gender or age group was less obvious in specific gravity adjustment than in creatinine adjustment. Thus, urinary cadmium adjusted for creatinine is more affected by age, gender, body size and meat intake than is specific gravity adjustment. When comparing individuals or populations with large differences in muscle mass or meat intake, such effects can be especially important. In such studies, specific gravity adjustment seems to be more appropriate.

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Runcorn has been a site of chemical industry activity for over a century, where tons of toxic chemicals are released annually to air and water. Excess kidney disease mortality (nephritis, nephrotic syndrome, and nephrosis) was found in the population living within 2 km of the industrial plants (standardised mortality ratio (SMR) in males 131 (95% CI 90 to 185) and females 161 (95% CI 118 to 214)) compared to a reference population (northwest England)). Risk of hospital admissions for kidney disease in Halton (comprising the towns of Runcorn and Widnes) was higher than in the less industrial, nearby town of Warrington. The standardised admission ratio (SAR) in Halton was 115 (95% CI 107 to 124) for males and 126 (95% CI 117 to 137) for females; and in Warrington 91 (95% CI 85 to 97) for males and 84 (95% CI 78 to 91) for females compared to the Warrington and Halton area as a whole. The excess risk of kidney disease in the Runcorn area requires further investigation.

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A recent study showed small excess risks of low birth weight, very low birth weight and certain congenital anomalies in populations living near landfill sites in Great Britain. The objective of the current study was to investigate the risk of adverse birth outcomes associated with residence near special waste landfill sites in Scotland. We studied risks of adverse birth outcomes in populations living within 2 km of 61 Scottish special waste landfill sites operational at some time between 1982 and 1997 compared with those living further away. 324,167 live births, 1,849 stillbirths, and 11,138 congenital anomalies (including terminations) were included in the study. Relative risks were computed for all congenital anomalies combined, some specific anomalies and prevalence of stillbirth and low and very low birth weight (< 2500 g and < 1500 g). For all anomalies combined, relative risk of residence near special waste landfill sites was 0.96 (99% confidence interval 0.89 to 1.02) adjusted for confounders. Adjusted risks were 0.71 (0.36 to 1.42) for neural tube defects, 1.03 (0.85 to 1.26) for cardiovascular defects, 0.84 (0.58 to 1.22) for hypospadias and epispadias (with no excess of surgical corrections), 0.78 (0.27 to 2.23) for abdominal wall defects (1.32 (0.42-4.17) for hospital admissions), 1.22 (0.28 to 5.38) for surgical correction of gastroschisis and exomphalos and 1.01 (0.96 to 1.07) and 1.01 (0.90 to 1.15) for low and very low birth weight respectively. There was no excess risk of stillbirth. In conclusion, we found no statistically significant excess risks of congenital anomalies or low birth weight in populations living near special waste landfill sites in Scotland.

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OBJECTIVE AND METHODS: In 1993, a special Amalgam Clinic was established at Huddinge University Hospital. Residents in the Stockholm County area with morbidity attributed to dental fillings ('amalgam disease'), were referred to this clinic. Patients were examined by a dentist (n 428), a physician (n 379), and a psychologist (n 360). Sixty-nine per cent were women and 31% men; the mean patient age was 46 years. RESULTS: Oral symptoms included tender or aching teeth (60%), metallic taste (54%), sore mouth (43%) and dry mouth (43%). Signs of moderate or severe temporomandibular joint dysfunction were found in 81 cases, glossitis in 30 and oral lichen in 26 cases. Common general symptoms included diffuse pain (78%), general weakness (75%), extreme fatigue (68%) and dizziness (68%). Seven per cent of the patients suffered from previously undiagnosed medical conditions (thyroid dysfunction, anaemia, cardiopathy, renal disease, cancer). In 26 subjects, skin patch testing revealed allergy to mercury, gold or palladium. The median concentration of mercury was 10 nmol L-1 in whole blood, 3 nmol L-1 in plasma and 10 nmol L-1 in urine, i.e. normal levels. Earlier mental trauma was common, and in the psychological questionnaire SCL-90, clear tendencies to somatization were found. Only a few cases of severe psychiatric illness were observed. No positive correlation was found between the amount of amalgam and somatic symptoms or psychological effect parameters. CONCLUSIONS: The results do not support the hypothesis that release of mercury from amalgam fillings is the cause of 'amalgam disease', but suggest that there may be various explanations for the patient's complaints.

