Environmental exposure to cadmium and risk of cancer: a prospective population-based study (original) (raw)
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Risk of mortality, cancer incidence, and stroke in a population potentially exposed to cadmium
Occupational and Environmental Medicine, 2000
Objectives-To follow up mortality and cancer incidence in a cohort potentially exposed to cadmium and to perform a geographical (ecological) analysis to further assess the health eVects of potential exposure to cadmium. Methods-The English village of Shipham has very high concentrations of cadmium in the soil. A previous cohort study of residents of Shipham in 1939 showed overall mortality below that expected, but a 40% excess of mortality from stroke. This study extends the follow up of the cohort for mortality to 1997, and includes an analysis of cancer incidence from 1971 to 1992, and a geographical study of mortality and cancer incidence. Standardised mortality and incidence ratios (SMRs and SIRs) were estimated with regional reference rates. Comparisons were made with the nearby village of Hutton. Results-All cause cohort mortality was lower than expected in both villages, although there was excess cancer incidence in both Shipham (SIR 167, 95% confidence interval (95% CI) 106 to 250) and Hutton (SIR 167, 95% CI 105 to 253). There was an excess of mortality from hypertension, cerebrovascular disease, and nephritis and nephrosis, of borderline significance, in Shipham (SMR 128, 95% CI 99 to 162). In the geographical study, all cause mortality in Shipham was also lower than expected (SMR 84, 95% CI 71 to 100). There was an excess in genitourinary cancers in both Shipham (SIR 160, 95% CI 107 to 239) and Hutton (SIR 153, 95% CI 122 to 192). Conclusion-No clear evidence of health eVects from possible exposure to cadmium in Shipham was found despite the extremely high concentrations of cadmium in the soil. (Occup Environ Med 2000;57:94-97)
Determinants of lung cancer risk among cadmium-exposed workers
Annals of Epidemiology, 1992
Workers at a cadmium recovery pIant in Globe, Colorado, showed an increased risk of lung cancer, which some investigators have attributed to cadmium exposure. We conducted a cohort mortality analysis of this work force and a case-control analysis of the lung cancer cases within this work force in order to assess the probable causes of the lung cancer excess. The Globe plant began as a lead smelter about 1886, switched to arsenic production in 1920, and became a cadmium metal production facility in 1926. Cadmium, arsenic, and cigarette smoking are three potential lung carcinogens found in this workplace. Industrial hygiene data collected from I943 onward served as the basis for the National Institute for Occupational Safety and Health (NIOSH)-derived exposure algorithm that assigned cadmium exposure estimates to employees based on their work area in the plant and calendar time. Few exposure data existed for substunces other than cadmium. Feedstock ore concentrations were used us a surrogate measure of air arsenic levels. The arsenic content of the fines used as feedstock prior to I940 was considerably higher than rhat of the fines used after 1940. Smoking histories had been obtained previously for 45% of the workers. A case-control analysis of the 25 cases of lung cancer known to have occurred among these workers through 1982 was conducted using three controls per case, matched by closest data of hire and age at hire. Porenrial causal agents for lung cancer included cadmium exposure, cigarette smoking, and arsenic exposure. Exposure variables for each case and control included estimated cumulative cadmium exposure in milligram-years per cubic meter, cigarette smoking history, and plant arsenic exposure status at the time of hire. Estimated cumuhtiwe cadmium exposures of cases and controls did not differ overall or within the date-of-hire strata. Cases were more than eight rimes more likely to have been cigarette smokers than were controls. Lung cancer risk in this workplace was more closely related to the period of hire, not to the cumulative cadmium eqosure. The period of hire appears to be a surrogate for arsenic exposure as related to feedstock. The measures used here seem to indicate that exposure to arsenic and cigarette particulates, rather than to cadmium particulates, may have caused the increased rate of lung cancer of these workers. Ann Epidemiol I992;2; 195-2 11.
