Obesity Research and Resources

Obesity's impact is now worldwide. On this page, we share information about environmental contributors to the obesity epidemic.

graphic based on data from the World Health Organization, ©CHE

Prevalence and Trends

Obesity has more than doubled worldwide between 1980 and 2014. Most of the world's population live in countries where overweight and obesity kill more people than underweight, according to the World Health Organization (WHO).1

The rates of obesity in the United States reflect this global trend, with adult rates doubling since 1970.2 Currently over one-third of adults in the US are obese.3

obesity prevalence in the US

Race and Ethnicity. Race and ethnicity influence the risk of obesity in the United States, with non-Hispanic blacks and Mexican-Americans experiencing higher rates.4


Body Mass Index

Obesity is generally indicated by body mass index (BMI), calculated as weight (mass) in kilograms divided by height in meters squared. Calculate your BMI on the National Heart, Lung and Blood Institute website.5 This measure is not always accurate in diagnosing obesity, but it is useful for public health screening.

Obese individuals are at risk for a variety of health problems including these:6

Environmental Contributors

Many factors are known to contribute to obesity, including both chemical exposures and lifestyle factors, which we discuss here in turn.

Toxic Chemical Exposures

Chemicals that promote fat development are referred to as obesogens. According to the National Institute of Environmental Health Sciences (NIEHS), these exposures do not cause obesity directly, but are thought to increase an individual’s susceptibility for gaining weight, especially when exposure occurs during development.9

Here we summarize what we know about obesogenic chemicals, grouped by the strength of evidence10 (all references are from Heindel et al.11 unless otherwise noted):

 Chemical  Sources of Exposure Effects   

Strong Evidence


DDT is a pesticide used to kill mosquitos; the body metabolizes it into DDE. Prenatal DDE is associated with increased infant growth.

Air pollution


Combustion of fuels (diesel exhaust and biomass), dust and other contaminants in air Increases fat and inflammation in adolescents whose mothers were exposed.

Tobacco smoke


First-hand and Second-hand Smoking during pregnancy is strongly associated with the child's obesity.
Good Evidence
Flame retardants

Chemicals applied to furniture, electronics, children’s clothing, foam, and insulation Increased rate of fat accumulation.
Pesticides13 Chemicals used to control weeds, insects, and other unwanted organisms; widely used in homes, schools, and businesses as well as in agriculture. Affect pancreatic function, cause abnormalities in lipid metabolism; promote obesity in response to increased dietary fat.

Endocrine Disrupting Chemicals

Many of the chemicals discussed here are part of a group called endocrine disrupting chemicals (EDCs). These chemicals interfere with the human body’s hormones, disrupting their process and effects. Obesogenic EDCs are thought to stimulate fat storage and negatively impact metabolism by disrupting the hormones involved in appetite control through multiple mechanisms.14 See the EDCs webpage.

Limited or conflicting evidence regarding other toxicants' links to obesity are listed in CHE's Toxicant and Disease Database.

Lifestyle Factors

Diet and Exercise. An energy-dense diet, and especially foods high in fat and/or sugar,15 and lack of exercise and physical activity are strongly associated with obesity.16

Modern society has reworked our systems of food and agriculture to make unhealthy food choices both more available and less expensive than healthier foods (see the Food and Agriculture Environment webpage). Many of our neighborhoods, our transportation systems, our work and school environments, and our recreational activities have likewise been altered or engineered to promote less physical activity as the norm in our lives17 (see the Built Environment webpage).

Governmental interest in addressing obesity is increasing, in part because of the huge economic and societal costs. Government actions include these:

Sleep and Stress. Evidence also links both sleep and stress to obesity.24 Research has found a strong association between individuals' working night shifts and increased body weight,25 with some evidence that poor sleep quality causes negative changes in metabolic, inflammatory, neuroendocrine, and antioxidant biomarkers.26 See our Psychosocial Environment page for more information on the effects of stress on health.

Genetics and Epigenetic Programming

Genes play a role in obesity, causing some obesity disorders. However, having a specific gene variant, or set of variants, does not always mean that an individual will be obese. Often with genetic components of diseases and disorders, an individual's environment—nutrition, activity, chemical exposures, sleep quality and so on—can either promote or inhibit the physical expression of genes.

The term "epigenetic programming" refers to mechanisms that can turn on or off genes or sections of chromosomes, changing their functioning. These changes are maintained as the cell replicates, and some research has shown that these changes can pass down to offspring. Changes in a fetus's genes by the mother's nutritional status during pregnancy are an example of epigenetic programming.27 See the Gene-Environment Interactions webpage.

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Other Environmental Factors

Mother's Nutrition. Severe undernourishment (famine) by a pregnant woman has been associated with an increased risk of obesity in her child. When the mother is malnourished, the baby's genes involved with appetite regulators, pancreatic development, and obesity-associated genes can be affected, and these changes can last throughout the child's life.28

Maternal obesity also increases the risk of developing insulin resistance and has been associated with an increased risk of large gestational weight, fat accumulation, and type 2 diabetes in youth.29

Socioeconomic Status. From 1999-2010, higher educational attainment has consistently been associated with a lower risk of obesity in white women. The association is less clear or consistent in men and non-white women.30 A similar pattern was found in an earlier report that included income: The prevalence of obesity in white, non-Hispanic females of all ages falls as family income rises. A similar association was found in white, non-Hispanic males aged 2-19, but the association is weak or even reversed in other groups.31 Thus there is some connection between income, educational attainment and risk of obesity, but it is not always consistent or conclusive. See CHE's Socioeconomic Environment webpage.

Research has found that low-income communities and communities of color have more limited access to healthful foods than other communities.32

Costs of Obesity

chart showing medical costs of obesity


data from Cawley et al.33

Studies estimating costs of obesity-related illness in the United States show total costs in the billions. Studies in 200934 and 201135 estimate medical costs to be between $147 billion and $190 billion per year. This accounts for roughly 20% of US annual health expenditures.

These estimates do not include many indirect costs of obesity, such as work absences, decreased productivity while at work, and premature mortality and disability.36 An economic review of obesity discovered that obesity has overtaken cigarette smoking as the most costly and detrimental preventable disease.37

Ethical Considerations

Obesity is a complex issue that involves many aspects of society. To best prevent the development of obesity and to support those that are obese, community responsibility must be addressed along with individual choices. Community, governmental and societal actions will be needed to provide health-promoting food options, encourage physical activity, educate the public, and regulate the foods and chemicals that are associated with obesity.

See more about environmental contributors to obesity in the list of CHE publications and Dig Deeper resources in the right sidebar.

This page was last revised by student intern Jessica Hale and Nancy Hepp, with review by Sarah Howard, in August 2016.

CHE invites our partners to submit corrections and clarifications to this page. Please include links to research to support your submissions through the comment form on our Contact page.

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