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Previous studies have raised concerns about possible excess risks of bladder, brain and hepatobiliary cancers and leukaemias near landfill sites. Several cancers have been implicated, but no consistent pattern has emerged. We present a large nationwide analysis of selected cancers near landfill sites in Great Britain. The base population comprised people living within 2 km of 9565 (from a total of 19 196) landfill sites that were operational at some time from 1982 to 1997, with populations living more than 2 km from a landfill as reference. Risks of cancers at the above sites were computed with adjustment for age, sex, year of diagnosis, region and deprivation. National post-coded registers provided a total of 341 856 640 person-years for the adult cancer analyses and 113 631 443 person-years for childhood leukaemia. There were 89 786 cases of bladder cancer, 36 802 cases of brain cancer, 21 773 cases of hepatobiliary cancer, 37 812 cases of adult leukaemia and 3973 cases of childhood leukaemia. In spite of the very large scale of this national study, we found no excess risks of cancers of the bladder and brain, hepatobiliary cancer or leukaemia, in populations living within 2 km of landfill sites. The results were similar if the analysis were restricted to landfill sites licensed to carry special (hazardous) waste. Our results do not support suggestions of excess risks of cancer associated with landfill sites reported in other studies.

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OBJECTIVES: To examine the associations between temperature, housing, deprivation and excess winter mortality using census variables as proxies for housing conditions. DESIGN: Small area ecological study at electoral ward level. Setting Great Britain between 1986 and 1996. PARTICIPANTS: Men and women aged 65 and over. MAIN OUTCOME MEASURES: Deaths from all causes (International Classification of Diseases, Ninth Revision [ICD-9] codes 0-999), coronary heart disease (ICD-9 410-414), stroke (ICD-9 430-438) and respiratory diseases (ICD-9 460-519). Odds of death occurring in winter period of the four months December to March compared to the rest of the year. RESULTS: During the study period (excluding the influenza epidemic year of 1989/90), a total of 1,682,687 deaths occurred in winter and 2,825,223 deaths occurred during the rest of the year among people aged > or =65 (around 30,000 excess winter deaths per year). A trend of higher excess winter mortality with age was apparent across all disease categories (P < 0.01). There was a significant association between winter mortality and temperature with a 1.5% higher odds of dying in winter for every 1 degrees C reduction in 24-h mean winter temperature. The amount of rain, wind and hours of sunshine were inversely associated with excess winter mortality. Selected housing variables derived from the English House Condition Survey showed little agreement with census-derived variables at electoral ward level. For all-cause mortality there was little association between deprivation and excess winter mortality, although lack of central heating was associated with a higher risk of dying in winter (odds ratio [OR] = 1.016, 95% CI : 1.009-1.022). CONCLUSIONS: Excess winter mortality continues to be an important public health problem in Great Britain. There was a strong inverse association with temperature. Lack of central heating was associated with higher excess winter mortality. Further work is needed to disentangle the complex relationships between different indicators of housing quality and other measures of socioeconomic deprivation and their relationship to the high number of excess winter deaths in Great Britain.

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OBJECTIVES: To investigate whether there is a relation between residential exposure to aircraft noise and hypertension. METHODS: The study population comprised two random samples of subjects aged 19-80 years, one including 266 residents in the vicinity of Stockholm Arlanda airport, and another comprising 2693 inhabitants in other parts of Stockholm county. The subjects were classified according to the time weighted equal energy and maximum aircraft noise levels at their residence. A questionnaire provided information on individual characteristics including history of hypertension. RESULTS: The prevalence odds ratio for hypertension adjusted for age, sex, smoking, and education was 1.6 (95% confidence interval (95% CI) 1.0 to 2.5) among those with energy averaged aircraft noise levels exceeding 55 dBA, and 1.8 (95% CI 1.1 to 2.8) among those with maximum aircraft noise levels exceeding 72 dBA. An exposure-response relation was suggested for both exposure measures. The exposure to aircraft noise seemed particularly important for older subjects and for those not reporting impaired hearing ability. CONCLUSIONS: Community exposure to aircraft noise may be associated with hypertension.

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Environmental exposure to cadmium may cause kidney damage and tubular proteinuria. We investigated the relationship between low-level cadmium exposure and end-stage renal disease (ESRD), indicated by renal replacement therapy (RRT), in a Swedish population environmentally or occupationally exposed to cadmium. Based on records of all persons in the population previously or presently employed in cadmium-battery production or residing in cadmium-polluted areas near the battery plants, we defined exposure as high (occupational), moderate (domicile < 2 km from a plant), low (domicile 2 to 10 km from a plant), or no exposure (domicile > 10 km from a plant). Comprehensive data were available for all individuals undergoing RRT since 1978. The annual incidence of RRT increased from 41 per million in the age group 20 to 29 years to 243 per million in the age group 70 to 79 years and was greater in a priori-defined populations with cadmium exposure. Adjusting for age and sex gave an increased Mantel-Haenszel rate ratio (MH-RR) of 1.8 (95% confidence interval [CI], 1.3 to 2.3) for RRT in the cadmium-exposed population compared with the unexposed group; the MH-RR was even higher for women (MH-RR, 2.3; 95% CI, 1.5 to 3.5). Directly age-standardized rate ratios for RRT and cadmium exposure increased from 1.4 (95% CI, 0.8 to 2.0) in the low-exposure group to 1.9 (95% CI, 1.3 to 2.5) and 2.3 (95% CI, 0.6 to 6.0) in the moderate- and high-exposure groups, respectively. We conclude that exposure to occupational or relatively low environmental levels of cadmium appears to be a determinant for the development of ESRD.

