Introduction

Tobacco smoke and tobacco products, such as cigars, pipes, and smokeless tobacco, contain many harmful and potentially harmful constituents (HPHC) [1, 2] that affect different organ systems and physiological processes in a tissue-specific manner. Smoking is reported to be a risk factor for type 2 diabetes mellitus [3, 4]. Furthermore, the most recent Surgeon General’s report concluded that smoking is a cause of type 2 diabetes and that the risk of developing type 2 diabetes increases with the cumulative number of cigarettes smoked [5] and this idea has been supported by several meta-analysis as well [6, 7]. In fact, compared with non-smokers, current smokers have been reported to have a 30–40% increased risk of type 2 diabetes [5]. Less is currently understood about other forms of tobacco relationship with type 2 diabetes, but there are some reported links to an increased risk for type 2 diabetes [8, 9]. Multiple mechanisms of tobacco exposure’s causation of diabetes have been proposed, including that tobacco exposure directly causes insulin resistance [10, 11].

The relationship between tobacco use and insulin resistance may be confounded by multiple associated variables. For example, Insulin resistance is often associated with an increase body habitus and increased BMI is a known risk factor for diabetes [12]. Smoking has also been linked to an overall lower BMI than that seen in non-smokers [13] however, smoking has be linked to increased central adiposity [11]. The increase in central adiposity may contribute to insulin resistance and diabetes proposed in smokers [11]. Moreover, there is evidence of different patterns of insulin resistance based on race [14] and gender [15]. Furthermore, smoking trends differ between race/ethnicity and genders, which may create different exposure patterns based on race/ethnicity or gender leading to different patterns of IR or incident diabetes. Of note the Hispanic/Latino populations tend to have low rates of smoking [16] while African American populations tend to have greater use of cigarettes that contain menthol [17].

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Temporal trends in tobacco use may also influence the association of IR and incident diabetes. Over the decades the changing composition of cigarettes including the introduction of filters on cigarettes in the mid to late 1950’s which did not gain popularity until the 1980’s [18] and introduction of low tar cigarettes in the 1980’s [19]. Moreover, curing of tobacco and flavoring of tobacco affects the amount and type of HPHC in the product [20, 21], therefore different tobacco use patterns lead to varying exposure to these HPHC’s. There is little research into how these different HPHC’s impact IR and incident diabetes between races.

Indeed, there is a body of evidence showing no relationship between tobacco use and IR or incident diabetes. Current research demonstrates heterogeneity in the association between smoking and glycated hemoglobin (HbA1c) levels, fasting blood glucose levels and 2 hour- post-challenge glycaemia (2H-PG) [22–25]. Furthermore it has been suggested the effect of smoking is not seen in lean individuals, instead only in obese men [26]. Two meta-analysis used to support the causal relationship between tobacco use and diabetes show considerable heterogeneity in the evidence used to complete the study [5, 6]. Indeed, extant meta-analyses used prior studies that often examined the association of smoking and type 2 diabetes in participants of similar race and gender, typically Caucasian males [5, 7].

In light of the heterogeneity of evidence available we aimed to identify whether the association between tobacco use IR and type 2 diabetes suggested in previous studies is also evident in large well characterized multi-ethnic cohort with multiple validated markers of insulin resistance (IR). Moreover, we sought to identify if there were markers of IR sensitive to smoking that may help identify a group of tobacco product users who are at an increased risk of type 2 diabetes. Identifying IR and incident diabetes risk in these in a contemporary multi-ethnic population seemed important as tobacco exposure patterns and metabolism of tobacco differs by race [27–30], and gender, [25, 28, 31]. We therefore examined the relationship between tobacco exposure, cross-sectional insulin resistance (IR) at baseline, and prospective incident type 2 diabetes over the course of 10 years in a contemporary multi-ethnic cohort.