Tag Archives: epidemiology

Dose-response meta-analysis of lung cancer risk and inorganic arsenic

Yuan T, Zhang H, Chen B, Zhang H, Tao S. Association between lung cancer risk and inorganic arsenic concentration in drinking water: a dose-response meta-analysis. Toxicol Res (Camb). 2018 Sep 18;7(6):1257-1266. doi: 10.1039/c8tx00177d.

High dose arsenic in drinking water (≥100 μg L-1) is known to induce lung cancer, but lung cancer risks at low to moderate arsenic levels and its dose-response relationship remains inconclusive. We conducted a systematic review of cohort and case-control studies that quantitatively reported the association between arsenic concentrations in drinking water and lung cancer risks by searching the PubMed database till June 14, 2018. Pooled relative risks (RRs) of lung cancer associated with full range (10 μg L-1-1000 μg L-1) and low to moderate range (<100 μg L-1) of water arsenic concentrations were calculated using random-effects models. A dose-response meta-analysis was performed to estimate the pooled associations between restricted cubic splines of log-transformed water arsenic and the lung cancer risks. Fifteen studies (9 case-control and 6 cohort studies) involving a total of 218 481 participants met the inclusion criteria. Meta-analysis identified significantly increased risks of lung cancer on exposure to both full range (RR = 1.21; 95% confidence interval [CI] = 1.05-1.37; heterogeneity I 2 = 54.3%) and low to moderate range (RR = 1.18; 95%CI = 1.00-1.35; I 2 = 56.3%) of arsenic-containing water. In the dose-response meta-analysis of eight case-control studies, we found no evidence of non-linearity, although statistical power was limited. The corresponding pooled RRs and their 95%CIs for exposure to 10 μg L-1, 50 μg L-1, and 100 μg L-1 water arsenic were 1.02 (1.00-1.03), 1.10 (1.04-1.15), and 1.20 (1.08-1.32), respectively. We provide evidence on the association between increased lung cancer risks and inorganic arsenic in drinking water across low, moderate and high levels. Minimizing arsenic levels in drinking water may be of public health importance.

Opportunities to reduce global cholera

Legros D; Partners of the Global Task Force on Cholera Control. Global Cholera Epidemiology: Opportunities to Reduce the Burden of Cholera by 2030. The Journal of infectious diseases. 2018 Sep 1. doi: 10.1093/infdis/jiy486.

While safe drinking water and advanced sanitation systems have made the Global North cholera-free for decades, the disease still affects 47 countries across the globe resulting in an estimated 2.86 million cases and 95,000 deaths per year worldwide. Cholera impacts communities already burdened by conflict, lack of infrastructure, poor health systems, and malnutrition. In October 2017, the Global Task Force on Cholera Control (GTFCC) launched an initiative titled Ending Cholera: A Global Roadmap to 2030, with the objective to reduce cholera deaths by 90% worldwide, and eliminate cholera in at least 20 countries by 2030. The GTFCC is working to position cholera control not as a vertical programme but instead using cholera as a marker of inequity and an indicator of poverty, linking the objectives of the Roadmap to the SDGs. The roadmap consists of targeted multi-sectoral interventions, supported by a coordination mechanism, along 3 axes: (1) early detection and quick response to contain outbreaks; (2) a multisectoral approach to prevent cholera recurrence in hotspots; (3) an effective partnership mechanism of coordination for technical support, countries capacity building, research and M&E, advocacy and resource mobilization. Every case and every death from cholera is preventable with the tools we have today.

PM2.5 not likely associated with premature deaths

James E. Enstrom. Scientific Distortions in Fine Particulate Matter Epidemiology. Journal of American Physicians and Surgeons Volume 23 Number 1 Spring 2018

The theoretical prevention of premature deaths from the inhalation of fine particulate matter is being used by the U.S. Environmental Protection Agency (EPA) to justify the National Ambient Air Quality Standard (NAAQS) and multibillion dollar regulations across the U.S., including the EPA Clean Power Plan and the California Air Resources Board (CARB) Truck and Bus Regulation. The epidemiology is severely flawed. Fine particulates probably make no significant contribution to premature mortality in the U.S. The publication of null findings has been blocked or marginalized and studies claiming excess mortality need to be reassessed. click here

Total THM long-term exposure not related to female breast cancer, Spain

Font-Ribera L, Gràcia-Lavedan E, Aragonés N, Pérez-Gómez B, Pollán M, Amiano P, Jiménez-Zabala A, Castaño-Vinyals G, Roca-Barceló A, Ardanaz E, Burgui R, Molina AJ, Fernández-Villa T, Gómez-Acebo I, Dierssen-Sotos T, Moreno V, Fernandez-Tardon G, Peiró R, Kogevinas M, Villanueva CM. Long-term exposure to trihalomethanes in drinking water and breast cancer in the Spanish multicase-control study on cancer (MCC-SPAIN). Environment international. 2017 Dec 28;112:227-234. doi: 10.1016/j.envint.2017.12.031.

