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1.  Epidemiologic study of renal function in copper smelter workers. 
A medical cross-sectional examination of a copper smelter work force was undertaken after environmental contamination with lead, cadmium and arsenic had been documented. A total of 920 subjects was examined, including active smelter employees, retired workers and copper mine employees who had never worked in the smelter. Slight to moderate absorption of lead and cadmium was definitely present in the active copper smelter employees, who had significantly higher levels of Pb-B, ZPP and Cd-B than retired employees and miners. Cd-U levels were higher in retired workers, who were also older and had, as a group, longer duration of exposure in the smelter. Cd-U did not exceed 10 micrograms/g creatinine, the level considered critical for nephrotoxicity, in any of the subjects. Median Cd-B level for active workers was 2.75 micrograms/L. Lead absorption was characterized by a relatively small proportion (16.7%) of active employees with Pb-B levels 40 micrograms/dL or higher. We were particularly interested in exploring the possibility that simultaneous exposure to lead and cadmium, although at levels not associated with nephrotoxicity for each metal separately, could result in renal function impairment. Distribution patterns of BUN and serum creatinine levels were unremarkable. Urinary beta 2-microglobulin levels were less than 200 micrograms/g creatinine in 95% of copper smelter employees. There were no significant correlations between urinary beta 2-microglobulin levels and Cd-U, Cd-B, Pb-B and ZPP or between urinary beta 2-microglobulin excretion and serum creatinine or BUN levels. Urinary beta 2-microglobulin levels were significantly correlated with age in the copper smelter workers, but not in the miners. Nevertheless, in the absence of any significant correlations between urinary beta 2-microglobulin and Cd-U, Cd-B, a causal relationship with cadmium absorption cannot be affirmed. That kidney function could be impaired by long-term exposure in the smelter was only indirectly suggested. Effects on renal function at the low levels of cadmium and lead absorption that were observed in this smelter population are minimal.
PMCID: PMC1568152  PMID: 6376092
2.  Arsenic exposure and mortality: a case-referent study from a Swedish copper smelter. 
An increased mortality from lung cancer, cardiovascular disease, haematolymphatic malignancy and cirrhosis of the liver has been reported among smelter workers and others exposed to arsenic. This study uses the case-referent (case-control) technique and is concerned with workers in a copper smelter in a complex work environment, characterised by the presence of trivalent arsenic in combination with sulphur dioxide and copper, and also with other agents. Lung cancer mortality was found to be increased about five-fold and cardiovascular disease about two-fold, showing a dose-response relationship to arsenic exposure. Mortality from malignant blood disease (leukaemia and myeloma) and cirrhosis of the liver was also slightly increased. This mortality pattern among the smelter workers is consistent with earlier reports. An increased mortality from cardiovascular disease in this type of industry is of particular interest as it has been reported only once before.
PMCID: PMC1008317  PMID: 629894
3.  Occupation and male lung cancer: a case-control study in northern Sweden. 
Using a case-control study comprising about 600 men with lung cancer in northern Sweden the potential risk of different occupations and groups of occupations was studied. Longitudinal data concerning occupation, employment, and smoking habits were obtained by questionnaires. Some occupational groups (underground miners, copper smelter workers, electricians, and plumbers) exposed to previously known lung carcinogenic agents such as radon daughters, arsenic, and asbestos, had considerably increased odds ratios, which persisted after adjustment for smoking. A slightly raised odds ratio was observed in a group of blue collar workers potentially exposed to lung carcinogenic agents; this rise in the group as a whole mainly disappeared after adjustment for smoking. Farmers and foresters had strikingly low odds ratios, which could only partly be explained by their more moderate smoking habits. The population aetiological fraction attributable to occupation was estimated as 9%.
