Study [reference] (Table from original publication) | Study locale | Outcome | ICD1 | Arsenic exposure assessment | Exposure [comments] | Cases: Controls | All participants | Never smokers | Ever smokers | Covariates assessed | |||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|
n | OR2, (95% CI) | n | OR, (95% CI) | n | OR, (95% CI) | ||||||||
Chen et al. 19863[25] (Table Four) | 4 neighbouring Blackfoot disease (BFD)-endemic areas, Taiwan | Mortality 1996-2000 | N/A | Individual level ‘estimated’ | Year of artesian water consumption: | 69:368 | age, sex, cigarette smoking, tea drinking habit, vegetarian habit, vegetable consumption frequency, fermented bean consumption frequency | ||||||
0 (referent) | 17 | 1.0 | – | – | – | – | |||||||
1 – 20 | 19 | 1.27 | – | – | – | – | |||||||
20 – 40 | 10 | 1.68 | – | – | – | – | |||||||
≥ 40 | 23 | 4.10 | – | – | – | – | |||||||
[Median arsenic content of artesian wells and (range): 780 μg˙•L-1 (350 – 1,140). History of artesian well water noted.] | |||||||||||||
Bates et al. 1995 [31] (Table Three) | Utah, USA | Incidence | N/A | Individual level ‘measured’ | Cumulative dose index of arsenic (mg): | 117:266 | age, sex, smoking, exposure to chlorinated surface water, history of bladder infection, education, urbanization of the place of longest lifetime residence, and ever employed in high-risk occupation | ||||||
Diagnosis in a 1-year period around 1978 | < 19 (referent) | 14 | 1.0 | 10 | 1.0 | 4 | 1.0 | ||||||
19 to < 33 | 21 | 1.56 (0.8–3.2) | 10 | 1.09 (0.4–3.1) | 11 | 3.33 (1.0–10.8) | |||||||
33 to < 53 | 17 | 0.95 (0.4–2.0) | 7 | 0.68 (0.2–2.3) | 10 | 1.93 (0.6–6.2) | |||||||
≥ 53 | 19 | 1.41 (0.7–2.9) | 4 | 0.53 (0.1–1.9) | 15 | 3.32 (1.1–10.3) | |||||||
[Arsenic water concentration ranged 0.5 - 160 μg˙•L and averaged 5 μg˙•L. Data on arsenic levels in public drinking water supplies were collected in 1978–79. Results are based on the 71 cases who had lived in study towns for at least half of their lives. Residential history and water source used in exposure assessment.] | |||||||||||||
* Kurttio et al. 1999 [20] (Tables Six, Seven) | Areas in Finland with < 10% population with municipal drinking-water system | Incidence 1981-95 | N/A | Individual level ‘measured’ | Arsenic water concentration (μg˙•L-1): | 61:275 | age, sex, smoking | ||||||
< 0.1 | 23 | 1.0 | 8 | 1.0 | 8 | 1.0 | |||||||
1.1 -0.5 | 19 | 1.53 (0.75–3.09) | 4 | 0.95 (0.25–3.64) | 3 | 1.10 (0.19–6.24) | |||||||
≥ 0.5 | 19 | 2.44 (1.11–5.37) | 5 | 0.87 (0.25–3.02) | 7 | 10.3 (1.16–92.6) | |||||||
(log) continuous [Only subjects with drilled wells; median total arsenic concentration of 0.1 μg˙•L ; max.concentration of 64 μg˙•L and 1% exceeding 10 μg˙•L. Water sampled from wells used by the study population at least for 1967–80. Exposure in the 3rd-9th calendar year prior to cancer diagnosis. Residential history and drinking water consumption used in exposure assessment.] | 61 | 1.37 (0.95–1.96) | – | – | |||||||||
Chen et al. 2003 [91] (Table Two) | Southwestern Taiwan | Incidence 1996-99 | ICD9 188 | Individual level ‘estimated’ | Cumulative arsenic exposure (mg˙•L-1•year): | 49:224 | age, sex, BMI, cumulative arsenic exposure, cigarette smoking, hair dye usage, education | ||||||