Environmental Health Perspectives, 2008
BACKGROUND: Few population studies have reported on the long-term changes in the internal cadmium dose and simultaneously occurring mortality. OBJECTIVE: We monitored blood cadmium (BCd), 24-hr urinary cadmium (UCd), and mortality in an environmentally exposed population. METHODS: Starting from 1985, we followed BCd (until 2003), UCd (until 1996), and mortality (until 2007) among 476 and 480 subjects, randomly recruited from low-exposure areas (LEA) and high-exposure areas (HEA). The last cadmium-producing plant in the HEA closed in 2002. RESULTS: From 1985-1989 to 1991-1996, BCd decreased by 40.3% and 18.9% in the LEA and HEA, respectively (p < 0.0001 for between-area difference). From 1991-1996 until 2001-2003, BCd remained unchanged in the HEA (+ 1.8%) and increased by 19.7% in the LEA (p < 0.0001). Over the entire follow-up period, the annual decrease in BCd averaged 2.7% in the LEA (n = 258) and 1.8% in the HEA (n = 203). From 1985-1989 to 1991-1996, UCd fell by 12.9% in the LEA and by 16.6% in the HEA (p = 0.22), with mean annual decreases of 2.7% (n = 366) and 3.4% (n = 364). Over 20.3 years (median), 206 deaths (21.5%) occurred. At baseline, BCd (14.6 vs. 10.2 nmol/L) and UCd (14. nmol/24-hr) were higher in deaths than in survivors. The risks (p ≤ 0.04) associated with a doubling of baseline UCd were 20% and 44% for total and noncardiovascular mortality, and 25% and 33% for a doubling of BCd. CONCLUSIONS: Even if zinc-cadmium smelters close, historical environmental contamination remains a persistent source of exposure. Environmental exposure to cadmium increases total and noncardiovascular mortality in a continuous fashion without threshold.
Cancer mortality of cadmium workers
Occupational and Environmental Medicine, 1985
Several epidemiological studies of workers exposed to cadmium indicate an increased risk of lung and prostatic cancer. The increase is statistically significant in some of the studies but the SMR is greater than 100 in almost all. A cohort study of the mortality among 522 Swedish workers exposed to cadmium for at least one year in a nickel-cadmium battery plant support the earlier findings. The SMR for lung and prostatic cancer increased with increasing dose and latency but did not obtain statistical significance. A combination of all the available data from the most recent follow up of causes of death among cadmium workers in six different cohorts shows 28 cases of prostatic cancer (SMR = 162) and 195 cases of lung cancer (SMR = 121). This new analysis suggests that long term, high level exposure to cadmium is associated with an increased risk of cancer. The role of concomitant exposure to nickel needs further study.
Environmental Research, 2001
This report covers part of the assessment of a site in northern France polluted by industrial metal emissions. Our objectives were to assess the cadmium burden in children aged 8 to 11 years and look for factors that affected it. A cross-sectional population-based study took place in 1996+1997 and included 400 children (200 in the metal-polluted area). The geometric mean of the blood cadmium (CdB) levels of children living on the polluted site was 0.51 g/L (95% CI ؍ [0.49+0.53]); that of the nonexposed children was 0.47 g/L (95% CI ؍ [0.45+0.49]) (P < 0.01). The geometric mean of the urinary cadmium (CdU) levels of children living on the polluted site was 1.16 g/g creatinine (95% CI ؍ [1.01+1.34]); that of the nonexposed children was 0.99 g/g creatinine (95% CI ؍ [0.86+1.14]) (P ؍ 0.10). Mean CdB was higher among children within 4 km of a zinc smelter and consuming 5500 ml of tap water daily ( ؋ 1.34; 95% CI ؍ [1.14+1.51]) compared with children living more than 4 km away and consuming < 500 ml of tap water daily. Independently of this association, consumption of Ash and shellAsh (5once a week vs < once a week) and homegrown vegetables (5once daily vs < once daily) was associated with higher mean CdB levels, respectively: ؋ 1.14; 95% CI ؍ [1.07+1.21] and ؋ 1.25; 95% CI ؍ [1.04+1.50]. Neither sex nor age was associated with CdB. Mean CdU was associated with paternal occupational cadmium exposure.
Cadmium Exposure and Breast Cancer Risk
JNCI Journal of the National Cancer Institute, 2006
Cadmium, a highly persistent heavy metal, has been categorized as a probable human carcinogen by the U.S. Environmental Protection Agency. Primary exposure sources include food and tobacco smoke. We carried out a population-based case -control study of 246 women, aged 20 -69 years, with breast cancer and 254 agematched con trol subjects. We measured cadmium levels in urine samples by inductively coupled plasma mass spectrometry and conducted interviews by telephone to obtain information on known breast cancer risk factors. Odds ratios (ORs) and 95% confi dence intervals (CIs) for breast cancer by creatinine-adjusted cadmium levels were calculated by multivariable analysis. Statistical tests were two-sided. Women in the highest quartile of creatinine-adjusted cadmium level ( ≥ 0.58 µg/g) had twice the breast cancer risk of those in the lowest quartile (<0.26 µg/g; OR = 2.29, 95% CI = 1.3 to 4.2) after adjustment for established risk factors, and there was a statistically signifi cant increase in risk with increasing cadmium level ( P trend = .01). Based on this study, the absolute risk difference is 45 (95% CI = 0 to 77) per 100 000 given an overall breast cancer rate of 124 per 100 000. Whether increased cadmium is a causal factor for breast cancer or refl ects the effects of treatment or disease remains to be determined. [J Natl Cancer Inst 2006;98: 869 -73 ]
Biological Effects of Human Exposure to Environmental Cadmium
Biomolecules
Cadmium (Cd) is a toxic metal for the human organism and for all ecosystems. Cd is naturally found at low levels; however, higher amounts of Cd in the environment result from human activities as it spreads into the air and water in the form of micropollutants as a consequence of industrial processes, pollution, waste incineration, and electronic waste recycling. The human body has a limited ability to respond to Cd exposure since the metal does not undergo metabolic degradation into less toxic species and is only poorly excreted. The extremely long biological half-life of Cd essentially makes it a cumulative toxin; chronic exposure causes harmful effects from the metal stored in the organs. The present paper considers exposure and potential health concerns due to environmental cadmium. Exposure to Cd compounds is primarily associated with an elevated risk of lung, kidney, prostate, and pancreatic cancer. Cd has also been linked to cancers of the breast, urinary system, and bladder. ...