PMCID: PMC1007858  PMID: 3620367
4.  Protective effect of selenium on lung cancer in smelter workers. 
A possible protective effect of selenium against lung cancer has been indicated in recent studies. Workers in copper smelters are exposed to a combination of airborne selenium and carcinogens. In this study lung tissue concentrations of selenium, antimony, arsenic, cadmium, chromium, cobalt, lanthanum, and lead from 76 dead copper smelter workers were compared with those of 15 controls from a rural area and 10 controls from an urban area. The mean exposure time for the dead workers was 31.2 years, and the mean retirement time after the end of exposure 7.2 years. Lung cancer appeared in the workers with the lowest selenium lung tissue levels (selenium median value 71 micrograms/kg wet weight), as compared with both the controls (rural group, median value 110; urban group, median value 136) and other causes of death among the workers (median value 158). The quotient between the metals and selenium was used for comparison: a high quotient indicating a low protective effect of selenium and vice versa. The median values of the quotients between antimony, arsenic, cadmium, lanthanum, lead, chromium, and cobalt versus selenium were all numerically higher among the cases of lung cancer, the first five significantly higher (p less than 0.05) in 28 of the 35 comparisons between the lung cancer group and all other groups of smelter workers and controls. The different lung metal concentrations for each person were weighted according to their carcinogenic potency (Crx4 + Asx3 + Cdx2 + Sbx1 + Cox1 + Lax1 + Pbx1) against their corresponding selenium concentrations. From these calculations the protective effect of selenium was even more pronounced.
PMCID: PMC1007544  PMID: 4041390
5.  The carcinogenicity of arsenic. 
A carcinogenic role of inorganic arsenic has been suspected for nearly a century. Exposure to inorganic arsenic compounds occurs in some occupational groups, e.g., among smelter workers and workers engaged in the production and use of arsenic containing pesticides. Substantial exposure can also result from drinking water in certain areas and the use of some drugs. Tobacco and wine have had high As concentrations due to the use of arsenic containing pesticides. Inorganic arsenic compounds interfere with DNA repair mechanisms and an increased frequency of chromosomal aberrations have been observed among exposed workers and patients. Epidemiological data show that inorganic arsenic exposure can cause cancer of the lung and skin. The evidence of an etiologic role of arsenic for angiosarcoma of the liver is highly suggestive; however, the association between arsenic and cancer of other sites needs further investigation. No epidemiological data are available on exposure to organic arsenic compounds and cancer. Animal carcinogenicity studies involving exposure to various inorganic and organic arsenic compounds by different routes have been negative, with the possible exception of some preliminary data regarding lung cancer and leukemia. Some studies have indicated an increased mortality from lung cancer in populations living near point emission sources of arsenic into the air. The role of arsenic cannot be evaluated due to lack of exposure data. Epidemiological data suggest that the present WHO standard for drinking water (50 micrograms As/l.) provides only a small safety margin with regard to skin cancer.
PMCID: PMC1568809  PMID: 7023936
6.  Survey of antimony workers: mortality 1961-1992. 
The mortality of a census population and a prospective cohort of men employed on an antimony smelter in the north east of England was followed up from 1961-1992. The workers studied were exposed to a variety of agents including antimony and its oxides, arsenic and arsenic oxides, sulphur dioxide, and polycyclic aromatic hydrocarbons. The regional mortality rates were used to calculate expected deaths and a group of zircon sand workers employed on the site were used as a comparison group. For the census population of men working on the smelter before 1961 a significant increase in deaths from lung cancer was found (32 observed v 14.7 expected, P < 0.001). A similar excess was seen among maintenance men (12 observed v 5.3 expected P = 0.016). No such excess was found in the cohort recruited after 1960 (5 observed v 9.2 expected, maintenance workers 3 observed v 2.8 expected). There was evidence of a minimum latency period of around 20 years between first exposure and death from lung cancer. No evidence was found for a correlation between length of time worked and mortality from lung cancer. The results show that an increased risk of lung cancer existed in the workers employed before 1961, but it was not possible to attribute this excess to any particular agent. Mortality analysed by five year calendar periods of first exposure show a lessening of effect after 1955. Although the power of the study is clearly less for more recent periods of exposure the absence of any excess in the population after 1960 is encouraging.
PMCID: PMC1128103  PMID: 7849856
7.  Arsenic and selenium in lung, liver, and kidney tissue from dead smelter workers. 
Concentrations of arsenic and selenium in lung, liver, and kidney tissue from dead smelter workers and from a control group have been determined with the aid of neutron activation analysis. A sevenfold increase of arsenic was found in lung tissue from the exposed workers compared with the control group. The median value of arsenic in lung tissue from workers dead from respiratory cancer was not higher than corresponding values from workers dead from other malignancies or from cardiovascular or other diseases. With increasing period of retirement the malignancies or from cardiovascular or other diseases. With increasing period of retirement the arsenic content diminished in liver tissue but not in lung tissue, indicating a long biological half life of arsenic in lung tissue. The workers dead from malignancies had a higher As/Se quotient than workers dead from other diseases, which does not contradict the protective theory of selenium. Accumulation of antimony, cadmium, lead and lanthanum was observed in lung tissue from the exposed workers. Six of the workers died from lung cancer and the highest concentrations of any of the elements were always observed in the lung tissue from these six cases. This observation speaks in favour of a multifactorial cause behind the excess mortality from lung cancer in smelter workers.
