MORTALITY OF SHIPHAM RESIDENTS: 40-YEAR FOLLOW-UP

doi:10.1016/S0140-6736(82)92163-8

The Lancet

Volume 319, Issue 8277, 17 April 1982, Pages 896-899

https://doi.org/10.1016/S0140-6736(82)92163-8 Get rights and content

Abstract

The 1939 populations of Shipham, a village in Somerset with high soil-cadmium levels, and a nearby control village have been followed for 40 years. Death certificates were obtained for those who had died, and the mortality rates were compared with those for England and Wales. Small excesses of hypertensive, cerebrovascular, and genitourinary disease were noted in Shipham but not in the control village. These conditions have been associated with cadmium toxicity, and so it is possible that cadmium had some influence on the disease pattern in Shipham; but if so, the effect was slight. By contrast, fewer deaths than expected from respiratory disease and cancers were observed in both villages. This gave rise to all-cause mortality rates in Shipham and the control village which were similar and well below the national average.

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Cited by (54)

Cadmium
2021, Handbook on the Toxicology of Metals: Fifth Edition
Cadmium (Cd) occurs with zinc and lead in sulfide ores. Elevated concentrations in air, water, and soil may occur close to nonferrous mining and metal refining industries. Cadmium metal has been used as an anticorrosive when electroplated onto steel. Cd compounds are used in batteries, as pigments and in solar panels. Between 10% and 50% of inhaled Cd will be absorbed and 5%–10% of ingested Cd. The accumulation of Cd in humans occurs in many tissues, with particularly long half-lives (10–30 years) in muscle, bone, kidney, and liver. Cd bound to metallothionein in plasma is filtered through the renal glomeruli and reabsorbed in the tubuli, where the metal ion is released and toxic effects occur. The average amount of Cd ingested in Japan and most European and North American countries is <10–20 μg/day. The corresponding average urinary excretion of Cd is <0.5–1.0 μg/day and the blood concentration is 0.2–0.7 μg/L in nonsmokers; it is twice as high in smokers. Acute inhalation of Cd in air, for example, from soldering or welding fumes, may lead to severe chemical pneumonitis. Long-term exposure to low air levels may lead to chronic obstructive lung disease and possibly to lung cancer. Long-term excessive exposure from the air or food leads to renal tubular dysfunction with low molecular weight proteinuria. It may also lead to disturbance of calcium metabolism, osteoporosis, and osteomalacia, mainly among postmenopausal women. A disease exhibiting these features—called itai-itai disease—occurred in the 1950s in a Cd-polluted area of Japan. Cd-induced cancer of the lungs, prostate, and other organs in animals and increased rates of cancer of the lungs and other organs in humans. The International Agency for Research on Cancer (IARC) classified Cd as a human carcinogen (Group 1). Adverse kidney effects occur in sensitive occupational groups, as well as in general population groups, after lifelong exposures giving rise to urinary Cd (UCd) of 2–4 μg/g creatinine. At such exposures, bone effects including osteoporosis and fractures may also occur in sensitive groups. Adverse bone and kidney effects may occur in a small but sensitive population group as a result of lifelong cadmium exposure with UCd of approximately 1 μg/g creatinine and higher, but the evidence is still inconclusive. This level of exposure occurs within general population groups in many countries. Osteomalacia is treated with large doses of vitamin D, but there is no effective treatment for other Cd-related effects. Because of the long half-life of Cd and the irreversibility of bone effects and some kidney effects, primary prevention is essential. The toxicological and environmental aspects of Cd have been reviewed in detail by Friberg et al. (1974, 1985, 1986), Tsuchiya (1978), Nriagu (1980, 1981), the WHO/IPCS (1992), the IARC (1993, 2012), Järup et al. (1998c), the Agency for Toxic Substances and Disease Registry (ATSDR, 1999), Nordberg and Nordberg (2002), the European Union (EU, 2003, 2007; ECHA 2020), Satarug and Moore (2004), and the World Health Organization Food and Agriculture Organization (JECFA, 2004, 2012), the European Food Safety Authority (EFSA, 2009, 2012), Akesson et al. (2014), the Scientific Committee on Occupational Exposure Limits (SCOEL, 2017), and the International Union of Pure and Applied Chemistry (Nordberg et al., 2018).
Cadmium
2015, Handbook on the Toxicology of Metals: Fourth Edition