Cadmium-induced cancers in animals and in humans
International journal of occupational and environmental health
Discovered in the early 1800s, the use of cadmium and various cadmium salts started to become industrially important near the close of the 19th century, rapidly thereafter began to flourish, yet has diminished more recently. Most cadmium used in the United States is a byproduct from the smelting of zinc, lead, or copper ores, and is used to manufacture batteries. Carcinogenic activity of cadmium was discovered first in animals and only subsequently in humans. Cadmium and cadmium compounds have been classified as known human carcinogens by the International Agency for Research on Cancer and the National Toxicology Program based on epidemiologic studies showing a causal association with lung cancer, and possibly prostate cancer, and studies in experimental animals, demonstrating that cadmium causes tumors at multiple tissue sites, by various routes of exposure, and in several species and strains. Epidemiologic studies published since these evaluations suggest that cadmium is also asso...
Cadmium Toxicity in Nature Generates the Cancerous Problems
Pollution Research
A naturally occurring metal, cadmium is noticed in tiny amounts in a variety of sources such as food, water, soil, and the atmosphere. Cadmium may be edified in all soils and rocks, including coal and mineral fertilizers. In general, non-smoker people are getting affected by food contamination. The main theme of this paper is cancer activity by cadmium pollution of our environment. Foods are getting contaminated by industrial wastes. Wastes have Cd2+ ions which can bind with plant materials and also bind with animal muscles. On the other hand, the smoker people take the cadmium by smoking tobacco. The cadmium can easily bind up with the organs like the lung, prostate, breast, bone, etc. When industrial wastes are thrown into rivers, ponds, or open spaces, particularly in South Asian nations, the water becomes poisoned and the soil becomes deteriorated; as a result, the environment becomes more hazardous. In consequence, people can be oppressed by significant sicknesses that occurred...
Cadmium exposure in the population: from health risks to strategies of prevention
BioMetals, 2010
We focus on the recent evidence that elucidates our understanding about the effects of cadmium (Cd) on human health and their prevention. Recently, there has been substantial progress in the exploration of the shape of the Cd concentrationresponse function on osteoporosis and mortality. Environmental exposure to Cd increases total mortality in a continuous fashion without evidence of a threshold, independently of kidney function and other classical factors associated with mortality including age, gender, smoking and social economic status. Pooled hazard rates of two recent environmental population based cohort studies revealed that for each doubling of urinary Cd concentration, the relative risk for mortality increases with 17% (95% CI 4.2-33.1%; P \ 0.0001). Tubular kidney damage starts at urinary Cd concentrations ranging between 0.5 and 2 lg urinary Cd/g creatinine, and recent studies focusing on bone effects show increased risk of osteoporosis even at urinary Cd below 1 lg Cd/g creatinine. The non-smoking adult population has urinary Cd concentrations close to or higher than 0.5 lg Cd/g creatinine. To diminish the transfer of Cd from soil to plants for human consumption, the bioavailability of soil Cd for the plants should be reduced (external bioavailability) by maintaining agricultural and garden soils pH close to neutral (pH-H 2 O of 7.5; pH-KCL of 6.5). Reducing the systemic bioavailability of intestinal Cd can be best achieved by preserving a balanced iron status. The latter might especially be relevant in groups with a lower intake of iron, such as vegetarians, and women in reproductive phase of life. In exposed populations, house dust loaded with Cd is an additional relevant exposure route. In view of the insidious etiology of health effects associated with low dose exposure to Cd and the current European Cd intake which is close to the tolerable weekly intake, one should not underestimate the importance of the recent epidemiological evidence on Cd toxicity as to its medical and public health implications.