PMCID: PMC1008843  PMID: 7236543
8.  Peripheral leucocyte count and longitudinal decline in lung function. 
Thorax  1988;43(6):462-466.
A six year follow up study of 750 aluminium smelter workers was undertaken to evaluate the relationship between the leucocyte count at the start of the study and the rate of decline in lung function. An inverse relationship between the leucocyte count and the forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) was present cross sectionally irrespective of cigarette smoking habit. The initial leucocyte count was also significantly related to the mean annual decline in FEV1 in smokers (p = 0.04) but not in former smokers or those who had never smoked. These observations suggest that the leucocyte count is a factor influencing the annual decline in FEV1 in smokers.
PMCID: PMC461311  PMID: 3420557
9.  Respiratory Cancer and Inhaled Inorganic Arsenic in Copper Smelters Workers: A Linear Relationship with Cumulative Exposure that Increases with Concentration 
Environmental Health Perspectives  2008;116(12):1661-1665.
Inhalation of high levels of airborne inorganic arsenic is a recognized cause of respiratory cancer. Although multiple epidemiologic studies have demonstrated this association, there have been few analyses of the mathematical relationship between cumulative arsenic exposure and risk of respiratory cancer, and no assessment as to whether and how arsenic concentration may modify this association.
The objective is an evaluation of the shape of the relationship between respiratory cancer mortality and cumulative inhaled arsenic exposure among copper smelter workers, and the modification of that relationship by arsenic concentration.
We used Poisson regression methods to analyze data from a cohort of arsenic-exposed copper smelter workers under a linear-exponential model for the excess relative risk.
Within categories of arsenic concentration, the association between respiratory cancer and cumulative arsenic exposure was consistent with linearity. The slope of the linear relationship with cumulative exposure increased with increasing arsenic concentration category.
Our results suggested a direct concentration effect from inhaled inorganic arsenic, whereby the excess relative risk for a fixed cumulative exposure was greater when delivered at a higher concentration and shorter duration than when delivered at a lower concentration and longer duration.
PMCID: PMC2599760  PMID: 19079717
arsenic; dose; response relationship; lung neoplasms; occupational diseases
10.  A new method for the analysis of cohort studies: implications of the multistage theory of carcinogenesis applied to occupational arsenic exposure. 
Implications of the multistage theory of carcinogenesis for evaluating the effect of exposure to carcinogens in the workplace are described. This theory predicts different patterns of excess risk related to duration of exposure, age at initial exposure, and follow-up time since exposure stopped, depending upon which stage of the carcinogenic process is affected by the carcinogen, i.e., action at an early stage or a late stage. New statistical methodologies are proposed to examine these patterns and are applied to the lung cancer mortality experience from a cohort study of smelter workers exposed to arsenic. Under this multistage hypothesis, the results indicate that arsenic exerts a definite late stage effect though an additional effect at the initial stage cannot be ruled out. The possibilities of biased conclusions resulting from incomplete exposure histories and lack of smoking information are also discussed as well as implications of these results to experimental animal studies.
PMCID: PMC1569231  PMID: 6873020
11.  Prevalence of beryllium sensitization among aluminium smelter workers 
Background Beryllium exposure occurs in aluminium smelters from natural contamination of bauxite, the principal source of aluminium.
Aims To characterize beryllium exposure in aluminium smelters and determine the prevalence rate of beryllium sensitization (BeS) among aluminium smelter workers.
Methods A population of 3185 workers from nine aluminium smelters owned by four different aluminium-producing companies were determined to have significant beryllium exposure. Of these, 1932 workers participated in medical surveillance programmes that included the serum beryllium lymphocyte proliferation test (BeLPT), confirmation of sensitization by at least two abnormal BeLPT test results and further evaluation for chronic beryllium disease in workers with BeS.