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OBJECTIVE: To investigate the risk of adverse birth outcomes associated with residence near landfill sites in Great Britain. DESIGN: Geographical study of risks of adverse birth outcomes in populations living within 2 km of 9565 landfill sites operational at some time between 1982 and 1997 (from a total of 19 196 sites) compared with those living further away. SETTING: Great Britain. SUBJECTS: Over 8.2 million live births, 43 471 stillbirths, and 124 597 congenital anomalies (including terminations). MAIN OUTCOME MEASURES: All congenital anomalies combined, some specific anomalies, and prevalence of low and very low birth weight (<2500 g and <1500 g). RESULTS: For all anomalies combined, relative risk of residence near landfill sites (all waste types) was 0.92 (99% confidence interval 0.907 to 0.923) unadjusted, and 1.01 (1.005 to 1.023) adjusted for confounders. Adjusted risks were 1.05 (1.01 to 1.10) for neural tube defects, 0.96 (0.93 to 0.99) for cardiovascular defects, 1.07 (1.04 to 1.10) for hypospadias and epispadias (with no excess of surgical correction), 1.08 (1.01 to 1.15) for abdominal wall defects, 1.19 (1.05 to 1.34) for surgical correction of gastroschisis and exomphalos, and 1.05 (1.047 to 1.055) and 1.04 (1.03 to 1.05) for low and very low birth weight respectively. There was no excess risk of stillbirth. Findings for special (hazardous) waste sites did not differ systematically from those for non-special sites. For some specific anomalies, higher risks were found in the period before opening compared with after opening of a landfill site, especially hospital admissions for abdominal wall defects. CONCLUSIONS: We found small excess risks of congenital anomalies and low and very low birth weight in populations living near landfill sites. No causal mechanisms are available to explain these findings, and alternative explanations include data artefacts and residual confounding. Further studies are needed to help differentiate between the various possibilities.

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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.

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Increases in testicular cancer incidence have been reported in several countries over a long period. Geographical variability has also been reported in some studies. We have investigated temporal trends and spatial variation of testicular cancer at ages 20-49 in Britain. Temporal trends in testicular cancer incidence were examined, 1974 to 1991 and in mortality, 1981-1997. Spatial variation in incidence was analysed across electoral wards, 1975 to 1991. We used Poisson regression to examine for regional and socio-economic effects and Bayesian mapping techniques to analyse small-area spatial variability. Incidence increased from 6.5 to 11.1 per 100 000 in men at ages 20-34, and from 5.6 to 9.7 per 100 000 in men at ages 35-49, while mortality declined by 50% in both age groups. Risks of testicular cancer varied across regional cancer registries, ranging from 0.79 (95% CI: 0.73-0.84) to 1.32 (95% CI: 1.25-1.38), and was higher in the most affluent compared with the most deprived areas. Analyses within 2 regions (one predominantly urban, the other predominantly rural) did not indicate any localized geographical clustering. The increasing incidence contrasted with a decreasing mortality over time in Great Britain, similar to that found in other countries. The higher risk in more affluent areas is not consistent with findings on social class at the individual level. The absence of any marked geographical variability at small area scale argues against a geographically varying environmental factor operating strongly in the aetiology of testicular cancer.

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BACKGROUND: The incidence of hospital admissions for respiratory and cardiovascular diseases in areas close to operating coke works in England and Wales was investigated. METHODS: A small area study using distance from source as a proxy for exposure was undertaken in subjects aged 65 or over and children under 5 years within 7.5 km of four coke works (1991 estimated populations 87 760 and 43 932, respectively). The main outcome measures were emergency hospital admissions in 1992/3-1994/5 with a primary diagnosis of coronary heart disease (ICD 410-414), stroke (ICD 431-438), all respiratory diseases (ICD 460-519), chronic obstructive pulmonary disease (ICD 491-492), and asthma (ICD 493) in those aged 65 or over, and all respiratory and asthma admissions in children under 5 years of age. RESULTS: At age 65 or over the combined estimate of relative risk with proximity to coke works (per km) ranged from 0.99 (95% CI 0.90 to 1.09) for chronic obstructive pulmonary disease to 1.03 (95% CI 0.94 to 1.13) for asthma. For children under 5 years the combined estimate of risk was 1.08 (95% CI 0.98 to 1.20) for all respiratory disease and 1.07 (95% CI 0.98 to 1.18) for asthma. There was evidence of significant heterogeneity in risk estimates between coke work groups, especially in children under 5 years (p<0.001 and p=0.004 for respiratory disease and asthma, respectively). For the Teesside coke works in North East England the relative risk with proximity (per km) was 1.09 (95% CI 1.06 to 1.12) for respiratory disease and 1.09 (95% CI 1.04 to 1.15) for asthma. CONCLUSIONS: No evidence overall was found for an association between hospital admissions and living near operational coke works in England and Wales. Trends of a higher risk of hospital admission for respiratory disease and asthma among children with proximity to the Teesside plant require further investigation.