0 – 2 | 30 | 1.0 | – | – | – | – | |||||||
> 2 – 12 | 4 | 0.6 (-1.1–3.0) | – | – | – | – | |||||||
> 12 | 10 | 1.86 (0.2–5.10) | – | – | – | – | |||||||
[Arsenic concentration in artesian well water from survey of 83,656 wells between 1974–76. Questionnaires used to determine village in which subjects lived 30 years ago. Residential history and duration and; source of drinking water used in exposure assessment.] | |||||||||||||
Steinmaus et al. 2003 [92] (Tables Three, Four) | 6 counties in Nevada; 1 county in California, USA | Incidence 1994-2000 | N/A | Individual level ‘estimated’ | Cumulative exposure to arsenic in water (mg˙•L-1•year): | 181:328 | OR for all participants adjusted for age, gender, occupation, smoking history (<1 pack per day (ppd), ≥1 ppd, former smoker, never smoker), income, education and race | ||||||
< 6.4 | 153 | 1.0 | 23 | 1.0 | 130 | 1.0 | |||||||
6.4 – 82.8 | 9 | 1.63 (0.64–4.13) | 3 | 2.65 (0.49–14.2) | 6 | 1.06 (0.34–3.33) | |||||||
> 82.8 | 19 | 1.40 (0.73–2.70) | 3 | 0.50 (0.12–2.05) | 13 | 2.25 (0.97–5.20) | |||||||
[Arsenic concentration from 7,000 samples from community and domestic wells. Results for a 40 years lagged exposure; 88.4% of cases and 91.8% of controls being exposed to arsenic levels ranging from 0 to 19 μg˙•L, respectively. Residential history, source of drinking water and intake used in exposure assessment.] | |||||||||||||
* Bates et al. 2004 [93] (Tables Two, Three) | Cordoba, Argentina | Incidence 1996-2000 | N/A | Individual level ‘measured’ | Arsenic water concentration (μg˙•L-1): | 114:114 | mate con bombilla consumption, education, and home tap-water consumption in all groups; and adjusted for the highest daily number of cigarettes subjects reported ever having smoked in the smoker group | ||||||
0–50 | 70 | 1.0 | 22 | 1.0 | 65 | 1.0 | |||||||
51–100 | 13 | 0.88 (0.3–2.3) | 2 | 1.05 (0.2–6.9) | 7 | 1.29 (0.3–5.0) | |||||||
101–200 | 22 | 1.02 (0.5–2.3) | 3 | 1.10 (0.2–6.3) | 10 | 0.96 (0.3–3.0) | |||||||
> 200 | 9 | 0.60 (0.2–1.7) | 1 | 0.58 (0.1–6.2) | 2 | 0.17 (0.0–1.0) | |||||||
[Average arsenic concentration of 5 years of highest exposure during the period 6–40 years before interview. On average, cases and controls had 25.7 and 25.6 years of well-water consumption, respectively; also approximately 50% of all well years were derived from proxy-well data. Results shown for transitional cell bladder cancer.] | |||||||||||||
Karagas et al. 2004 [94] (Table Two) | New Hampshire, USA | Incidence 1994-98 | N/A | Individual level ‘measured’ | Arsenic toenail concentration (μg˙•g-1): | 383:641 | age, sex, smoking status (ever/never) | ||||||
0.009–0.059 | 90 | 1.0 | 15 | 1.0 | 75 | 1.0 | |||||||
0.060–0.086 | 119 | 1.37 (0.96–1.96) | 20 | 0.85 (0.38–1.91) | 99 | 1.53 (1.02–2.29) | |||||||
0.087–0.126 | 88 | 1.08 (0.74–1.58) | 22 | 1.18 (0.53–2.66) | 66 | 1.02 (0.66–1.56) | |||||||
0.127–0.193 | 48 | 1.04 (0.66–1.63) | 11 | 1.10 (0.42–2.90) | 37 | 1.00 (0.60–1.67) | |||||||
0.194–0.277 | 2 | 1.33 (0.71–2.49) | 3 | 0.49 (0.12–2.05) | 18 | 1.78 (0.86–3.67) | |||||||
0.278–0.330 | 3 | 0.41 (0.11–1.50) | 0 | – | 3 | 0.50 (0.13–1.88) | |||||||
0.331–2.484 | 14 | 1.36 (0.63–2.90) | 0 | – | 14 | 2.17 (0.92–5.11) | |||||||