Results Personal beryllium samples obtained from the nine aluminium smelters showed a range of <0.01–13.00 μg/m3 time-weighted average with an arithmetic mean of 0.25 μg/m3 and geometric mean of 0.06 μg/m3. Nine workers were diagnosed with BeS (prevalence rate of 0.47%, 95% confidence interval = 0.21–0.88%).
Conclusions BeS can occur in aluminium smelter workers through natural beryllium contamination of the bauxite and further concentration during the refining and smelting processes. Exposure levels to beryllium observed in aluminium smelters are similar to those seen in other industries that utilize beryllium. However, compared with beryllium-exposed workers in other industries, the rate of BeS among aluminium smelter workers appears lower. This lower observed rate may be related to a more soluble form of beryllium found in the aluminium smelting work environment as well as the consistent use of respiratory protection.
PMCID: PMC3716328  PMID: 20610489
Aluminium; beryllium; sensitization; smelter; surveillance
12.  Renal function in relation to low levels of cadmium exposure in a group of smelter workers. 
Blood and urine samples were obtained from 274 smelter workers and urine samples from 48 controls. Cadmium, beta 2-microglobulin, and creatinine were estimated in blood and urine, and total protein in urine. Concentrations of cadmium in urine (mean 2.0 nmole/mmole creatinine) and blood (mean 21.8 nmole/L) observed in the smelter workers confirmed that this group had absorbed more cadmium than the general population, but less than most other occupationally exposed groups studied. Mean beta 2-microglobulin in urine was not significantly different in the smelter workers and the controls. The mean total protein in urine was 20% higher in the smelter workers, a difference which was significant (p congruent to 0.01). There was no consistent picture within the smelter workers of a relationship between history of cadmium exposure and the effect measures of beta 2-microglobulin in urine and blood, total protein in urine, creatinine clearance and relative beta 2-microglobulin clearance. Small but significant positive correlation coefficients were observed between cadmium in urine and beta 2-microglobulin in urine (r = 0.13), total protein in urine (r = 0.23) and beta 2-microglobulin clearance (r = 0.15), although these may be artifactual.
PMCID: PMC1568191  PMID: 6734555
13.  High exposure of Chinese mercury mine workers to elemental mercury vapor and increased methylmercury levels in their hair 
The aim of this study was to determine the level of exposure of mercury (Hg) miners and smelter workers to elemental mercury (Hg0) vapor in China, who work in Hg mines without using protective equipment against Hg0 vapor. In addition, the level of methylmercury (MeHg) intake by the workers was estimated from the MeHg concentration in their hair.
Urinary total mercury (THg) and hair THg and MeHg concentrations were measured in 26 Hg miners and smelter workers (i.e., exposed group), and 48 unexposed people (unexposed group).
The exposed group showed high geometric mean THg concentrations in urine (258 ng/ml, 226 μg/g creatinine) and hair (20.0 μg/g). The urinary THg concentration of the smelter workers in particular was extremely high (338 μg/g creatinine in urine). The highest urine THg concentration reached 4577 μg/g creatinine. THg concentrations in urine and hair showed a significant correlation in the exposed group (r=0.62), indicating the adhesion of Hg0 vapor to hair. However, no such significant correlation was found in the unexposed group. Hair MeHg concentration in the exposed group (1.97 μg/g) was about threefold higher than that in the unexposed group (0.60 μg/g).
This study shows that smelter workers in a Chinese Hg mine are exposed to extremely high levels of Hg0 vapor, and that Hg miners are exposed to higher levels of MeHg than the unexposed subjects. Further study is needed to determine the cause of the higher hair MeHg concentration in the exposed group.
PMCID: PMC2723641  PMID: 21431821
mercury mine; elemental mercury; hair; urine; methylmercury
14.  Some aspects of the environmental exposure to arsenic in Romania. 
The main sources of arsenic emission in Romania are ore smelters and refineries. Arsenic determinations were carried out by the silver diethyldithiocarbamate spectrophotometric method on hair and urine samples taken from smelter workers and individuals residing in two polluted areas and three areas not polluted by arsenic. Arsenic in hair was found to be a more reliable biologic test than tests on urine, obviously reflecting the differences in arsenic concentrations in workroom air. Repeated determinations for arsenic content after 3 years revealed a twofold increased rate in the 48 re-examined workers. Hair arsenic analysis in people living in two locations near an ore smelter and a refinery indicated high-levels compared to those of individuals residing in nonpolluted areas. Epidemiological studies are necessary in order to ascertain effects of heavy arsenic exposure in relation with concurrent exposures to respiratory irritants and metals.