Cadmium (Cd) occurs naturally with zinc and lead in sulfide ores. Elevated concentrations in air, water, and soil may occur close to industrial emission sources, particularly those of nonferrous mining and metal refining industries. Cadmium metal has been used as an anticorrosive when electroplated onto steel. Cd compounds are used in batteries and as pigments. Cd is increasingly used in solar panels. Dispersive use of Cd is restricted by law in the European Union. Absorption of Cd compounds through the skin is negligible. Between 10% and 50% of inhaled Cd will be absorbed. Humans absorb 5-10% of ingested Cd. A low intake of calcium, zinc, or iron increases the degree of absorption. Cadmium is transported in plasma when bound to metallothionein (MT), a low molecular weight protein, and/or to certain high molecular weight proteins. The accumulation of Cd occurs in many tissues, with particularly long half-lives (10-30 years) in muscle, bone, kidney, and liver. MT-bound Cd in plasma is filtered through the renal glomeruli and reabsorbed in the tubuli, where the metal ion is released. When not all Cd is bound, toxic effects occur.
The average amount of Cd ingested in European and North American countries is 10-20 μg/day. The corresponding average urinary excretion is 0.5-1.0 μg/day and the blood concentration is 0.5-1.0 μg/L in nonsmokers; it is twice as high in smokers. The intake of Cd through food used to be higher in Japan than in Europe, but it has decreased and is currently similar to levels reported in European countries with high intakes.
Acute inhalation of Cd in air, for example from soldering or welding fumes, may lead to severe chemical pneumonitis. Long-term exposure to low air levels may lead to chronic obstructive lung disease and possibly to lung cancer. Long-term excessive exposure from the air or food leads to renal tubular dysfunction. The first sign of damage is low molecular weight proteinuria.
Long-term exposure from food, often combined with other means of delivery, may also lead to disturbance of calcium metabolism, osteoporosis, and osteomalacia, mainly among postmenopausal women. A disease exhibiting these features—called itai-itai disease—occurred in the 1950s in a Cd-polluted area of Japan: 124 cases were diagnosed up to 1970, and 196 cases in total were diagnosed up to 2011.
In laboratory animals, Cd has been shown to induce cancer of the lungs, prostate, and other organs. Epidemiological studies have found increased rates of cancer of the lungs and in some studies also in other organs. Cadmium is classified as a human carcinogen (Group 1) by the International Agency for Research on Cancer (IARC).
Exposure to Cd in the air at concentrations of 5-10 μg/m³ during a working life of 45 years may give rise to renal tubular dysfunction in a small proportion of exposed workers. At approximately 100 μg/m³, signs of chronic obstructive lung disease may develop. Epidemiological data shows that adverse kidney effects occur in sensitive occupational groups, as well as in general population groups, after lifelong exposures giving rise to urinary Cd (UCd) of 4 μg/g creatinine. At such exposures, bone effects including osteoporosis and increased risk of fractures may also occur in sensitive groups, mainly among postmenopausal women. Adverse bone and kidney effects may occur in a small but sensitive population group as a result of lifelong cadmium exposure with UCd of approximately 1 μg/g creatinine and higher, but the evidence is still inconclusive. Such exposure occurs in general population groups in many countries. There is no specific treatment for Cd poisoning. When there are signs of osteomalacia, large doses of vitamin D should be given. Because of the long half-life of Cd and the irreversibility of bone effects and some kidney effects primary prevention is essential.
The toxicological and environmental aspects of Cd have been reviewed in detail by Friberg et al., 1974, Friberg et al., 1985, Friberg et al., 1986, Tsuchiya, 1978, Nriagu, 1980, Nriagu, 1981, the WHO/IPCS (1992), the IARC, 1993, IARC., 2012, Järup et al., 1998c, the Agency for Toxic Substances and Disease Registry (ATSDR, 1999), Nordberg and Nordberg (2002), the European Union (EU, 2003, EU, 2007), Satarug and Moore (2004), and the World Health Organization (WHO) Food and Agriculture Organization (JECFA, 2004, JECFA., 2012), the European Food Safety Authority (EFSA, 2009, EFSA, 2012), and Akesson et al. (2014).
Landfill waste and recycling: Use of a screening-level risk assessment tool for end-of-life cadmium telluride (CdTe) thin-film photovoltaic (PV) panels
2014, Energy Policy
Citation Excerpt :
At the waste volumes used in our analysis, the carcinogenic risks were all below the critical risk level of 1 in 100,000. Most epidemiological studies suggest that cadmium is a human carcinogen by inhalation exposure from fumes or particulate, and there is no compelling evidence for the carcinogenicity of cadmium via the oral or dermal routes of exposure (ATSDR (Agency for Toxic Substances and Disease Registry), 2008; Inskip et al., 1982; Lauwerys and De Wals, 1981; Nakagawa et al., 1987; Thun et al., 1985). Thus, the only contribution to carcinogenic risk was via the surface pathway through particle inhalation, as shown in Table 2.
