Health Stream Literature Summary - Issue 58 - June 2010

Kidney cancer mortality: Fifty-year latency patterns related to arsenic exposure.
Yuan Y, Marshall G, Ferreccio C, Steinmaus C, Liaw J, Bates M and Smith AH. (2010) Epidemiology, 21(1); 103-108.

Arsenic in drinking water has been found to be associated with increased risks of kidney cancer in several countries, although the evidence for causation is currently regarded as insufficient by the International Agency for Research on Cancer. This study investigated kidney cancer mortality in the northern region of Chile before, during and after a period of high arsenic exposure from drinking water.

More than half of the population of Region II in Chile resides in the cities of Antofagasta and Mejillones which share the same water source. The arsenic concentration in the drinking water for these cities increased in 1958 from 90 micro g/L to an average of 870 micro g/L when water began to be drawn from highly contaminated rivers. When a water treatment plant was introduced in 1971, Antofagasta's water arsenic concentration dropped to about 110 micro g/L and further reductions occurred with further improvements in treatment. As a comparison population, Region V of Chile was selected. The major city of this region (Valparaiso) has had water arsenic concentrations close to 1 micro g/L. Information on mortality in men and women aged 30 years and above from 1950 to 2000 was collected for Region II and Region V. Causes of death were coded according to the International Classification of Diseases, Ninth Revision (ICD-9). The National Institute of Statistics provided annual estimates of the population living in Regions II and V stratified by age and sex for the period 1950-2000.

The kidney cancer mortality rates increased rapidly from 1950 through 2000 in both regions. Age-adjusted kidney cancer mortality rate ratios (RRs) for Region II compared with Region V started to increase about 10 years after high arsenic exposure began in 1958. There was an RR of 2.5 (95% confidence interval (CI) = 1.2-5.2) among men for the 5-year period centred in 1967, and an RR of 3.7 (1.8-7.6) for women for the 5-year period centred in 1972. For men, the peak kidney cancer mortality rate ratio was 3.4 (2.2-5.1) in 1981-1985, with a decline to 1.6 (1.2-2.1) in 1996-2000. For women, mortality RRs reached 2.9 (1.8-4.7) in 1981-1985 but remained higher for longer than men, with an RR of 4.4 (3.0-6.4) in 1991-1995 and then a decline to 2.3 (1.6-3.3) in 1996-2000. The effect of high arsenic exposure in early life was assessed by comparing young adults in Antofagasta and Mejillones aged 30-39 years (born during and just before the high-exposure period), and people aged 40 and above (born before 1950 and therefore without early life exposure). Standardised mortality ratios (SMRs) for kidney cancer mortality for these groups were calculated and compared with the rest of Chile. For those aged 30-39 years who had early life exposure, the SMR was 7.1 (3.1-14). For those aged 40 and above, the SMR was 3.1 (2.7-3.6).

This 50-year mortality study showed a distinct increase in deaths from kidney cancer in both regions of Chile over the study period. However the pattern of increase for Region II showed a greater increase than Region V with a long latency relative to the period of high arsenic exposure. Increased kidney cancer mortality rate ratios continued for at least 25 years after the high exposure levels began to decline. The latency patterns are consistent with the causal interpretation and add strength to the epidemiological evidence that arsenic in water causes increased rates of kidney cancer mortality.

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