PMCID: PMC1637413  PMID: 908284
15.  Diabetes mellitus and arsenic exposure: a second look at case-control data from a Swedish copper smelter. 
OBJECTIVES--To find out whether a newly found association between diabetes mellitus and arsenic in drinking water in Taiwan could be reproduced in copper smelters with arsenic exposure. METHODS--Extended analysis of a previous case-control study from 1978 was based on death records and objective exposure information from the company. The final analysis included only those employed at the smelter. Cases were 12 people with diabetes mellitus on the death certificate and those for whom there was clinical information on this disease. Controls were 31 people without cancer, cardiovascular and cerebrovascular disease as these disease categories had been associated with arsenic exposure in the original study and elsewhere. RESULTS--The odds ratios found for diabetes mellitus with increasing arsenic exposure categories were (reference level = 1), 2.0, 4.2, and 7.0, but the 95% confidence intervals included unity. Unstratified test for trend was weakly significant, P = 0.03. CONCLUSIONS--Although based on small numbers, the findings provide some support for the suggestion that arsenic exposure could sometimes play a part in the development of diabetes mellitus.
PMCID: PMC1128360  PMID: 8535499
16.  Increased lung cancer risks are similar whether arsenic is ingested or inhaled 
In 1980, the International Agency for Research on Cancer (IARC) determined there was sufficient evidence that inorganic arsenic was a human lung carcinogen based on studies involving exposure through inhalation. In 2004, IARC listed arsenic in drinking water as a cause of lung cancer, making arsenic the first substance established to cause human cancer by two unrelated pathways of exposure. It may initially seem counterintuitive that arsenic in drinking water would cause human lung cancer, and even if it did, one might expect risks to be orders of magnitude lower than those from direct inhalation into the lungs. In this paper we consider lung cancer dose-response relationships for inhalation and ingestion of arsenic by focusing on two key studies, a cohort mortality study in the United States involving Tacoma smelter workers inhaling arsenic, and a lung cancer case-control study involving ingestion of arsenic in drinking water in northern Chile. When exposure was assessed based on absorbed dose identified by concentrations of arsenic in urine, there was very little difference in the dose-response findings for lung cancer relative risks between inhalation and ingestion. The lung cancer mortality rate ratio estimate was 8.0 (95% CI 3.2-16.5, p<0.001) for an average urine concentration of 1179 μg/L following inhalation, and the odds ratio estimate of the lung cancer incidence rate ratio was 7.1 (95% CI 3.4-14.8, p<0.001) for an estimated average urine concentration of 825 μg/L following ingestion. The slopes of the linear dose-response relationships between excess relative risk (RR-1) for lung cancer and urinary arsenic concentration were similar for the two routes of exposure. We conclude that lung cancer risks probably depend on absorbed dose, and not on whether inorganic arsenic is ingested or inhaled.
PMCID: PMC2682945  PMID: 19190673
lung cancer; arsenic; inhalation; ingestion
17.  Biological indicators of exposure to total and respirable aluminium dust fractions in a primary aluminium smelter. 
OBJECTIVES: The study attempts to define biological indicators of aluminium uptake and excretion in workers exposed to airborne aluminium compounds in a primary aluminium smelter. Also, this study defines the total and respirable aluminium dust fractions in two different potrooms, and correlates their concentrations with biological indicators in this group of workers. METHODS: Air was sampled at defined work sites. Non-destructive and conventional techniques were used to find total and respirable aluminium content of the dust. Blood and urine was collected from 84 volunteers employed at various work stations throughout the smelter and from two different cohorts of controls matched for sex, age, and socioeconomic status. Aluminium in serum samples and urine specimens was measured by flameless atomic absorption with a PE 4100 ZL spectrometer. RESULTS: The correlation of aluminium concentrations in serum and urine samples with the degree of exposure was assessed for three arbitrary exposure categories; low (0.036 mg Al/m3), medium (0.35 mg Al/m3) and high (1.47 mg Al/m3) as found in different areas of the smelter. At medium and high exposure, the ratio of respirable to total aluminium in the dust samples varied significantly. At high exposure, serum aluminium, although significantly raised, was still within the normal range of an unexposed population. The workers with low exposure excreted aluminium in urine at levels significantly higher than the controls, but still within the normal range of the population. However, potroom workers with medium and high exposure had significantly higher urinary aluminium than the normal range. CONCLUSIONS: It is concluded that only urinary aluminium constitutes a practical index of occupational exposure at or above 0.35 mg Al/m3, and that the respirable fraction of the dust may play a major role in the biological response to exposure to aluminium in a smelter environment.