Grid-connected solar photovoltaic (PV) power is currently one of the fastest growing power-generation technologies in the world. While PV technologies provide the environmental benefit of zero emissions during use, the use of heavy metals in thin-film PV cells raises important health and environmental concerns regarding the end-of-life disposal of PV panels. To date, there is no published quantitative assessment of the potential human health risk due to cadmium leaching from cadmium telluride (CdTe) PV panels disposed in a landfill. Thus, we used a screening-level risk assessment tool to estimate possible human health risk associated with disposal of CdTe panels into landfills. In addition, we conducted a literature review of potential cadmium release from the recycling process in order to contrast the potential health risks from PV panel disposal in landfills to those from PV panel recycling. Based on the results of our literature review, a meaningful risk comparison cannot be performed at this time. Based on the human health risk estimates generated for PV panel disposal, our assessment indicated that landfill disposal of CdTe panels does not pose a human health hazard at current production volumes, although our results pointed to the importance of CdTe PV panel end-of-life management.
Cadmium
2014, Handbook on the Toxicology of Metals
Cadmium (Cd) occurs naturally with zinc and lead in sulfide ores. Elevated concentrations in air, water, and soil may occur close to industrial emission sources, particularly those of nonferrous mining and metal refining industries. Cadmium metal has been used as an anticorrosive when electroplated onto steel. Cd compounds are used in batteries and as pigments. Cd is increasingly used in solar panels. Dispersive use of Cd is restricted by law in the European Union. Absorption of Cd compounds through the skin is negligible. Between 10% and 50% of inhaled Cd will be absorbed. Humans absorb 5-10% of ingested Cd. A low intake of calcium, zinc, or iron increases the degree of absorption. Cadmium is transported in plasma when bound to metallothionein (MT), a low molecular weight protein, and/or to certain high molecular weight proteins. The accumulation of Cd occurs in many tissues, with particularly long half-lives (10-30 years) in muscle, bone, kidney, and liver. MT-bound Cd in plasma is filtered through the renal glomeruli and reabsorbed in the tubuli, where the metal ion is released. When not all Cd is bound, toxic effects occur.
The average amount of Cd ingested in European and North American countries is 10-20 μg/day. The corresponding average urinary excretion is 0.5-1.0 μg/day and the blood concentration is 0.5-1.0 μg/L in nonsmokers; it is twice as high in smokers. The intake of Cd through food used to be higher in Japan than in Europe, but it has decreased and is currently similar to levels reported in European countries with high intakes.
Acute inhalation of Cd in air, for example from soldering or welding fumes, may lead to severe chemical pneumonitis. Long-term exposure to low air levels may lead to chronic obstructive lung disease and possibly to lung cancer. Long-term excessive exposure from the air or food leads to renal tubular dysfunction. The first sign of damage is low molecular weight proteinuria.
Long-term exposure from food, often combined with other means of delivery, may also lead to disturbance of calcium metabolism, osteoporosis, and osteomalacia, mainly among postmenopausal women. A disease exhibiting these features—called itai-itai disease—occurred in the 1950s in a Cd-polluted area of Japan: 124 cases were diagnosed up to 1970, and 196 cases in total were diagnosed up to 2011.
In laboratory animals, Cd has been shown to induce cancer of the lungs, prostate, and other organs. Epidemiological studies have found increased rates of cancer of the lungs and in some studies also in other organs. Cadmium is classified as a human carcinogen (Group 1) by the International Agency for Research on Cancer (IARC).
Exposure to Cd in the air at concentrations of 5-10 μg/m³ during a working life of 45 years may give rise to renal tubular dysfunction in a small proportion of exposed workers. At approximately 100 μg/m³, signs of chronic obstructive lung disease may develop. Epidemiological data shows that adverse kidney effects occur in sensitive occupational groups, as well as in general population groups, after lifelong exposures giving rise to urinary Cd (UCd) of 4 μg/g creatinine. At such exposures, bone effects including osteoporosis and increased risk of fractures may also occur in sensitive groups, mainly among postmenopausal women. Adverse bone and kidney effects may occur in a small but sensitive population group as a result of lifelong cadmium exposure with UCd of approximately 1 μg/g creatinine and higher, but the evidence is still inconclusive. Such exposure occurs in general population groups in many countries. There is no specific treatment for Cd poisoning. When there are signs of osteomalacia, large doses of vitamin D should be given. Because of the long half-life of Cd and the irreversibility of bone effects and some kidney effects primary prevention is essential.