[Levels of arsenic in toenails reflect exposures occurring between 9–15 months prior to sample collection. On average cases and controls had 16.5 and 17.2 years exposure to their water system. Results shown for transitional cell bladder cancer.] | |||||||||||||
Michaud et al. 2004 [95] (Table Two) | Southwestern Finland | Incidence 1985-99 | ICD9 188, 233.7 | Individual level ‘measured’ | Arsenic toenail concentration (μg˙•g-1): | 280:293 | age, toenail collection date, intervention group, number of cigarettes per day, and number of years smoking | ||||||
< 0.105 | – | – | – | – | 136 | 1.0 | |||||||
0.105–0.160 | – | – | – | – | 73 | 1.10 (0.73–1.64) | |||||||
0.161–0.259 | – | – | – | – | 37 | 0.93 (0.56–1.54) | |||||||
0.260–0.399 | – | – | – | – | 20 | 1.38 (0.68–2.80) | |||||||
> 0.399 | – | – | – | – | 14 | 1.14 (0.52–2.51) | |||||||
† Pu et al. 2007 [51] (Tables Four, Five) | Taiwan | Incidence 2002-04 | N/A | Individual level ‘measured’ | Arsenic urine concentration (μg˙•g-1 creatine): | 177:313 | OR (all participants): age, sex, education, parents’ ethnicity, alcohol drinking, pesticides use | ||||||
≤ 15.4 | 24 | 1.0 | – | – | – | – | |||||||
15.5–26.4 | 44 | 1.9 (1.1–3.4) | – | – | – | – | |||||||
>26.4 | 109 | 5.3 (3.1–9.0) | – | – | – | – | |||||||
≤ 20.3 | – | – | 17 | 1.0 | 21 | 1.0 | OR (never/ever smokers): age, sex | ||||||
≥ 20.3 | – | – | 68 | 4.4 (2.3–8.5) | 61 | 8.2 (3.8–17.8) | |||||||
[Smokers include current and former smokers. Non-smokers with ≤ 20.3 (μg˙•g-1 creatine) was used as referent category.] | |||||||||||||
*†Meliker et al. 2010 [87] (Table Three) | 11 counties of Southeastern Michigan, USA | Incidence 2000-04 | N/A | Individual level ‘measured’ | Arsenic water concentration (μg˙•L-1): | 411:566 | age, sex, race, smoking history, education, history of employment in high risk occupation, family history of bladder cancer | ||||||
< 1 | 187 | 1.0 | – | – | – | – | |||||||
1–10 | 182 | 0.84 (0.63–1.12) | – | – | – | – | |||||||
> 10 | 38 | 1.10 (0.65–1.86) | – | – | – | – | |||||||
[Arsenic water concentrations obtained from: 6,050 private untreated wells sampled between 1993–2002; 371 well water measurements from participants’ current residence and; 1,675 measurements from public well water supplies collected between 1983–2004, which were used to estimate arsenic concentrations at past residences.] | |||||||||||||
*†Steinmaus et al. 2013 [67] (Table Two) | Region I and II, northern Chile | Incidence 2007-10 | N/A | Individual level ‘estimated’ | Arsenic water concentration (μg˙•L-1): | 306:640 | no covariates assessed, although subjects were frequency matched on age, sex | ||||||
0–59 | 23 | 1.0 | – | – | – | – | |||||||
60–199 | 27 | 0.84 (0.46–1.52) | – | – | – | – | |||||||
200–799 | 60 | 2.50 (1.48–4.22) | – | – | – | – | |||||||
> 800 | 122 | 4.44 (2.75–7.15) | – | – | – | – | |||||||
[Each city/town of residence in which each subject lived was linked to a water arsenic measurement for that city/town so that an arsenic concentration could be assigned to each year of each subject’s life. Study also present OR in relation to various metrics of arsenic exposure such as lifetime and cumulative average exposure and; lifetime and cumulative intake. Residential history used in exposure assessment.] |