PMCID: PMC1128499  PMID: 8758038
18.  Arsenic and cancer. 
Palmar and plantar keratoses developed in seven patients many years after ingeston of trivalent inorganic arsenic. Six had basal cell carcinoma (superficial multicentric type in five), carcinoma "in situ" or squamous cell carcinoma of the skin. Two had systemic carcinoma--one, bilateral breast adenocarcinoma and one, carcinoma of the colon. From these observations and from the findings of a review of the literature, there seems no question that long-term arsenic ingestion can cause palmar and plantar keratoses and skin cancer, particularly basal cell carcinoma of the superficial multicentric type, usually on the torso. It is suspected but not proved to cause other cancers. Although over the last 50 years general exposure to arsenic has greatly decreased, particularly that from insecticides, this element is still found occasionally in drinking water (naturally or as a smelter byproduct), in certain foods and in cigarette smoke.
PMCID: PMC1956632  PMID: 125622
19.  Various effects of arsenic in Japan depending on type of exposure. 
Since 1955, a number of outbreaks of arsenic poisoning have occurred throughout Japan among industrial workers and the general population. The sources and types of exposure differ according to the incident, and the victims vary in sex and age. These incidents include arsenic poisoning in milk, soy sauce, and well water, pollution originating from the Toroku Mine on the island of Kyushu, the Matsuo Mine in Shimane Prefecture and Saganoseki Smelter on Kyushu. The type, routes, and dose of exposure as well as major symptoms are given. The clinical signs and symptoms are discussed in relation to the various types of exposure which occurred in these incidents. Dose-response relationships will be considered where data are available.
PMCID: PMC1637385  PMID: 561692
20.  Mortality and lead exposure: a retrospective cohort study of Swedish smelter workers. 
The study is based on the work histories and mortality data for 3832 male workers first employed before 1967 at a copper smelter in northern Sweden and followed up from 1950 to 1981. From the 3832 workers a lead cohort consisting of 437 workers employed for at least three years at sites with considerable lead exposure during 1950-74 was selected. These workers had regularly had blood lead measurements performed since 1950. Based on the cumulative blood lead dose 1950-74 and peak blood lead values, the cohort was subdivided into high mean, low mean, high peak, and low peak groups. Standardised mortality ratios (SMR) were calculated for the six groups using general and local reference populations. The original cohort of 3832 workers showed considerable excess of deaths for total mortality, malignant neoplasms especially lung and stomach cancer, ischaemic heart diseases, and cerebrovascular diseases when compared with the general population. In the lead cohort where the workers had been subjected to a considerable lead exposure only the raised SMR for lung cancer was sustained (SMR = 162; not significant). No significant differences were found between high lead and low lead exposed smelter workers.
PMCID: PMC1007741  PMID: 3778840
21.  Geographical patterns in blood lead in relation to industrial emissions and traffic in Swedish children, 1978–2007 
BMC Public Health  2009;9:225.
Blood lead concentrations (B-Pb) were measured in 3 879 Swedish school children during the period 1978–2007. The objective was to study the effect of the proximity to lead sources based on the children's home and school location.
The children's home address and school location were geocoded and their proximity to a lead smelter and major roads was calculated using geographical information system (GIS) software. All the statistical analyses were carried out using means of generalized log-linear modelling, with natural-logarithm-transformed B-Pb, adjusted for sex, school year, lead-exposing hobby, country of birth and, in the periods 1988–1994 and 1995–2007, parents' smoking habits.
The GIS analysis revealed that although the emission from the smelter and children's B-Pb levels had decreased considerably since 1978, proximity to the lead smelter continued to affect levels of B-Pb, even in recent years (geometric mean: near smelter: 22.90 μg/l; far from smelter 19.75 μg/l; p = 0.001). The analysis also revealed that proximity to major roads noticeably affected the children's B-Pb levels during the period 1978–1987 (geometric mean near major roads: 44.26 μg/l; far from roads: 38.32 μg/l; p = 0.056), due to the considerable amount of lead in petrol. This effect was, however, not visible after 1987 due to prohibition of lead in petrol.