The toxicological and environmental aspects of Cd have been reviewed in detail by Friberg et al., 1974, Friberg et al., 1985, Friberg et al., 1986, Tsuchiya, 1978, Nriagu, 1980, Nriagu, 1981, the WHO/IPCS (1992), the IARC, 1993, IARC., 2012, Järup et al., 1998c, the Agency for Toxic Substances and Disease Registry (ATSDR, 1999), Nordberg and Nordberg (2002), the European Union (EU, 2003, EU, 2007), Satarug and Moore (2004), and the World Health Organization (WHO) Food and Agriculture Organization (JECFA, 2004, JECFA., 2012), the European Food Safety Authority (EFSA, 2009, EFSA, 2012), and Akesson et al. (2014).
Cadmium exposure in association with history of stroke and heart failure
2010, Environmental Research
Citation Excerpt :
In the English village of Shipham, where soil levels and dietary intake of cadmium were very high, researchers found no evidence of adverse effects on blood pressure and hepatic, renal and skeletal systems (Morgan and Simms, 1988; Strehlow and Barltrop, 1988). However, in research based in the same geographical area, a 40-year cohort study found significant excess mortality from stroke, and a follow-up ecological study reported borderline significant excess stroke mortality (Elliott et al., 2000; Inskip et al., 1982). HF is a disabling and deadly disease whose prevalence continues to rise in the US despite a decline in general cardiovascular disease morbidity and mortality (Bahrami et al., 2008).
It is unclear whether environmental cadmium exposure is associated with cardiovascular disease, although recent data suggest associations with myocardial infarction and peripheral arterial disease.
The objective of this study was to evaluate the association of measured cadmium exposure with stroke and heart failure (HF) in the general population.
We analyzed data from 12,049 participants, aged 30 years and older, in the 1999–2006 National Health and Nutrition Examination Survey (NHANES) for whom information was available on body mass index, smoking status, alcohol consumption, and socio-demographic characteristics.
At their interviews, 492 persons reported a history of stroke, and 471 a history of HF. After adjusting for demographic and cardiovascular risk factors, a 50% increase in blood cadmium corresponded to a 35% increased odds of prevalent stroke [OR: 1.35; 95% confidence interval (CI): 1.12–1.65] and a 50% increase in urinary cadmium corresponded to a 9% increase in prevalent stroke [OR: 1.09; 95% CI: 1.00–1.19]. This association was higher among women [OR: 1.38; 95% CI: 1.11–1.72] than men [OR: 1.30; 95% CI: 0.93–1.79] (p-value for interaction=0.05). A 50% increase in blood cadmium corresponded to a 48% increased odds of prevalent HF [OR: 1.48; 95% CI: 1.17–1.87] and a 50% increase in urinary cadmium corresponded to a 12% increase in prevalent HF [OR: 1.12; 95% CI: 1.03–1.20], with no difference in sex-specific associations.
Environmental exposure to cadmium was associated with significantly increased stroke and heart failure prevalence. Cadmium exposure may increase these important manifestations of cardiovascular disease.
Review of cadmium transfers from soil to humans and its health effects and Jamaican environment
2008, Science of the Total Environment
Concerns about the effects of cadmium on human health have led to numerous guidelines and regulations limiting its concentrations in soils and food and allowable human intakes. These have socio-economic consequences in terms of land use and the marketing of food. The bauxite soils in Jamaica, which are both aluminium ores and agricultural soils contain orders of magnitude higher than world normal concentrations of cadmium resulting in elevated Cd concentrations in several foodstuffs and significant transfers to humans, which would seem to represent a risk factor for increased mortality and/or morbidity in the local populations. But, as in Shipham and other examples, there is no evidence of cadmium-related human distress. Macro-indicators like life expectancy and median ages of death do not show cadmium related geographical distributions. The present review focuses on the soils and foods and illnesses of high incidence especially cancers and renal disease that have been traditionally associated with cadmium. In view of the remarkable concentrations of cadmium involved in Jamaica, and often contradictory reports in the literature, it appears that much remains to be learned about certain details of cadmium toxicity.

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Public HealthMORTALITY OF SHIPHAM RESIDENTS: 40-YEAR FOLLOW-UP

Abstract

J Chron Dis

Lancet

Lancet

J Chron Dis

Lancet

Lancet

Lancet

The Wolfson geochemical atlas of England and Wales

Health hazards in the manufacture of alkaline accumulators with special reference to chronic cadmium poisoning

Acta Med Scand

Renal tubular malfunction and pulmonary emphysema in cadmium pigment workers

Quart J Med

Cadmium in the environment

Cadmium, chromium and cardiovascular disease

Circulation

Public Health
MORTALITY OF SHIPHAM RESIDENTS: 40-YEAR FOLLOW-UP