Back in the days when drinking water epidemiology studies were useful, this type of study would not have gotten off the ground because exposure is not directly measured. Why is this important? Because if enough assumptions are made using computer models an association can be found just about anywhere between anything. And that looks to be what has happened here. These authors in many respects have simply ended up assuming their way to the desired conclusion without realizing it. Having said that, it is reasonable to expect arsenic exposure to have a role in CHD and the Alamosa area is known for high ground water arsenic concentrations. (The town of Alamosa now has treatment for arsenic removal.) At issue is whether there is an effect at concentrations below 50 ug/L (the old limit) or even 10 ug/L (the new standard). As with the Alan Smith internal cancer study in 1991, advocates will grab on to this study to make alarming political statements.
As a side note, whether funding was provided for the study (and if so from who) really has no role in defining the credibility of the study. The authors state they were not financially supported. But this is irrelevant. Of most importance are the assumptions behind the analysis many of which are unstated. And of course, if they are employed someone pays them for their work. A lot of work went into this study and some aspects are useful. The weakness is in the underlying data, analysis and interpretation. Data and analysis are not neutral. The presuppositions and assumptions of the researchers define the outcome.
Finally, EHP is government funded and run publication that generally publishes papers from a particular point of view regardless of the strength of the study.
James KA, Byers T, Hokanson JE, Meliker JR, Zerbe GO, Marshall JA. Association between Lifetime Exposure to Inorganic Arsenic in Drinking Water and Coronary Heart Disease in Colorado Residents. Environ Health Perspect. 2014 Oct 28.
BACKGROUND: Chronic diseases, including coronary heart disease, have been associated with ingestion of drinking water with high levels of inorganic arsenic (over 1000 μg/L). However, associations have been inconclusive in populations with lower levels (<100 μg/L) of inorganic arsenic exposure.
OBJECTIVES: We conducted a case-cohort study based on individual estimates of lifetime arsenic exposure to examine the relationship between chronic low-level arsenic exposure and risk of CHD.
METHODS: This study included 555 participants with 96 CHD events diagnosed between 1984 and 1998 for which individual lifetime arsenic exposure estimates were determined using data from structured interviews and secondary data sources to determine lifetime residence which was linked to a, geospatial model of arsenic concentrations in drinking water, which were correlated with historically collected urinary arsenic concentrations. A Cox proportional hazards model with time-dependent CHD risk factors was used to assess the association between lifetime exposure to low-level inorganic arsenic in drinking water and incident CHD.
RESULTS: We estimated a positive association between low-level inorganic arsenic exposure and CHD risk (Hazard Ratio (HR): =1.38, 95%=1.09 1.78 per 15 μg/L) while adjusting for age, gender, first-degree family history of CHD, and serum low density lipoprotein levels. The risk of CHD increased monotonically with increasing TWAs for inorganic arsenic exposure in water relative to < 20 μg/L (HR=1.2; 95% CI: 0.6, 2.2 for 20-30 μg/L, HR=2.2; 95% CI: 1.2, 4.0 for 30-45 μg/L, and HR=3; 95% CI: 1.1, 9.1 for 45-88 μg/L).
CONCLUSIONS: Lifetime exposure to low-level inorganic arsenic in drinking water was associated with increased risk for CHD in this population.
The study is here.