The results show that proximity to the lead smelter still has an impact on the children's B-Pb levels. This is alarming since it could imply that living or working in the vicinity of a former lead source could pose a threat years after reduction of the emission. The analysis also revealed that urban children exposed to lead from traffic were only affected during the early period, when there were considerable amounts of lead in petrol, and that the prohibition of lead in petrol in later years led to reduced levels of lead in the blood of urban children.
PMCID: PMC2724513  PMID: 19591669
22.  Mortality in a region surrounding an arsenic emitting plant 
The purpose of the investigation is to study whether an increased mortality from certain causes exists in an area around the Rönnskärsverken smelter works in northern Sweden. Founded in 1928, this metallurgical plant processing mainly nonferrous metals has since its initial operations been using ore with a high arsenic content. This has resulted in environmental pollution to air and water of arsenic, as well as other metals and sulfur dioxide.
The causes of death for the population of two parishes in the vicinity of the plant were listed from the National Sedish Register on Death Causes. A reference area in the same part of Sweden with similar degree of urbanization, occupational profile, and age distribution was chosen. The causes of death for the two populations were followed during a period of 14 yr. A significantly higher mortality rate for lung cancer was noted in men in the exposed area. However, this increase was no longer significant when the occupationally exposed at Rönnskärsverken were excluded. The latter showed a highly significant excess mortality due to primary respiratory cancer.
A continuation of this investigation in the form of a cohort study of both the mortality and cancer incidence is currently under way.
PMCID: PMC1637390  PMID: 908290
23.  Carcinoma of Bronchus and the Smoking Habit in Rhodesian Africans 
British Medical Journal  1968;3(5616):468-469.
Comparison of the smoking habits of 32 adult male Africans with carcinoma of the bronchus and 32 controls showed that 87.5% of the patients with lung cancer were cigarette smokers compared with only 22% of the controls. The distribution of histological types of growth confirmed findings by other workers.
The absence of atmospheric pollution in Rhodesia makes it likely that cigarette-smoking is the most important causative factor in the aetiology of lung cancer among Rhodesian Africans. Further work is needed to determine the level of consumption of cigarettes and type of smoking habits which lead to a serious risk of cancer.
PMCID: PMC1986403  PMID: 5666805
24.  Combined effect of asbestos and smoking on mortality from lung cancer and mesothelioma in factory workers. 
The mortality of over 1250 male and 420 female asbestos factory workers was observed over the period 1971-80. Smoking habits were obtained from the subjects in 1971 before the start of the follow up period. Mortality due to lung cancer and to mesothelioma was related to smoking habits. After allowing for the effect of smoking on lung cancer the relative risk due to asbestos was highest for those who had never smoked, lowest for current smokers, and intermediate for ex-smokers; the trend was statistically significant (p less than 0.05). There was no significant association between smoking and deaths due to mesothelioma. Data from several studies are reviewed, and although overall non-smokers have a relative risk of lung cancer due to asbestos that is 1.8 times that of smokers, there is some uncertainty on the accuracy of this figure because of possible biases and sampling variation. Overall the evidence is that mesothelioma risk is independent of smoking.
PMCID: PMC1007410  PMID: 3965010
25.  Pulmonary function in aluminium smelters. 
Thorax  1984;39(10):743-751.
Two studies were conducted at an aluminum smelter employing 113 male workers in the smelting process. Twenty one of the 111 men in the first study experienced chest tightness more often than once a week and had a higher prevalence of cough, dyspnoea, and nasal symptoms but not of positive skin test responses than symptomless men. Lung function in these men did not differ significantly from that in the symptomless men at the beginning of the working week and only marginal deterioration occurred over the week. In the second study serial spirometric measurements were obtained over several shifts in a subset of 31 men from the first study. Impairment of ventilatory function on exposure to smelting fumes was demonstrated in 18 men. Analysis of all data from the 31 subjects revealed that ventilatory function varied significantly in association with heavy exposure to potfumes and a history of recurrent chest tightness. The findings of these two studies indicate that aluminum smelting fumes can cause bronchoconstriction in susceptible individuals. The reaction is dose dependent and is more severe in those with a history of recurrent chest tightness.
PMCID: PMC459912  PMID: 6495242

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