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OBJECTIVES: To study the dose-response relation between cadmium dose and renal tubular damage in a population of workers and people environmentally or occupationally exposed to low concentrations of cadmium. METHODS: Early kidney damage in 1021 people, occupationally or environmentally exposed to cadmium, was assessed from cadmium in urine to estimate dose, and protein HC (alpha(1)-microglobulin) in urine to assess tubular proteinuria. RESULTS: There was an age and sex adjusted correlation between cadmium in urine and urinary protein HC. The prevalence of tubular proteinuria ranged from 5% among unexposed people to 50% in the most exposed group. The corresponding prevalence odds ratio was 6.0 (95% confidence interval (95% CI) 1.6 to 22) for the highest exposure group, adjusted for age and sex. Multiple logistic regression analysis showed an increasing prevalence of tubular proteinuria with urinary cadmium as well as with age. After adjustment to the mean age of the study population (53 years), the results show an increased prevalence of 10% tubular proteinuria (taking into account a background prevalence of 5%) at a urinary cadmium concentration of 1.0 nmol/mmol creatinine. CONCLUSION: Renal tubular damage due to exposure to cadmium develops at lower levels of cadmium body burden than previously anticipated.

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Osteoporosis is a major cause of morbidity worldwide. A number of risk factors, such as age and gender, are well established. High cadmium exposure causes renal damage and in severe cases also causes osteoporosis and osteomalacia. We have examined whether long-term low-level cadmium exposure increases the risk of osteoporosis. Bone mineral density (BMD) in the forearm was measured in 520 men and 544 women, aged 16-81 years, environmentally or occupationally exposed to cadmium, using dual-energy X-ray absorptiometry (DXA) technique. Cadmium in urine was used as the dose estimate and protein HC was used as a marker of renal tubular damage. There was a clear dose-response relation between cadmium dose and the prevalence of tubular proteinuria. Inverse relations were found between cadmium dose, tubular proteinuria, and BMD, particularly apparent in persons over 60 years of age. There was a dose-response relation between cadmium dose and osteoporosis. The odds ratios (ORs) for men were 2.2 (95% CI, 1.0-4.8) in the dose group 0.5-3 nmol Cd/mmol creatinine and 5.3 (2.0-14) in the highest dose category (> or = 3 nmol/mmol creatinine) compared with the lowest dose group (< 0.5 nmol Cd/mmol creatinine). For women, the OR was 1.8 (0.65-5.3) in the dose group 0.5-3 nmol Cd/mmol creatinine. We conclude that exposure to low levels of cadmium is associated with an increased risk of osteoporosis.

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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.

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This case-referent study investigated the lung cancer risk from occupational exposure to diesel exhaust, mixed motor exhaust, other combustion products, asbestos, metals, oil mist, and welding fumes. All cases of lung cancer in males aged 40-75 years among stable residents of Stockholm County, Sweden, were identified from 1985 to 1990. Referents were selected as a stratified (age, inclusion year) random sample. Information on lifetime occupational history, residency, and tobacco smoking was obtained from the study subjects or from next of kin. Response rates of 87% and 85% resulted in 1,042 cases and 2,364 referents, respectively. Occupational exposures were assessed by an occupational hygienist who coded the intensity and probability of each exposure. Risk estimates were adjusted for tobacco smoking, other occupational exposures, residential radon, and environmental exposure to traffic-related air pollution. For the highest quartile of cumulative exposure versus no exposure, the relative risk was 1.63 (95% confidence interval (CI): 1.14, 2.33) for diesel exhaust, 1.60 (95% CI: 1.09, 2.34) for combustion products, and 1.68 (95% CI: 1.15, 2.46) for asbestos. Dose-response analyses indicated an increase in lung cancer risk of 14% per fiber-year/ml for asbestos exposure. No increased risk was found for the other exposure factors. An overall attributable proportion of 9.5% (95% CI: 5.5, 13.9) was estimated for lung cancer related to diesel exhaust, other combustion products, and asbestos.

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