BACKGROUND: Exposure to trihalomethanes (THMs) in drinking water has consistently been associated with an increased risk of bladder cancer, but evidence on other cancers including the breast is very limited.

OBJECTIVES: We assessed long-term exposure to THMs to evaluate the association with female breast cancer (BC) risk.

METHODS: A multi case-control study was conducted in Spain from 2008 to 2013. We included 1003 incident BC cases (women 20-85 years old) recruited from 14 hospitals and 1458 population controls. Subjects were interviewed to ascertain residential histories and major recognized risk factors for BC. Mean residential levels of chloroform, brominated THMs (Br-THMs) and the sum of both as total THM (TTHMs) during the adult-lifetime were calculated.

RESULTS: Mean adult-lifetime residential levels ranged from 0.8 to 145.7μg/L for TTHM (median=30.8), from 0.2 to 62.4μg/L for chloroform (median=19.7) and from 0.3 to 126.0μg/L for Br-THMs (median=9.7). Adult-lifetime residential chloroform was associated with BC (adjusted OR=1.47; 95%CI=1.05, 2.06 for the highest (>24μg/L) vs. lowest (<8μg/L) quartile; p-trend=0.024). No association was detected for residential Br-THMs (OR=0.91; 95%CI=0.68, 1.23 for >31μg/L vs. <6μg/L) or TTHMs (OR=1.14; 95%CI=0.83, 1.57 for >48μg/L vs. <22μg/L).

CONCLUSIONS: At common levels in Europe, long-term residential total THMs were not related to female breast cancer. A moderate association with chloroform was suggested at the highest exposure category. This large epidemiological study with extensive exposure assessment overcomes several limitations of previous studies but further studies are needed to confirm these results.

Taiwan Arsenic Study of Limited Value

The confidence intervals on the data analysis presented here are very wide. A lower confidence interval of 1 indicates no effect. Studies such as this showing no association or a weak association are of very limited usefulness.

Hsu LI, Hsieh FI, Wang YH, Lai TS, Wu MM, Chen CJ, Chiou HY, Hsu KH. Arsenic Exposure From Drinking Water and the Incidence of CKD in Low to Moderate Exposed Areas of Taiwan: A 14-Year Prospective Study. Am J Kidney Dis. 2017 Aug 23. pii: S0272-6386(17)30800-4. doi: 10.1053/j.ajkd.2017.06.012.

BACKGROUND: Arsenic exposure is associated with decreased kidney function. The association between low to moderate arsenic exposure and kidney disease has not been fully clarified.

STUDY DESIGN: The association between arsenic exposure from drinking water and chronic kidney disease (CKD) was examined in a long-term prospective observational study.

SETTING & PARTICIPANTS: 6,093 participants 40 years and older were recruited from arseniasis-endemic areas in northeastern Taiwan. Arsenic levels were 28.0, 92.8, and 295.7μg/L at the 50th, 75th, and 90th percentiles, respectively.

PREDICTOR: Well-water arsenic and urinary total arsenic (inorganic plus methylated arsenic species) concentrations, adjusted for urinary creatinine concentration.

OUTCOMES: Kidney diseases (ICD-9 codes: 250.4, 274.1, 283.11, 403.*1, 404.*2, 404.*3, 440.1, 442.1, 447.3, or 580-589) and CKD (ICD-9 code: 585) ascertained using Taiwan’s National Health Insurance database 1998 to2011.

MEASUREMENTS: HRs contrasting CKD risk across arsenic exposure levels were estimated using Cox regression. Prevalence ORs for proteinuria (protein excretion ≥ 200mg/g) comparing quartiles of total urinary arsenic concentrations were estimated using logistic regression.

RESULTS: We identified 1,104 incident kidney disease cases, including 447 CKD cases (incidence rates, 166.5 and 67.4 per 104 person-years, respectively). A dose-dependent association between well-water arsenic concentrations and kidney diseases was observed after adjusting for age, sex, education, body mass index, cigarette smoking, alcohol consumption, and analgesic use. Using arsenic concentration ≤ 10.0μg/L as reference, multivariable-adjusted HRs for incident CKD were 1.12 (95% CI, 0.88-1.42), 1.33 (95% CI, 1.03-1.72), and 1.33 (95% CI, 1.00-1.77) for arsenic concentrations of 10.1 to 49.9, 50.0 to 149.9, and ≥150.0μg/L, respectively (P for trend=0.02). The association between arsenic concentration and kidney diseases was stronger for women (P for interaction=0.06). Arsenic values in the range of 50th to 75th and 75th to 100th percentiles of total urinary arsenic concentrations were associated with 50% and 67% higher prevalences, respectively, of proteinuria.

