Introduction

Chemical exposure has been linked to obesity and type 2 diabetes (T2DM) development and thus may also limit success of weight loss diets for obesity and T2DM management.

Aims

We aimed to determine the effect of environmental chemical exposure on mass loss and glycaemic control during diet-induced weight management.

Method

We systematically searched PubMed, Web of Knowledge, and Scopus. Study selection, screening and data extraction followed preferred reporting items for systematic review and meta analysis (PRISMA) guidelines. The protocol is registered in PROSPERO (CRD42022339993). Independent selection and screening were performed by 2 evaluators. Risk of bias was performed using established tools and nested meta-analysis of comparable studies performed using the rma.mv function in the metafor package in R.

Results

We retrieved 178 unique records from databases, and 34 from citing and cited papers. Six papers directly examined impacts of environmental contaminant exposure on diet-induced weight loss and/or glycaemic control in humans and five in animals. One targeted people with T2DM. In humans, one paper linked phthalates and parabens, but not bisphenols, with slower fat loss. Two showed per- and polyfluoroalkyl substances (PFAS) were not associated with mass loss, but with faster subsequent mass regain. One explored BMI improvements in relation to air pollutants. Two papers reported weight loss-induced elevation in plasma organochlorines associated with altered glycaemic control. There were insufficient papers on any one contaminant group to perform meta-analyses for human studies. Risk of bias was moderate to serious , primarily from potential for deviation from intended diet, and statistics and reporting.

In rodents, high fat diet was used to induce obesity and impaired glycaemic control. One paper examined PFAS, one examined the organochlorine pesticide, dichloro-diphenyl-trichloroethane (DDT), and three explored polychlorinated biphenyl 77 (CB77). Perfluro-octane sulphonate (PFOS) impaired glycaemic control, but not weight loss, in obese male C57BL/6 mice. DDT did not impair weight loss in Sprague Dawley rats. CB77 did not affect final mass of C57BL/6 mice after four weeks of calorie restriction (standardised mean difference = -0.35 [-0.87, 0.18]; n = 5 (experiments); n = 3 (papers)), but impaired glucose control in glucose tolerance tests (standardised mean difference = -1.30 [-1.80, -0.79]; n = 6 (experiments); n = 3 (papers)) and insulin tolerance tests (standardised mean difference = -1.54 [-2.32, -0.77] n = 3 (experiments); n = 2 (papers)). Heterogeneity was low and did not differ between animal models (I²= 0; tau² = 0; p > 0.1) but experiments on CB77 were underpowered and came from the same research group. All studies were at moderate to serious risk of bias, largely due to lack of reported detail.

Conclusions

Human and animal studies suggest some chemical groups, especially PCB and PFAS, could impair management of body mass and glucose control, but the evidence is sparse and at high risk of bias. Studies that robustly address whether chemical exposure can impair weight loss and resumption of glycaemic control are urgently needed to help determine whether chemical exposure history should be considered when delivering care for obesity and T2DM.