LIMITATIONS: Kidney diseases and CKD outcomes were based on diagnostic codes. Glomerular filtration rates were not available. Other heavy metals were not measured.

CONCLUSIONS: This study describes the temporal relationship between arsenic concentrations ≥ 10μg/L in drinking water and CKD. A dose-dependent association between well-water arsenic concentration and kidney diseases was observed. Higher creatinine-adjusted urinary total arsenic concentrations were associated with a higher prevalence of proteinuria.

Ohio Arsenic Study Exposure Assessment Inadequate, Inconclusive

Alarming as this study may appear, it is simply another in a long line of weak ecologic studies examining birth outcomes and drinking water that rely on an inadequate exposure assessment. The exposure was not directly measured and is unknown. In studies such as this statistical manipulations simply cannot reliably compensate for an inadequate assessment of contaminant exposure.

Almberg KS, Turyk ME, Jones RM, Rankin K, Freels S, Graber JM, Stayner LT. Arsenic in drinking water and adverse birth outcomes in Ohio. Environ Res. 2017 May 15;157:52-59. doi: 10.1016/j.envres.2017.05.010.

BACKGROUND: Arsenic in drinking water has been associated with adverse reproductive outcomes in areas with high levels of naturally occurring arsenic. Less is known about the reproductive effects of arsenic at lower levels.

OBJECTIVES: This research examined the association between low-level arsenic in drinking water and small for gestational age (SGA), term low birth weight (term LBW), very low birth weight (VLBW), preterm birth (PTB), and very preterm birth (VPTB) in the state of Ohio.

METHODS: Exposure was defined as the mean annual arsenic concentration in drinking water in each county in Ohio from 2006 to 2008 using Safe Drinking Water Information System data. Birth outcomes were ascertained from the birth certificate records of 428,804 births in Ohio from the same time period. Multivariable generalized estimating equation logistic regression models were used to assess the relationship between arsenic and each birth outcome separately. Sensitivity analyses were performed to examine the roles of private well use and prenatal care utilization in these associations.

RESULTS: Arsenic in drinking water was associated with increased odds of VLBW (AOR 1.14 per µg/L increase; 95% CI 1.04, 1.24) and PTB (AOR 1.10; 95% CI 1.06, 1.15) among singleton births in counties where <10% of the population used private wells. No significant association was observed between arsenic and SGA, or VPTB, but a suggestive association was observed between arsenic and term LBW.

CONCLUSIONS: Arsenic in drinking water was positively associated with VLBW and PTB in a population where nearly all (>99%) of the population was exposed under the current maximum contaminant level of 10µg/L. Current regulatory standards may not be protective against reproductive effects of prenatal exposure to arsenic.

Atrazine in Drinking Water Not Associated with Overian Cancer, Iowa

Inoue-Choi M, Weyer PJ, Jones RR, Booth BJ, Cantor KP, Robien K, Ward MH Atrazine in public water supplies and risk of ovarian cancer among postmenopausal women in the Iowa Women’s Health Study. Occupational and Environmental Medicine. 2016 Jul 1. pii: oemed-2016-103575. doi: 10.1136/oemed-2016-103575.

BACKGROUND: Few studies have evaluated environmental chemical exposures in relation to ovarian cancer. We previously found an increased risk of ovarian cancer among postmenopausal women in Iowa associated with higher nitrate levels in public water supplies (PWS). However, elevated nitrate levels may reflect the presence of other agricultural chemicals, such as atrazine, one of the most commonly detected pesticides in Iowa PWS.

METHODS: We evaluated the association between atrazine in drinking water and incident ovarian cancer (N=145, 1986-2010) among 13 041 postmenopausal women in the Iowa Women’s Health Study who used their PWS for ≥11 years as reported in 1989. Average levels of atrazine (1986-1987), nitrate-nitrogen (NO3-N, 1955-1988) and estimated levels of total trihalomethanes (TTHM, 1955-1988) from PWS monitoring data were linked to the participants’ cities of residence. We computed HRs and 95% CIs by categories of the average atrazine level (not detected, ≤ or >0.37 parts per billion=median) using Cox proportional hazards regression adjusting for ovarian cancer risk factors.

RESULTS: Atrazine was detected in water samples from 69 cities where 4155 women (32%) lived and levels were moderately correlated with NO3-N (ρ=0.35) and TTHM (ρ=0.24). Atrazine levels were not associated with ovarian cancer risk with or without adjusting for NO3-N and TTHM levels (p-trend=0.50 and 0.81, respectively). Further, there was no evidence for effect modification of the atrazine association by NO3-N or TTHM levels.

CONCLUSIONS: In our study with low atrazine detection rates, we found no association between atrazine in PWS and postmenopausal ovarian cancer risk.